| 95332324 | ing tyrosine kinase Syk. In contrast, integrin ligation with antibodies induces | tyrosine phosphorylation | of Syk but not of FAK or paxillin. In adhering cells, pre-treatment with cytoch |
| 95332324 | AK or paxillin. In adhering cells, pre-treatment with cytochalasin D suppresses | tyrosine phosphorylation | of FAK and paxillin but not of Syk, while IL-1 beta message induction is unaffe |
| 96085174 | sm of several cytokines. IL-7 was observed to induce a rapid and dose-dependent | tyrosine phosphorylation | of Jak 1 and Jak 3 and concomitantly, the tyrosine phosphorylation and DNA bind |
| 96085174 | se-dependent tyrosine phosphorylation of Jak 1 and Jak 3 and concomitantly, the | tyrosine phosphorylation | and DNA binding activity of multiple STAT proteins. The STAT proteins utilized |
| 96329553 | ophages by culture in macrophage-CSF ( M-CSF ) , we measured the GM-CSF induced | tyrosine phosphorylation | of STAT5A, STAT5B, and any lower molecular weight STAT5 isoforms. Freshly isola |
| 97054651 | ol 12 myristate 13-acetate treatment had weak effects on proliferation. Rather, | tyrosine phosphorylation | was shown to be directly involved in mediating CD40-dependent signals. The use |
| 97207294 | lly, we detected signal transducers and activators of transcription 6 ( STAT6 ) | tyrosine phosphorylation | and DNA binding activity in X-SCID B cells with a wide range of gammac mutation |
| 99168986 | tivate binding of STAT5 to the high-affinity IFP53 GAS site. IFN-alpha enhanced | tyrosine phosphorylation | of STAT1, STAT3, STAT4, STAT5a, and STAT5b. IL-12 induced STAT4 and IL-2 and IL |
| 99305241 | crophage colony-stimulating factor ( GM-CSF ) and interleukin ( IL ) -3 induced | tyrosine phosphorylation | of 92-kDa protein in normal human monocytes. We identified this 92-kDa protein |
| 99305241 | nyl-leucyl-phenylalanine ( FMLP ) and phorbol myristate acetate ( PMA ) induced | tyrosine phosphorylation | of 42- and 44-kDa proteins, which were identified as extracellular signal-regul |
| 99305241 | ocytes. In marked contrast to neutrophils and MO7e cells, GM-CSF did not induce | tyrosine phosphorylation | and activation of ERK in monocytes. Among upstream signaling molecules of ERK, |
| 95261059 | monocytic and neutrophilic cells. PU.1 is expressed at highest levels in mature | human monocytes | and human peripheral blood neutrophils. In contrast to PU.1, significant levels |
| 96075792 | ts were designed to analyse in detail the priming effect on the LPS response in | human monocytes | . Priming by IFN-gamma was primarily manifested at the level of TNF mRNA accumul |
| 96329553 | ne the activation of the STAT5 homologues and lower molecular weight variant in | human monocytes | and monocytes differentiated into macrophages by culture in macrophage-CSF ( M- |
| 97162234 | Nuclear factor-kappa B activation in | human monocytes | stimulated with lipopolysaccharide is inhibited by fibroblast conditioned mediu |
| 97162234 | ibit both TNF mRNA accumulation and protein release in peripheral blood-derived | human monocytes | ( PBM ) stimulated with lipopolysaccharide ( LPS ) . In this study we have inve |
| 99228708 | an important mediator of septic shock. Endotoxin ( LPS ) signal transduction in | human monocytes | leads to activation of nuclear factor-kappa B ( NF-kappa B ) and TNF-alpha rele |
| 99228708 | B DNA binding and TNF-alpha release in human monocytes. MATERIALS AND METHODS: | Human monocytes | were stimulated with PMA ( 50 ng / ml ) alone or LPS ( 100 ng / ml ) with and w |
| 99228708 | attenuated both LPS-induced NF-kappa B DNA binding and TNF-alpha production in | human monocytes | . Direct activation of PKC with PMA induced both NF-kappa B activation and TNF-a |
| 99228708 | of PKC with PMA induced both NF-kappa B activation and TNF-alpha production by | human monocytes | . CONCLUSIONS: These results suggest that LPS-induced NF-kappa B activation and |
| 99305241 | Signal transduction pathways in normal | human monocytes | stimulated by cytokines and mediators: comparative study with normal human neut |
| 99305241 | erleukin ( IL ) -3 induced tyrosine phosphorylation of 92-kDa protein in normal | human monocytes | . We identified this 92-kDa protein as STAT5, but not as STATs1, 3, and 6 nor c- |
| 99305241 | ns, which were identified as extracellular signal-regulated kinase ( ERK ) , in | human monocytes | . In marked contrast to neutrophils and MO7e cells, GM-CSF did not induce tyrosi |
| 99305241 | ylated and agonist-dependent phosphorylation and activation was not detected in | human monocytes | . Superoxide release stimulated by FMLP was inhibited partially by PD98059 or SB |
| 99305241 | rancriptional roles of STAT5 and functional roles of ERK and / or p38 in normal | human monocytes | stimulated by physiological receptor-mediated agonists GM-CSF and FMLP. Possibl |
| 99406845 | Glucocorticoids induce apoptosis in | human monocytes | : potential role of IL-1 beta. Glucocorticoids ( GC ) are potent anti-inflammato |
| 99406845 | still unknown. In our study, we determined the induction of apoptosis by GC in | human monocytes | . Peripheral blood monocytes were isolated by density centrifugation methods wit |
| 99406845 | L-1beta. This is the first study to demonstrate induction of apoptosis by GC in | human monocytes | . GC-induced monocyte apoptosis may be partially mediated through effects on IL- |
| 99305241 | DNA binding capacity, and potentiation of trancriptional activity by GM-CSF. N- | formyl-methionyl-leucyl-phenylalanine | ( FMLP ) and phorbol myristate acetate ( PMA ) induced tyrosine phosphorylation |
| 99305241 | of trancriptional activity by GM-CSF. N-formyl-methionyl-leucyl-phenylalanine ( | FMLP | ) and phorbol myristate acetate ( PMA ) induced tyrosine phosphorylation of 42- |
| 99305241 | tutively associated with Grb2 and was not tyrosine-phosphorylated by GM-CSF and | FMLP | , and Sos1 and c-Raf-1 were not phosphorylated by GM-CSF, IL-3, TNF, and FMLP in |
| 99305241 | nd FMLP, and Sos1 and c-Raf-1 were not phosphorylated by GM-CSF, IL-3, TNF, and | FMLP | in monocytes, whereas all these signaling molecules were affected and / or util |
| 99305241 | ctivation was not detected in human monocytes. Superoxide release stimulated by | FMLP | was inhibited partially by PD98059 or SB203580, a specific inhibitor of ERK or |
| 99305241 | man monocytes stimulated by physiological receptor-mediated agonists GM-CSF and | FMLP | . Possible roles of ERK in proliferation of transformed cells were also suggeste |
| 95399771 | nd inhibited the activity of granulocyte-macrophage colony-stimulating factor ( | GM-CSF | ) gene regulatory elements that use NFAT by 60%. CsA similarly mediated a reduc |
| 95399771 | ements that use NFAT by 60%. CsA similarly mediated a reduction of up to 65% in | GM-CSF | mRNA and protein expression in activated endothelial cells. CsA also suppressed |
| 95399771 | t the chromatin structure level, as DNasel hypersensitive sites within both the | GM-CSF | enhancer and the E-selectin promoter were suppressed by CsA. This represents th |
| 96075792 | ral hours of treatment, and the primed state was induced by either IFN-gamma or | GM-CSF | , but not M-CSF. Primed monocytes transcribed TNF mRNA at a higher rate than fre |
| 96329553 | peripheral blood monocytes. Granulocyte-macrophage colony-stimulating factor ( | GM-CSF | ) induces immediate effects in monocytes by activation of the Janus kinase ( JA |
| 96329553 | iated into macrophages by culture in macrophage-CSF ( M-CSF ) , we measured the | GM-CSF | induced tyrosine phosphorylation of STAT5A, STAT5B, and any lower molecular wei |
| 96329553 | . STAT5A-STAT5A homodimers and STAT5A-STAT5B heterodimers formed in response to | GM-CSF | . Therefore, activation of STAT5A predominates compared to STAT5B when assayed b |
| 96329553 | ide specificity and control to genes expressed in response to cytokines such as | GM-CSF | . |
| 99305241 | ctionality and cell biology. Granulocyte-macrophage colony-stimulating factor ( | GM-CSF | ) and interleukin ( IL ) -3 induced tyrosine phosphorylation of 92-kDa protein |
| 99305241 | f specific DNA binding capacity, and potentiation of trancriptional activity by | GM-CSF | . N-formyl-methionyl-leucyl-phenylalanine ( FMLP ) and phorbol myristate acetate |
| 99305241 | ( ERK ) , in human monocytes. In marked contrast to neutrophils and MO7e cells, | GM-CSF | did not induce tyrosine phosphorylation and activation of ERK in monocytes. Amo |
| 99305241 | was constitutively associated with Grb2 and was not tyrosine-phosphorylated by | GM-CSF | and FMLP, and Sos1 and c-Raf-1 were not phosphorylated by GM-CSF, IL-3, TNF, an |
| 99305241 | sphorylated by GM-CSF and FMLP, and Sos1 and c-Raf-1 were not phosphorylated by | GM-CSF | , IL-3, TNF, and FMLP in monocytes, whereas all these signaling molecules were a |
| 99305241 | cytes, whereas all these signaling molecules were affected and / or utilized by | GM-CSF | in MO7e cells. In contrast to neutrophils, p38 was constitutively phosphorylate |
| 99305241 | e release was resistant to these two inhibitors in monocytes. PD98059 inhibited | GM-CSF | -dependent proliferation of MO7e cells. Present results indicate trancriptional |
| 99305241 | n normal human monocytes stimulated by physiological receptor-mediated agonists | GM-CSF | and FMLP. Possible roles of ERK in proliferation of transformed cells were also |
| 98438422 | fect of translocations involving the inactive X chromosome: physical linkage to | XIC | / XIST does not lead to long-range de novo inactivation in human differentiated |
| 98438422 | X-chromosome inactivation ( X inactivation ) in relation to the position of the | X-inactivation center | ( XIC ) /XIST in differentiated cells. Autosome / Xi translocations were detect |
| 98438422 | n ( X inactivation ) in relation to the position of the X-inactivation center ( | XIC | ) /XIST in differentiated cells. Autosome / Xi translocations were detected by |
| 98438422 | her BrdU incorporated at late S phase or acetylated histone H4. The position of | XIC | / XIST in the reciprocal products of the translocation was determined by XIST-s |
| 98438422 | c FISH and computer enhancement. In other experiments, the Xq13 region carrying | XIC | / XIST was localized by computer enhancement of the DAPI banding pattern. Our s |
| 98438422 | ferentiated cells provides a visual demonstration that physical separation from | XIC | / XIST does not result in reactivation of inactive X-chromosome material and th |
| 98438422 | ion is not spread to the translocated autosomes irrespective of the position of | XIC | / XIST. This observation suggests that physical linkage to XIC / XIST does not |
| 98438422 | the position of XIC / XIST. This observation suggests that physical linkage to | XIC | / XIST does not lead to de novo inactivation of autosomal material. |
| 92215726 | ocation and turnover of the vitamin D receptor in human HL60 leukemia cells and | peripheral blood lymphocytes | -coincident rise of DNA-relaxing activity in nuclear extracts. High affinity rec |
| 92215726 | ( calcitriol ) are expressed in HL60 human leukemia cells and in low numbers in | peripheral blood lymphocytes | ( PBL ) . HL60 cells, expressing some characteristics of promyelocytes, can be |
| 92215726 | HL60 human leukemia cells and in low numbers in peripheral blood lymphocytes ( | PBL | ) . HL60 cells, expressing some characteristics of promyelocytes, can be induce |
| 92215726 | s a maximum of approximately 310 binding sites / nucleus was found after 3 h in | PBL | . Pulse exposure of HL60 to radiolabeled hormone for 3 h followed by culture in |
| 92215726 | difference of VDR retention in pulse and pulse / chase-experiments was seen in | PBL | , where VDR halflife was approximately 30 min. No specific translocation into th |
| 92215726 | ation with calcitriol ( final ethanol concentration 0.0001% v / v ) in HL60 and | PBL | . The enhanced activity disappeared after 2 h in PBL, whereas it was still enhan |
| 92215726 | 0.0001% v / v ) in HL60 and PBL. The enhanced activity disappeared after 2 h in | PBL | , whereas it was still enhanced by 4 h in HL60. No effect was seen in ethanol tr |
| 99007236 | combination, the polyamides inhibit virus replication by >99% in isolated human | peripheral blood lymphocytes | , with no detectable cell toxicity. The ability of small molecules to target pre |
| 99294118 | Binding characteristics of the glucocorticoid receptor in | peripheral blood lymphocytes | in multiple sclerosis. Although the exact etiology of multiple sclerosis ( MS ) |
| 99294118 | portion of patients. We characterized glucocorticoid receptor ( GR ) binding in | peripheral blood lymphocytes | from 39 MS patients and 14 age- and sex-matched controls with respect to dissoc |
| 96239534 | Transcriptional activation of RNA polymerase III-dependent genes by the | human T-cell leukemia virus | type 1 tax protein. The human T-cell leukemia virus-encoded tax protein is a po |
| 96239534 | III-dependent genes by the human T-cell leukemia virus type 1 tax protein. The | human T-cell leukemia virus | -encoded tax protein is a potent activator of many viral and cellular genes tran |
| 96239534 | y RNA polymerase II. We find that both chromatin and cell extracts derived from | human T-cell leukemia virus | type 1-infected human T lymphocytes support higher levels of 5S rRNA and tRNA g |
| 96279111 | ry mechanisms responsible for human interleukin 9 ( IL-9 ) gene expression in a | human T cell leukemia virus | type I-transformed human T cell line, C5MJ2, were investigated. We demonstrated |
| 91190842 | Purification of TCF-1 alpha, a | T-cell-specific transcription factor | that activates the T-cell receptor C alpha gene enhancer in a context-dependent |
| 91190842 | ctive extracts from Jurkat but not HeLa cells, confirming that TCF-1 alpha is a | T-cell-specific transcription factor | . Curiously, the TCF-1 alpha binding element was inactive in vivo when removed f |
| 95166251 | in T cells throughout their development, supporting the notion that PEBP2 is a | T-cell-specific transcription factor | . Transcripts of mouse AML1 / PEBP2 alpha B were also detected in day 12 fetal h |
| 95399771 | FAT. Nuclear factor of activated T cells ( NFAT ) was originally described as a | T-cell-specific transcription factor | athat supported the activation of cytokine gene expression and mediated the imm |
| 96184791 | nd. The IL-13 gene 5' flank region included a segment with sequence homology to | P elements | of the IL-4 promoter involved in transcriptional activation in T cells. Mutatio |
| 96184791 | omoter involved in transcriptional activation in T cells. Mutation of the IL-13 | P element | site significantly reduced IL-13 promoter activity in response to T-cell activa |
| 96184791 | in response to T-cell activation. Oligonucleotides containing the IL-13 or IL-4 | P element | sites specifically bound the transcriptional activator protein, nuclear factor- |
| 96184791 | e primed T cells contain higher levels of nuclear NF-ATp, capable of binding to | P elements | of the IL-4 and IL-13 promoters, than do freshly-isolated T cells, the NF-AT-bi |
| 96184791 | e IL-4 and IL-13 promoters, than do freshly-isolated T cells, the NF-AT-binding | P elements | are attractive candidates to mediate the coordinate expression of these two cyt |
| 97456880 | Four | P-like elements | are required for optimal transcription of the mouse IL-4 gene: involvement of a |
| 97456880 | hokine element 0 ( CLE0 ) , P, P2, P3 and P4. To characterize the role of these | P-like elements | and their binding factors in the native promoter, we did transient transfection |
| 97456880 | ction of EL-4 cells with the IL-4 promoter-reporter constructs carrying mutated | P-like elements | showed that four P-like elements, CLE0, P, P2 and P4, but not P3, were required |
| 97456880 | promoter-reporter constructs carrying mutated P-like elements showed that four | P-like elements | , CLE0, P, P2 and P4, but not P3, were required for optimal activation of the IL |
| 97456880 | AT / AP-1 complex formed only with P and P2. Cross-competition assays among the | P-like elements | revealed element-specific and common complexes. Six tandem repeats of the P ele |
| 97456880 | ments revealed element-specific and common complexes. Six tandem repeats of the | P element | linked to the SV40 promoter responded to phorbol 12-myristate 13-acetate, while |
| 98438422 | autosomes to study the maintenance and spreading of X-chromosome inactivation ( | X inactivation | ) in relation to the position of the X-inactivation center ( XIC ) /XIST in dif |
| 98438422 | XIST does not result in reactivation of inactive X-chromosome material and that | X inactivation | is not spread to the translocated autosomes irrespective of the position of XIC |
| 99155344 | of the human androgen receptor gene ( HUMARA ) has been shown to correlate with | X-inactivation | . In this study, we have used the polymerase chain reaction ( PCR ) with nested |
| 99155344 | have used the polymerase chain reaction ( PCR ) with nested primers to analyze | X-inactivation | patterns of the HUMARA loci in purified eosinophils from female patients with e |
| 99155344 | om a female patient presenting with IHES were found to show a clonal pattern of | X-inactivation | . Eosinophil-depleted leukocytes from this patient were polyclonal by HUMARA ana |
| 99155344 | patient were polyclonal by HUMARA analysis, thus excluding skewedness of random | X-inactivation | . After corticosteroid suppression of her blood eosinophilia, a clonal populatio |
| 99155344 | o allergy, parasitic infection, or drug reaction showed a polyclonal pattern of | X-inactivation | by HUMARA analysis. The finding of clonal eosinophilia in a patient presenting |
| 93183827 | rin A sensitive in T cells. Few known genes ( IL-2, members of the IL-8 family, | interferon-gamma | ) are induced in T cells only through the combined effect of phorbol myristic a |
| 96075792 | IFN-gamma | priming of monocytes enhances LPS-induced TNF production by augmenting both tra | |
| 96075792 | l, highly regulated host defence response. The augmentation of LPS responses by | interferon gamma | ( IFN-gamma ) , referred to as priming, is well established. However, the mecha |
| 96075792 | host defence response. The augmentation of LPS responses by interferon gamma ( | IFN-gamma | ) , referred to as priming, is well established. However, the mechanism ( s ) b |
| 96075792 | in detail the priming effect on the LPS response in human monocytes. Priming by | IFN-gamma | was primarily manifested at the level of TNF mRNA accumulation. IFN-gamma pre-t |
| 96075792 | ng by IFN-gamma was primarily manifested at the level of TNF mRNA accumulation. | IFN-gamma | pre-treatment affected the magnitude rather than the sensitivity of the LPS res |
| 96075792 | ed after several hours of treatment, and the primed state was induced by either | IFN-gamma | or GM-CSF, but not M-CSF. Primed monocytes transcribed TNF mRNA at a higher rat |
| 96079922 | T cell lines were investigated. A comparison with the Stat proteins induced by | interferon-gamma | , PRL, and IL-6 in T47D mammary tumor cells was made. We found that these parame |
| 97064186 | a powerful skewer of CD4+ T cell responses toward the Th1 phenotype by inducing | IFN-gamma | production in naive Th cells. In the present study we addressed the question of |
| 97064186 | L-12 can reverse established Th2 responses into Th1 / Th0 responses by inducing | IFN-gamma | production in memory Th2 cells. To this aim, allergen-specific CD4+ T cell clon |
| 97064186 | TCC exhibited a strongly polarized Th2 cytokine profile, and the production of | IFN-gamma | could not be induced by exogenous IL-12. Only those TCC with low IFN-gamma leve |
| 97064186 | n of IFN-gamma could not be induced by exogenous IL-12. Only those TCC with low | IFN-gamma | levels in the absence of IL-12 responded to IL-12 by additional enhancement of |
| 97064186 | levels in the absence of IL-12 responded to IL-12 by additional enhancement of | IFN-gamma | production. The IL-12 nonresponsiveness of the Th2 clones was further evident b |
| 97064186 | e profiles do not respond to IL-12 and, therefore, cannot be induced to produce | IFN-gamma | . The apparent high frequency of IL-12-nonresponsive Th cells within the allerge |
| 98133462 | the latter group received prenatal steroid treatment. Seven preterms developed | neonatal respiratory distress syndrome | ( NRDS ) . The number of GR and the Kd were similar in the term and preterm ( w |
| 98133462 | id treatment. Seven preterms developed neonatal respiratory distress syndrome ( | NRDS | ) . The number of GR and the Kd were similar in the term and preterm ( with and |
| 98133462 | number of GR and the Kd were similar in the term and preterm ( with and without | NRDS | ) babies. The maximum ( 3H ) -thymidine incorporation into DNA of cord blood ly |
| 98133462 | rporation into DNA of cord blood lymphocytes from all preterms, with or without | NRDS | was suppressed when compared to that from term babies or adults. This could par |
| 98133462 | e to find a relation between the functionality of the GR and the development of | NRDS | . |
| 92362919 | as been found that the number of glucocorticoid receptors in lymphocytes of the | peripheral blood | of healthy elderly subjects increases, while the number of mineralocorticoid re |
| 95261059 | cells. PU.1 is expressed at highest levels in mature human monocytes and human | peripheral blood | neutrophils. In contrast to PU.1, significant levels of Spi-B mRNA and protein |
| 97064186 | this aim, allergen-specific CD4+ T cell clones ( TCC ) were generated from the | peripheral blood | of three atopic patients, and their cytokine profiles were analyzed. The majori |
| 97162234 | um ( FCM ) is able to inhibit both TNF mRNA accumulation and protein release in | peripheral blood | -derived human monocytes ( PBM ) stimulated with lipopolysaccharide ( LPS ) . In |
| 98230439 | immune system, we amplified and cloned LTRs from proviral DNA in HIV-1-infected | peripheral blood | . Sequence analysis of nineteen LTRs cloned from 2 adult and 3 pediatric patient |
| 99155344 | the HUMARA loci in purified eosinophils from female patients with eosinophilia. | Peripheral blood | eosinophils were isolated by their autofluoresence using flow cytometric sortin |
| 99091536 | T cells are considered to be unresponsive to testosterone due to the absence of | androgen receptors | ( AR ) . Here, we demonstrate the testosterone responsiveness of murine splenic |
| 99091536 | d to be unresponsive to testosterone due to the absence of androgen receptors ( | AR | ) . Here, we demonstrate the testosterone responsiveness of murine splenic T ce |
| 99091536 | onventional cell surface receptors for testosterone and classical intracellular | AR | . Binding sites for testosterone on the surface of both CD4 ( + ) and CD8 ( + ) |
| 99091536 | terone-BSA-induced Ca2+ import is not affected by cyproterone, a blocker of the | AR | . In addition, AR are not detectable on the surface of intact T cells when using |
| 99091536 | d Ca2+ import is not affected by cyproterone, a blocker of the AR. In addition, | AR | are not detectable on the surface of intact T cells when using anti-AR antibodi |
| 99091536 | ddition, AR are not detectable on the surface of intact T cells when using anti- | AR | antibodies directed against the amino and carboxy terminus of the AR, although |
| 99091536 | using anti-AR antibodies directed against the amino and carboxy terminus of the | AR | , although T cells contain AR, as revealed by reverse transcription-polymerase c |
| 99091536 | cted against the amino and carboxy terminus of the AR, although T cells contain | AR | , as revealed by reverse transcription-polymerase chain reactions and Western bl |
| 99091536 | ealed by reverse transcription-polymerase chain reactions and Western blotting. | AR | can be visualized with the anti-AR antibodies in the cytoplasm of permeabilized |
| 99091536 | merase chain reactions and Western blotting. AR can be visualized with the anti- | AR | antibodies in the cytoplasm of permeabilized T cells by using CLSM, though AR a |
| 99091536 | i-AR antibodies in the cytoplasm of permeabilized T cells by using CLSM, though | AR | are not detectable in cytosol fractions when using the charcoal binding assay w |
| 99091536 | ions when using the charcoal binding assay with 3H-R1881 as ligand. Cytoplasmic | AR | do not translocate to the nucleus of T cells in the presence of testosterone, i |
| 99091536 | nucleus of T cells in the presence of testosterone, in contrast to cytoplasmic | AR | in human cancer LNCaP cells. These findings suggest that the classical AR prese |
| 99091536 | asmic AR in human cancer LNCaP cells. These findings suggest that the classical | AR | present in splenic T cells are not active in the genomic pathway. By contrast, |
| 97468093 | possibility that this enzyme can exert its hydrolytic activity independently of | protein tyrosine kinase activation | . |
| 99356019 | ime ELISA, EMSA ( electromobility shift assay ) and RT-PCR were used to measure | protein tyrosine kinase activity | , protein activity of NF-kappa B and cytokine ( IL-1beta, IL-6, TNF-alpha ) spec |
| 99356019 | , TNF-alpha ) specific mRNA levels in BEAS-2B cells. We observed an increase in | protein tyrosine kinase activity | ( up to 1.8 +/- 0.5-fold ) and NF-kappa B protein activity in BEAS-2B cells aft |
| 99356019 | IL-1beta-, IL-6- and TNF-alpha-mRNA were elevated ( up to 1.9 +/- 0.58-fold ) . | Protein tyrosine kinase activity | , NF-kappa B activity, and the synthesis of cytokine-specific mRNA were inhibite |
| 96338163 | CTL | recognition of an altered peptide associated with asparagine bond rearrangement | |
| 96338163 | d post-translationally modified amino acid side chains are recognized by primed | CTL | has not been clearly defined. We report on the CTL recognition of a MHC class I |
| 96338163 | ins are recognized by primed CTL has not been clearly defined. We report on the | CTL | recognition of a MHC class I-restricted peptide containing a cyclized asparagin |
| 96338163 | aining amino acids and also occurs as a side reaction in peptide synthesis. The | CTL | specifically recognized the succinimide-containing peptide showing only weak cr |
| 96338163 | ncentrations of the parent peptide containing unmodified asparagine. Similarly, | CTL | raised against the parent peptide did not recognize the succinimide derivative |
| 99102590 | c cells. The conventional means of studying Epstein-Barr virus ( EBV ) -induced | cytotoxic T-lymphocyte | ( CTL ) memory, by in vitro stimulation with the latently infected autologous l |
| 99102590 | means of studying Epstein-Barr virus ( EBV ) -induced cytotoxic T-lymphocyte ( | CTL | ) memory, by in vitro stimulation with the latently infected autologous lymphob |
| 99102590 | epitope peptide-loaded dendritic cells ( DCs ) , which allows one to probe the | CTL | repertoire for any individual reactivity of choice; this method proved signific |
| 99102590 | ntified by T cells during primary EBV infection are regularly detectable in the | CTL | memory of virus carriers; this implies that in such carriers chronic virus repl |
| 99102590 | ns, can be reactivated by DC stimulation and selectively expanded as polyclonal | CTL | lines; the adoptive transfer of such preparations may be of value in targeting |
| 95065655 | Epstein-Barr virus | SM protein. The protein products of the Epstein-Barr virus ( EBV ) BMLF1 open r | |
| 95065655 | Epstein-Barr virus SM protein. The protein products of the | Epstein-Barr virus | ( EBV ) BMLF1 open reading frame have been characterized in the early productiv |
| 95065655 | Epstein-Barr virus SM protein. The protein products of the Epstein-Barr virus ( | EBV | ) BMLF1 open reading frame have been characterized in the early productive cycl |
| 95065655 | ing BSLF2 to BMLF1 is much the most abundant protein. SM is a phosphoprotein in | EBV | -infected cells and can be phosphorylated in vitro with casein kinase II ( CKII |
| 95065655 | other herpesviruses and revealed consensus CKII sites near the N termini of the | EBV | SM protein, the herpes simplex virus ( HSV ) ICP27 protein and the herpesvirus |
| 95065655 | ading frame 57 protein. Site-directed mutagenesis of the consensus CKII site in | EBV | SM greatly reduced the in vitro phosphorylation of SM by CKII. The mechanism of |
| 97054651 | cell surface. The nature of CD40-dependent signals in proliferating fresh human | Epstein-Barr virus | -negative B lymphocytes is currently unknown. In this study, a CD40-dependent B |
| 98406200 | The | Epstein-Barr virus | Rta protein activates lytic cycle genes and can disrupt latency in B lymphocyte |
| 98406200 | s lytic cycle genes and can disrupt latency in B lymphocytes. The transition of | Epstein-Barr virus | ( EBV ) from latency into the lytic cycle is associated with the expression of |
| 98406200 | nd can disrupt latency in B lymphocytes. The transition of Epstein-Barr virus ( | EBV | ) from latency into the lytic cycle is associated with the expression of two im |
| 98406200 | implicating ZEBRA in the activation of Rta, we suggest a cooperative model for | EBV | entry into the lytic cycle. Expression of either BZLF1 or BRLF1 triggers expres |
| 99102590 | Accessing | Epstein-Barr virus | -specific T-cell memory with peptide-loaded dendritic cells. The conventional me |
| 99102590 | memory with peptide-loaded dendritic cells. The conventional means of studying | Epstein-Barr virus | ( EBV ) -induced cytotoxic T-lymphocyte ( CTL ) memory, by in vitro stimulation |
| 99102590 | loaded dendritic cells. The conventional means of studying Epstein-Barr virus ( | EBV | ) -induced cytotoxic T-lymphocyte ( CTL ) memory, by in vitro stimulation with |
| 99102590 | inant and subdominant lytic cycle epitopes identified by T cells during primary | EBV | infection are regularly detectable in the CTL memory of virus carriers; this im |
| 99102590 | the adoptive transfer of such preparations may be of value in targeting certain | EBV | -positive malignancies. |
| 95202809 | was dose-dependently reduced by aspirin over the same range, while induction of | intercellular adhesion molecule-1 | ( ICAM-1 ) was hardly affected. Aspirin appeared to prevent VCAM-1 transcriptio |
| 95202809 | rin over the same range, while induction of intercellular adhesion molecule-1 ( | ICAM-1 | ) was hardly affected. Aspirin appeared to prevent VCAM-1 transcription, since |
| 98104459 | NF-kappa B / Rel family members regulating the | ICAM-1 | promoter in monocytic THP-1 cells. A kappa B-site was identified in the promote |
| 98104459 | in monocytic THP-1 cells. A kappa B-site was identified in the promoter of the | intercellular adhesion molecule-1 | ( ICAM-1 ) gene, which is involved in regulation of ICAM-1 expression by tumor |
| 98104459 | -site was identified in the promoter of the intercellular adhesion molecule-1 ( | ICAM-1 | ) gene, which is involved in regulation of ICAM-1 expression by tumor necrosis |
| 98104459 | ellular adhesion molecule-1 ( ICAM-1 ) gene, which is involved in regulation of | ICAM-1 | expression by tumor necrosis factor alpha ( TNF-alpha ) and glucocorticoids. We |
| 98104459 | tion factors which bind and transactivate this enhancer sequence. In vitro, the | ICAM-1 | kappa B site appeared to bind RelA and c-Rel homodimers as well as heterodimers |
| 98104459 | ition, both RelA and c-Rel, but not NF-kappa B1, were shown to transactivate an | ICAM-1 | kappa B-reporter construct. In monocytic THP-1 cells TNF-alpha induced two nucl |
| 98104459 | THP-1 cells TNF-alpha induced two nuclear complexes which in vitro bound to the | ICAM-1 | kappa B site. Using antibodies in an electrophoretic mobility supershift assay, |
| 98104459 | t. The second complex contained RelA, and exhibited higher affinity towards the | ICAM-1 | kappa B than to the HIV kappa B site. The glucocorticoid receptor was shown to |
| 98104459 | in vivo RelA homodimers are likely to play a dominant role in TNF-alpha-induced | ICAM-1 | transcription in monocytic cells. |
| 99369970 | CD3 ligation induces a delayed Stat3 binding to oligonucleotide probes from the | ICAM-1 | and IL-2R alpha promoter. CD3-mediated activation of Stat3 is almost completely |
| 97028169 | cating that murine adult HPCs transduced with dominant negative ATRA receptor ( | RAR | ) gene are immortalized and show a selective blockade of granulocytic different |
| 97028169 | hematopoiesis via a dual effect hypothetically mediated by interaction with the | RAR | / RXR heterodimer, ie, inhibition of HSC/ primitive HPC proliferation and induc |
| 98400423 | l development. Here we investigated the impact of retinoid X receptor ( RXR ) , | retinoic acid receptor | ( RAR ) , and of the c-erbA / thyroid hormone ( T3 ) receptor ( c-erbA / TR ) o |
| 98400423 | vestigated the impact of retinoid X receptor ( RXR ) , retinoic acid receptor ( | RAR | ) , and of the c-erbA / thyroid hormone ( T3 ) receptor ( c-erbA / TR ) on grow |
| 98400423 | vitro culture system of stem cell factor-dependent erythroid progenitors. RXR, | RAR | , and c-erbA / TR-specific ligands were found to induce erythroid-specific gene |
| 99408303 | ggested from a variety of sources. Here we present a review of the mechanism of | retinoic acid receptor | action and the major evidence showing that normal retinoid signaling is require |
| 99102590 | Accessing Epstein-Barr virus-specific T-cell memory with peptide-loaded | dendritic cells | . The conventional means of studying Epstein-Barr virus ( EBV ) -induced cytotox |
| 99102590 | alternative approach, based on in vitro stimulation with epitope peptide-loaded | dendritic cells | ( DCs ) , which allows one to probe the CTL repertoire for any individual react |
| 99102590 | ch, based on in vitro stimulation with epitope peptide-loaded dendritic cells ( | DCs | ) , which allows one to probe the CTL repertoire for any individual reactivity |
| 99102590 | though rarely undetectable in LCL-stimulated populations, can be reactivated by | DC | stimulation and selectively expanded as polyclonal CTL lines; the adoptive tran |
| 99172186 | N-acetyl-L-cysteine inhibits primary human T cell responses at the | dendritic cell | level: association with NF-kappa B inhibition. N-acetyl-L-cysteine ( NAC ) is a |
| 99172186 | NAC on the induction phase of T cell responses, we analyzed its action on human | dendritic cells | ( DC ) derived from adherent PBMC cultured with IL-4 and granulocyte-macrophage |
| 99172186 | on phase of T cell responses, we analyzed its action on human dendritic cells ( | DC | ) derived from adherent PBMC cultured with IL-4 and granulocyte-macrophage CSF. |
| 99172186 | a B. In parallel, NAC was shown to down-regulate the production of cytokines by | DC | as well as their surface expression of HLA-DR, CD86 ( B7-2 ) , and CD40 molecul |
| 99172186 | 0 molecules both at the basal state and upon LPS activation. NAC also inhibited | DC | responses induced by CD40 engagement. The inhibitory effects of NAC were not du |
| 99172186 | effects of NAC were not due to nonspecific toxicity as neither the viability of | DC | nor their mannose receptor-mediated endocytosis were modified by NAC. Finally, |
| 99172186 | , we found that the addition of NAC to MLR between naive T cells and allogeneic | DC | resulted in a profound inhibition of alloreactive responses, which could be att |
| 99172186 | inhibition of alloreactive responses, which could be attributed to a defect of | DC | as APC-independent T cell responses were not inhibited by NAC. Altogether, our |
| 99172186 | neration of primary immune responses in humans through its inhibitory action on | DC | . |
| 96185499 | ibits histone deacetylation in vivo and causes mammalian cells to arrest in the | cell cycle | . A trapoxin affinity matrix was used to isolate two nuclear proteins that copur |
| 98038749 | Regulation of Id3 | cell cycle | function by Cdk-2-dependent phosphorylation. The functions of basic helix-loop- |
| 98038749 | factors in activating differentiation-linked gene expression and in inducing G1 | cell cycle | arrest are negatively regulated by members of the Id family of HLH proteins. Th |
| 98038749 | r5 ) in Id2 has been shown to occur during late G1-to-S phase transition of the | cell cycle | , and this neutralizes the function of Id2 in abrogating E-box-dependent bHLH ho |
| 98038749 | M.Hall, and G.Peters, EMBO J.16:332-342, 1997 ) . We now show that an analogous | cell-cycle | -regulated phosphorylation of Id3 alters the specificity of Id3 for abrogating b |
| 98038749 | type Id3, an Id3 Asp5 mutant ( mimicking phosphorylation ) is unable to promote | cell cycle | S phase entry in transfected fibroblasts, whereas an Id3 Ala5 mutant ( ablating |
| 98038749 | ore provides a switch during late G1-to-S phase that both nullifies an early G1 | cell cycle | regulatory function of Id3 and modulates its target bHLH specificity. These dat |
| 98038749 | HLH specificity. These data also demonstrate that the ability of Id3 to promote | cell cycle | S phase entry is not simply a function of its ability to modulate bHLH heterodi |
| 99081619 | n-10 inhibition of T-helper cell activation by superantigen at the level of the | cell cycle | . We have analyzed the effects of interleukin-10 ( IL-10 ) on the entry of quies |
| 99081619 | f interleukin-10 ( IL-10 ) on the entry of quiescent CD4 ( + ) T cells into the | cell cycle | upon stimulation with the superantigen staphylococcal enterotoxin B ( SEB ) . I |
| 99081619 | ) , an inhibitory protein that controls progression out of the G0 phase of the | cell cycle | . IL-10 also prevented the upregulation of the G1 cyclins D2 and D3, proteins ne |
| 99081619 | nd D3, proteins necessary for entry and progression through the G1 phase of the | cell cycle | . Associated with the inhibition of the cell cycle, IL-10 suppressed SEB inducti |
| 99081619 | n through the G1 phase of the cell cycle. Associated with the inhibition of the | cell cycle | , IL-10 suppressed SEB induction of interleukin-2 ( IL-2 ) . Addition of exogeno |
| 99081619 | ( Kip1 ) and upregulation of D cyclins in T-cell activation and entry into the | cell cycle | . |
| 91190842 | ssed in mature and immature T-cell lines ( Jurkat, CCRF-CEM ) and not in mature | B cells | ( JY, Namalwa ) or nonlymphoid ( HeLa ) cell lines. A small 95-bp fragment of t |
| 95261059 | usly described as being predominantly expressed coordinately in macrophages and | B cells | , but their expression in early hematopoietic stages and during the course of my |
| 97025698 | he oligo sequence I stimulated proliferation of both T and, to a lesser extent, | B cells | . The percentage of cells expressing CD40 in T and B cell co-cultures increased |
| 97054651 | robe, revealed that both p65 ( RelA ) and c-Rel were present in CD40-stimulated | B cells | . While PKC depletion did not alter the NF-kappa B level, treatment of B lymphoc |
| 97207294 | mphocyte function and mediates its effects via a receptor that contains gammac. | B cells | derived from patients with X-linked severe combined immunodeficiency ( X-SCID ) |
| 97207294 | t in IL-4-mediated signaling. We found that although IL-4 stimulation of X-SCID | B cells | did not result in Janus tyrosine kinase-3 ( JAK3 ) phosphorylation, other IL-4 |
| 97207294 | ription 6 ( STAT6 ) tyrosine phosphorylation and DNA binding activity in X-SCID | B cells | with a wide range of gammac mutations. However, reconstitution of these X-SCID |
| 97207294 | with a wide range of gammac mutations. However, reconstitution of these X-SCID | B cells | with gammac enhanced IL-4-mediated responses including STAT6 phosphorylation an |
| 97207294 | expression. Thus, gammac is not necessary to trigger IL-4-mediated responses in | B cells | , but its presence is important for optimal IL-4-signaling. These results sugges |
| 97303223 | man interleukin 4 receptor alpha chain induces Cepsilon germline transcripts in | B cells | in the absence of the interleukin 2 receptor gamma chain. The cytokines interle |
| 97303223 | le in inducing Cepsilon germline transcripts and IgE isotype switching in human | B cells | . The IL-4 receptor ( IL-4R ) in B cells is composed of two chains, the IL-4-bin |
| 97303223 | ipts and IgE isotype switching in human B cells. The IL-4 receptor ( IL-4R ) in | B cells | is composed of two chains, the IL-4-binding IL-4Ralpha chain, which is shared w |
| 97303223 | IL-15R. IL-4 induces Cepsilon germline transcripts and IgE isotype switching in | B cells | from patients with gammac chain deficiency. Induction of Cepsilon germline tran |
| 97303223 | gammac chain deficiency. Induction of Cepsilon germline transcripts by IL-4 in | B cells | that lack the gammac chain may involve signaling via the IL-13R. Alternatively, |
| 97303223 | egion of IL-4Ralpha abolished signaling by this chimeric receptor. Furthermore, | B cells | transfected with a chimeric CD8alpha / IL-4Ralpha receptor, which is expressed |
| 91190842 | Purification of | TCF-1 alpha | , a T-cell-specific transcription factor that activates the T-cell receptor C al |
| 91190842 | ence this developmental process. We have purified a new T-cell-specific factor, | TCF-1 alpha | , that is implicated in the activation of genes encoding a major component of th |
| 91190842 | tion of genes encoding a major component of the human T-cell receptor ( TCR ) . | TCF-1 alpha | , originally identified and purified through its binding sites on the HIV-1 prom |
| 91190842 | n the TCR alpha gene ( e.g., p56 lck and CD3 delta ) . Sequences related to the | TCF-1 alpha | binding motif ( 5'--3' ) are also found in the human TCR delta ( and possibly T |
| 91190842 | naturation experiments with the use of purified protein fractions revealed that | TCF-1 alpha | activity is derived from a family of 57- to 53-kD proteins that are abundantly |
| 91190842 | lines. A small 95-bp fragment of the TCR alpha control region that contains the | TCF-1 alpha | binding site juxtaposed between a cAMP-response element ( the CRE or T alpha 1 |
| 91190842 | ll as resting and activated immature ( CCRF-CEM ) T-cell lines. Mutation of the | TCF-1 alpha | binding site diminished enhancer activity and disrupted the synergism observed |
| 91190842 | d disrupted the synergism observed in vivo between tandem enhancer repeats. The | TCF-1 alpha | binding site was also required for TCR alpha enhancer activity in transcription |
| 91190842 | anscriptionally active extracts from Jurkat but not HeLa cells, confirming that | TCF-1 alpha | is a T-cell-specific transcription factor. Curiously, the TCF-1 alpha binding e |
| 91190842 | ming that TCF-1 alpha is a T-cell-specific transcription factor. Curiously, the | TCF-1 alpha | binding element was inactive in vivo when removed from its neighboring elements |
| 91190842 | pies upstream of a heterologous promoter. Thus, the transcriptional activity of | TCF-1 alpha | appears to depend on the TCF-2 alpha and T alpha 1 ( CREB ) transcription facto |
| 95202809 | udied a potential inhibition of this pathway by acetylsalicylate ( aspirin ) in | human umbilical vein endothelial cells | ( HUVECs ) . METHODS AND RESULTS: Gel-shift analyses demonstrated dose-dependen |
| 95202809 | way by acetylsalicylate ( aspirin ) in human umbilical vein endothelial cells ( | HUVECs | ) . METHODS AND RESULTS: Gel-shift analyses demonstrated dose-dependent inhibit |
| 95202809 | TNF. As a functional consequence, adhesion of U937 monocytes to TNF-stimulated | HUVECs | was markedly reduced by aspirin due to suppression of VCAM-1 and E-selectin upr |
| 92052106 | kDa plus 50-kDa NF-kappa B heterodimer was preferentially lost. Adding purified | NF-kappa B protein | to nuclear extracts from cells with restricted expression overcomes this lack o |
| 92135145 | cell hybrids is accompanied by the nuclear localization of NF-kappa B. The two | nuclear proteins NF-kappa B | ( consisting of subunits p50 an dp65 ) and the DNA-binding subunit of NF-kappa |
| 96074632 | Down-regulation of | NF-kappa B protein | levels in activated human lymphocytes by 1,25-dihydroxyvitamin D3 [published er |
| 96074632 | were ineffective. Besides p50, 1,25 ( OH ) 2D3 decreased the levels of another | NF-kappa B protein | , namely c-rel. In addition, 1,25 ( OH ) 2D3 decreased the abundance of a specif |
| 97211823 | ence of in vitro treatment of these cells. In the present report, we identified | NF-kappa B proteins | extracted from human thymocyte nuclei as being p50 / p65 and p50 / c-Rel comple |
| 99356019 | an increase in protein tyrosine kinase activity ( up to 1.8 +/- 0.5-fold ) and | NF-kappa B protein | activity in BEAS-2B cells after particle or fibre exposure of co-cultured BM. C |
| 99228708 | uman monocytes leads to activation of nuclear factor-kappa B ( NF-kappa B ) and | TNF-alpha release | . Previous studies have implicated activation of both protein kinase C ( PKC ) a |
| 99228708 | ibitor bisindolylmaleimide ( Bis ) , or an inhibitor of PTK genistein ( Gen ) . | TNF-alpha release | in culture supernatants was measured by an ELISA. NF-kappa B DNA binding was ev |
| 99228708 | ytes. Nonspecific protein kinase inhibition inhibited NF-kappa B activation and | TNF-alpha release | , while specific PKC inhibition with Bis had no effect on LPS-induced NF-kappa B |
| 99228708 | PKC inhibition with Bis had no effect on LPS-induced NF-kappa B DNA binding or | TNF-alpha release | . PTK inhibition with Gen attenuated both LPS-induced NF-kappa B DNA binding and |
| 94238882 | on, both at the mRNA and protein level. The induced expression of IL-1 beta and | TNF alpha mRNA | in the monocytic THP-1 cell line increased as quickly as in primary cells. In c |
| 94238882 | e c-myc protein are involved in the MDHM-induced increase in IL-1 beta, IL-6 or | TNF alpha mRNA | levels. Furthermore, the present results demonstrate clearly that mycoplasma pr |
| 99356019 | particle or fibre exposure of co-cultured BM. Consecutive IL-1beta-, IL-6- and | TNF-alpha-mRNA | were elevated ( up to 1.9 +/- 0.58-fold ) . Protein tyrosine kinase activity, N |
| 91190842 | ified through its binding sites on the HIV-1 promoter, was found to bind to the | TCR alpha enhancer | and to promoters for several genes expressed at significantly earlier stages of |
| 91190842 | een tandem enhancer repeats. The TCF-1 alpha binding site was also required for | TCR alpha enhancer | activity in transcriptionally active extracts from Jurkat but not HeLa cells, c |
| 91190842 | element was inactive in vivo when removed from its neighboring elements on the | TCR alpha enhancer | and positioned in one or more copies upstream of a heterologous promoter. Thus, |
| 91190842 | 1 ( CREB ) transcription factors and the context of its binding site within the | TCR alpha enhancer | . |
| 95202809 | on and monocyte adhesion in stimulated human endothelial cells. BACKGROUND: The | induction of vascular cell adhesion molecule-1 | ( VCAM-1 ) and E-selectin by tumor necrosis factor-alpha ( TNF ) is mediated by |
| 95202809 | appa B mobilization by aspirin at concentrations ranging from 1 to 10 mmol / L. | Induction of VCAM-1 | and E-selectin surface expression by TNF was dose-dependently reduced by aspiri |
| 95202809 | n appeared to prevent VCAM-1 transcription, since it dose-dependently inhibited | induction of VCAM-1 | mRNA by TNF. As a functional consequence, adhesion of U937 monocytes to TNF-sti |
| 95202809 | e. CONCLUSIONS: Our data suggest that aspirin inhibits NF-kappa B mobilization, | induction of VCAM-1 | and E-selectin, and subsequent monocyte adhesion in endothelial cells stimulate |
| 93204975 | entic enhancer for high-level zeta 2 globin promoter activity in K562 cells, an | erythroid cell | line of embryonic and / or fetal origin. Although sequences located between -55 |
| 93204975 | onic zeta 2 globin gene and the fetal / adult alpha globin genes is mediated by | erythroid cell | -specific and developmental stage-specific nuclear factor-DNA complexes which fo |
| 98400423 | Retinoid X receptor and c-cerbA / thyroid hormone receptor regulate | erythroid cell | growth and differentiation. Nuclear receptors are important regulators of eryth |
| 98400423 | cell growth and differentiation. Nuclear receptors are important regulators of | erythroid cell | development. Here we investigated the impact of retinoid X receptor ( RXR ) , r |
| 98400423 | hyroid hormone ( T3 ) receptor ( c-erbA / TR ) on growth and differentiation of | erythroid cells | using an in vitro culture system of stem cell factor-dependent erythroid progen |
| 98400423 | rowth in culture. Thus, c-erbA / TR appears to act as a binary switch affecting | erythroid cell | fate: unliganded c-erbA / TR supports growth while ligand-activated c-erbA / TR |
| 98400423 | / TR induces differentiation. Additionally, to determine the impact of RXR for | erythroid cell | development, dominant interfering mutant RXRs, lacking the transcriptional acti |
| 98400423 | the RXR mutants devoid of AF-1 and / or AF-2 supported a transient outgrowth of | erythroid cells | . In marked contrast, expression of the dominant interfering deltaDNA-binding do |
| 98400423 | , containing a deletion of the entire DNA-binding domain, was incompatible with | erythroid cell | growth in vitro, suggesting a pivotal role of RXR for erythroid cell developmen |
| 98400423 | tible with erythroid cell growth in vitro, suggesting a pivotal role of RXR for | erythroid cell | development. |
| 99310627 | isms by which GATA-1 controls cell survival are unknown. Here we report that in | erythroid cells | , GATA-1 strongly induces the expression of the anti-apoptotic protein bcl-xL, b |
| 99310627 | tiated bcl-xL-/- embryonic stem cells fail to generate viable mature definitive | erythroid cells | , a phenotype resembling that of GATA-1 gene disruption. In addition, we show th |
| 99310627 | val, cooperates with GATA-1 to stimulate bcl-xL gene expression and to maintain | erythroid cell | viability during terminal maturation. Together, our data show that bcl-xL is es |
| 99155344 | Clonality of isolated eosinophils in the hypereosinophilic syndrome. The | idiopathic hypereosinophilic syndrome | ( IHES ) is a rare disorder characterized by unexplained, persistent eosinophil |
| 99155344 | in the hypereosinophilic syndrome. The idiopathic hypereosinophilic syndrome ( | IHES | ) is a rare disorder characterized by unexplained, persistent eosinophilia asso |
| 99155344 | typic abnormalities, there is no specific test to detect clonal eosinophilia in | IHES | . Analysis of X-chromosome inactivation patterns can be used to determine whethe |
| 99155344 | cytometric sorting. Eosinophils purified from a female patient presenting with | IHES | were found to show a clonal pattern of X-inactivation. Eosinophil-depleted leuk |
| 99155344 | UMARA analysis. The finding of clonal eosinophilia in a patient presenting with | IHES | indicates that such patients may have, in reality, a low-grade clonal disorder |
| 94209654 | ified serine / threonine kinases, including protein kinase A, protein kinase C, | casein kinase II | , MAP kinases, p70S6K and p90RSK. Fos kinase was purified by anion exchange chro |
| 95065655 | a phosphoprotein in EBV-infected cells and can be phosphorylated in vitro with | casein kinase II | ( CKII ) . Computer analysis of the SM protein sequence showed a C terminal sec |
| 95065655 | n EBV-infected cells and can be phosphorylated in vitro with casein kinase II ( | CKII | ) . Computer analysis of the SM protein sequence showed a C terminal section of |
| 95065655 | genome positional homologues of four other herpesviruses and revealed consensus | CKII | sites near the N termini of the EBV SM protein, the herpes simplex virus ( HSV |
| 95065655 | HVS ) open reading frame 57 protein. Site-directed mutagenesis of the consensus | CKII | site in EBV SM greatly reduced the in vitro phosphorylation of SM by CKII. The |
| 95065655 | ensus CKII site in EBV SM greatly reduced the in vitro phosphorylation of SM by | CKII | . The mechanism of transactivation by BMLF1 proteins has been controversial but |
| 95065655 | construct by increasing the amount of cytoplasmic CAT mRNA. Mutagenesis of the | CKII | site in SM made no difference to the transactivation in this transient transfec |
| 94238882 | Induction of proto-oncogene and cytokine expression in human | peripheral blood monocytes | and the monocytic cell line THP-1 after stimulation with mycoplasma-derived mat |
| 94238882 | ls by stimulating IL-6 release from adherent cells. This study shows that human | peripheral blood monocytes | ( PBMo ) also respond to MDHM with increases in IL-1 beta, IL-6 and TNF alpha e |
| 94238882 | e from adherent cells. This study shows that human peripheral blood monocytes ( | PBMo | ) also respond to MDHM with increases in IL-1 beta, IL-6 and TNF alpha expressi |
| 94238882 | ocytic THP-1 cell line increased as quickly as in primary cells. In contrast to | PBMo | , THP-1 and 14 other monocytic / myeloid leukemia-derived cell lines did not sec |
| 94238882 | though these data suggest AP-1 regulated cytokine mRNA expression, results from | PBMo | are not in accordance with this notion. In the primary cells MDHM-induced eleva |
| 94238882 | expression, constitutively high in THP-1 cells, was induced in MDHM-stimulated | PBMo | . In conclusion, MDHM-stimulated induction of cytokine mRNA expression was accom |
| 94238882 | tokine mRNA expression was accompanied by different proto-oncogene responses in | PBMo | and THP-1 cells. These differences may represent different regulatory pathways |
| 96329553 | preferentially activates the 94-kD STAT5A and an 80-kD STAT5A isoform in human | peripheral blood monocytes | . Granulocyte-macrophage colony-stimulating factor ( GM-CSF ) induces immediate |
| 99406845 | n our study, we determined the induction of apoptosis by GC in human monocytes. | Peripheral blood monocytes | were isolated by density centrifugation methods with a purity of >90% and were |
| 94254835 | sion in monocytic cells is mediated by binding of c-Rel / p65 heterodimers to a | kappa B-like site | . Exposure of monocytic cells to bacterial lipopolysaccharide ( LPS ) activates |
| 94254835 | haracterization of a nuclear complex from human monocytic cells that bound to a | kappa B-like site | , 5'--3', in the 5'-flanking region of the human TF gene. This nuclear complex w |
| 94254835 | ex and further showed that c-Rel / p65 heterodimers selectively bound to the TF | kappa B-like site | . Functional studies indicated that the TF site conferred LPS inducibility on a |
| 94254835 | r, our results demonstrated that binding of c-Rel / p65 heterodimers to a novel | kappa B-like site | mediated LPS induction of TF gene expression in monocytic cells. |
| 98104459 | / Rel family members regulating the ICAM-1 promoter in monocytic THP-1 cells. A | kappa B-site | was identified in the promoter of the intercellular adhesion molecule-1 ( ICAM- |
| 98104459 | ctors which bind and transactivate this enhancer sequence. In vitro, the ICAM-1 | kappa B site | appeared to bind RelA and c-Rel homodimers as well as heterodimers with NF-kapp |
| 98104459 | ells TNF-alpha induced two nuclear complexes which in vitro bound to the ICAM-1 | kappa B site | . Using antibodies in an electrophoretic mobility supershift assay, one of these |
| 98104459 | contain NF-kappa B1 and RelA, and to bind with higher affinity to the consensus | kappa B site | in the HIV long terminal repeat. The second complex contained RelA, and exhibit |
| 98104459 | RelA, and exhibited higher affinity towards the ICAM-1 kappa B than to the HIV | kappa B site | . The glucocorticoid receptor was shown to repress activity of both the RelA hom |
| 92135145 | Activity of the | kappa B enhancer | of the interleukin-2 receptor alpha chain in somatic cell hybrids is accompanie |
| 92135145 | 01.5. In order to define the roles of these two factors, which bind to the same | kappa B enhancers | , in transcription activation we have prepared somatic cell hybrids between IARC |
| 92135145 | th KBF1 and NF-kappa B in their nuclei, but one hybrid expresses only KBF1. The | kappa B enhancer | of the gene encoding the interleukin-2 ( IL-2 ) receptor alpha chain ( IL-2R al |
| 92135145 | ppa B. These findings show that nuclear NF-kappa B is necessary to activate the | kappa B enhancer | , while KBF1 by itself is not sufficient. We propose that KBF1 is a competitive |
| 92135145 | Activity of the kappa B enhancer of the interleukin-2 | receptor alpha chain | in somatic cell hybrids is accompanied by the nuclear localization of NF-kappa |
| 92135145 | only KBF1. The kappa B enhancer of the gene encoding the interleukin-2 ( IL-2 ) | receptor alpha chain | ( IL-2R alpha ) is functional only in the hybrids expressing nuclear NF-kappa B |
| 94107268 | activation such as surface expression of the CD69 antigen and the interleukin 2 | receptor alpha-chain | ( CD25 ) . Pervanadate synergized with signals delivered by T-cell antigen rece |
| 96322726 | e induction of expression of IL-2 receptor components, but did not inhibit IL-4 | receptor alpha-chain | and CD69 expression or the induction of activator protein 1 transcription facto |
| 97303223 | Homodimerization of the human interleukin 4 | receptor alpha chain | induces Cepsilon germline transcripts in B cells in the absence of the interleu |
| 94209654 | ine kinase that phosphorylated the proto-oncogene product, c-Fos, and is termed | Fos kinase | . Fos kinase was rapidly activated after ligation of the CD3 and CD2 receptors i |
| 94209654 | hat phosphorylated the proto-oncogene product, c-Fos, and is termed Fos kinase. | Fos kinase | was rapidly activated after ligation of the CD3 and CD2 receptors in Jurkat and |
| 94209654 | 0 and Ramos, respectively. The phorbol ester, PMA, was also a potent inducer of | Fos kinase | activity in all of the above populations, suggesting that PKC plays a role in t |
| 94209654 | populations, suggesting that PKC plays a role in the regulation of this enzyme. | Fos kinase | phosphorylates c-Fos at a site near the C-terminus, as well as a peptide derive |
| 94209654 | RKGSSSNEPSSD ) , and Fos peptide competitively inhibited c-Fos phosphorylation. | Fos kinase | was shown to be distinct from other identified serine / threonine kinases, incl |
| 94209654 | n kinase A, protein kinase C, casein kinase II, MAP kinases, p70S6K and p90RSK. | Fos kinase | was purified by anion exchange chromatography and exhibited an apparent M ( r ) |
| 94209654 | ography and exhibited an apparent M ( r ) = 65,000 and isoelectric point = 6.1. | Fos kinase | may play a role in transcriptional regulation through its capacity to phosphory |
| 98089072 | proteins. The estrogen receptor ( ER ) repressed erythroid differentiation and | erythroid-specific gene expression | . In this study, we investigated the effect of ER alpha ( referred to throughout |
| 98089072 | ) on DNA-binding activities of transcription factors involved in regulating the | expression of erythroid-specific genes | , and, in particular, the histone H5 gene. Using electrophoretic mobility shift |
| 98089072 | Both GATA-1 and-binding proteins are critical for the developmentally regulated | expression of erythroid-specific genes | . We hypothesize that interference in DNA-binding activities of GATA-1 and-bindi |
| 98400423 | id progenitors. RXR, RAR, and c-erbA / TR-specific ligands were found to induce | erythroid-specific gene expression | and to accelerate erythroid differentiation in culture, with T3 being most effe |
| 91363265 | coid receptors in human mononuclear cells: effects of glucocorticoid treatment, | Cushing's disease | and ketoconazole. Glucocorticoid receptors ( GcR ) were determined by a whole c |
| 91363265 | l subjects, patients receiving glucocorticoid therapy for systemic diseases and | Cushing's disease | patients with or without ketoconazole therapy. Prolonged corticosteroid treatme |
| 91363265 | id treatment resulted in down-regulation of GcR, while the mean level of GcR in | Cushing's disease | was normal. In this group, however, receptor levels and morning plasma cortisol |
| 91363265 | y showed very mild down-regulation in hypercortisolemic patients suffering from | Cushing's disease | . Finally, we did not observed either up-regulation or antagonism of GcR by keto |
| 91363265 | cR by ketoconazole treatment, at the time that cortisol levels of patients with | Cushing's disease | were reduced. This indicates that the beneficial effects of ketoconazole in Cus |
| 91363265 | ase were reduced. This indicates that the beneficial effects of ketoconazole in | Cushing's disease | are due to adrenal cortisol suppression and not to interaction with GcR of targ |
| 95202809 | s nuclear factor-kappa B mobilization and monocyte adhesion in stimulated human | endothelial cells | . BACKGROUND: The induction of vascular cell adhesion molecule-1 ( VCAM-1 ) and |
| 95202809 | zation, induction of VCAM-1 and E-selectin, and subsequent monocyte adhesion in | endothelial cells | stimulated by TNF, thereby providing an additional mechanism for therapeutic ef |
| 95399771 | f granulocyte-macrophage colony-stimulating factor and E-selectin expression in | endothelial cells | by cyclosporin A and the T-cell transcription factor NFAT. Nuclear factor of ac |
| 95399771 | munoregulatory effects of cyclosporin A ( CsA ) . As we observed that activated | endothelial cells | also expressed NFAT, we tested the antiinflammatory properties of CsA in endoth |
| 95399771 | cells also expressed NFAT, we tested the antiinflammatory properties of CsA in | endothelial cells | . Significantly, CsA completely suppressed the induction of NFAT in endothelial |
| 95399771 | helial cells. Significantly, CsA completely suppressed the induction of NFAT in | endothelial cells | and inhibited the activity of granulocyte-macrophage colony-stimulating factor |
| 95399771 | ted a reduction of up to 65% in GM-CSF mRNA and protein expression in activated | endothelial cells | . CsA also suppressed E-selectin, but not vascular cell adhesion molecule-1 ( VC |
| 95399771 | E-selectin, but not vascular cell adhesion molecule-1 ( VCAM-1 ) expression in | endothelial cells | , even though the E-selectin promoter is activated by NF-kappa B rather than NFA |
| 95399771 | s was reflected by a 29% decrease in neutrophil adhesion. The effects of CsA on | endothelial cells | were also detected at the chromatin structure level, as DNasel hypersensitive s |
| 95399771 | in promoter were suppressed by CsA. This represents the first report of NFAT in | endothelial cells | and suggests mechanisms by which CsA could function as an antiinflammatory agen |
| 95202809 | thelial cells. BACKGROUND: The induction of vascular cell adhesion molecule-1 ( | VCAM-1 | ) and E-selectin by tumor necrosis factor-alpha ( TNF ) is mediated by mobiliza |
| 95202809 | adhesion molecule-1 ( ICAM-1 ) was hardly affected. Aspirin appeared to prevent | VCAM-1 | transcription, since it dose-dependently inhibited induction of VCAM-1 mRNA by |
| 95202809 | to TNF-stimulated HUVECs was markedly reduced by aspirin due to suppression of | VCAM-1 | and E-selectin upregulation. These effects of aspirin were not related to the i |
| 95399771 | ression in activated endothelial cells. CsA also suppressed E-selectin, but not | vascular cell adhesion molecule-1 | ( VCAM-1 ) expression in endothelial cells, even though the E-selectin promoter |
| 95399771 | ls. CsA also suppressed E-selectin, but not vascular cell adhesion molecule-1 ( | VCAM-1 | ) expression in endothelial cells, even though the E-selectin promoter is activ |
| 96437028 | E3, a hematopoietic-specific transcript directly regulated by the | retinoic acid receptor alpha | . Retinoic acid ( RA ) -induced maturation mediated by the retinoic acid recepto |
| 96437028 | c acid receptor alpha. Retinoic acid ( RA ) -induced maturation mediated by the | retinoic acid receptor alpha | ( RAR alpha ) has been implicated in myeloid development. We have used differen |
| 96437028 | acid ( RA ) -induced maturation mediated by the retinoic acid receptor alpha ( | RAR alpha | ) has been implicated in myeloid development. We have used differential hybridi |
| 96437028 | HL60 cells, but not in an RA-resistant subclone, HL60R, that harbors a mutated | RAR alpha | gene. However, when HL60R cells were transduced with a functional copy of the R |
| 96437028 | a gene. However, when HL60R cells were transduced with a functional copy of the | RAR alpha | gene, RA induced a 10-fold increase in E3 mRNA levels. E3 transcripts are prese |
| 96437028 | is a hematopoietic-specific gene that is an immediate target for the activated | RAR alpha | during myelopoiesis. |
| 94254835 | Lipopolysaccharide induction of | tissue factor | gene expression in monocytic cells is mediated by binding of c-Rel / p65 hetero |
| 94254835 | teins and leads to the rapid induction of inflammatory gene products, including | tissue factor | ( TF ) . TF is the primary cellular initiator of the coagulation protease casca |
| 94254835 | to the rapid induction of inflammatory gene products, including tissue factor ( | TF | ) . TF is the primary cellular initiator of the coagulation protease cascades. |
| 94254835 | rapid induction of inflammatory gene products, including tissue factor ( TF ) . | TF | is the primary cellular initiator of the coagulation protease cascades. Here we |
| 94254835 | at bound to a kappa B-like site, 5'--3', in the 5'-flanking region of the human | TF | gene. This nuclear complex was activated by LPS with kinetics that preceded ind |
| 94254835 | clear complex was activated by LPS with kinetics that preceded induction of the | TF | gene. In vitro binding studies demonstrated that the TF site bound translated c |
| 94254835 | cluded binding of NF-kappa B. In fact, under low-ionic-strength conditions, the | TF | complex did not migrate with translated p50 / p65 dimers but instead comigrated |
| 94254835 | ng studies revealed the presence of c-Rel and p65 and the absence of p50 in the | TF | complex and further showed that c-Rel / p65 heterodimers selectively bound to t |
| 94254835 | mplex and further showed that c-Rel / p65 heterodimers selectively bound to the | TF | kappa B-like site. Functional studies indicated that the TF site conferred LPS |
| 94254835 | c-Rel / p65 heterodimers to a novel kappa B-like site mediated LPS induction of | TF | gene expression in monocytic cells. |
| 96079922 | f T cells. PRL and IL-2 receptor activation are both linked to the Jak / Stat ( | signal transducer | and activator of transcription ) pathway. We investigated the ability of PRL an |
| 96085174 | ne T cells. The activation of Janus protein tyrosine kinases ( Jak ) and STAT ( | signal transducer | and activator of transcription ) proteins has recently been linked to the signa |
| 96322726 | o effector phenotypes. The regulation of transcription factors belonging to the | signal transducer | and activator of transcription ( STAT ) family was analyzed in PHA-activated mo |
| 97064186 | s further evident by the total lack of IL-12-induced phosphorylation of STAT4 ( | signal transducer | and activator of transcription-4 ) , a transcription factor that is typically i |
| 97207294 | strates including JAK1 and IRS-1 were phosphorylated. Additionally, we detected | signal transducers | and activators of transcription 6 ( STAT6 ) tyrosine phosphorylation and DNA bi |
| 93204975 | Transcriptional activation of human zeta 2 | globin promoter | by the alpha globin regulatory element ( HS-40 ) : functional role of specific |
| 93204975 | complexes. We studied the functional interaction between human embryonic zeta 2 | globin promoter | and the alpha globin regulatory element ( HS-40 ) located 40 kb upstream of the |
| 93204975 | ression assay that HS-40 behaved as an authentic enhancer for high-level zeta 2 | globin promoter | activity in K562 cells, an erythroid cell line of embryonic and / or fetal orig |
| 93204975 | mids, they were required for the HS-40 enhancer-mediated activity of the zeta 2 | globin promoter | . Site-directed mutagenesis demonstrated that this HS-40 enhancer-zeta 2 globin |
| 93204975 | romoter. Site-directed mutagenesis demonstrated that this HS-40 enhancer-zeta 2 | globin promoter | interaction is mediated by the two GATA-1 factor binding motifs located at -230 |
| 93204975 | the functional core of HS-40 in the erythroid-specific activation of the zeta 2 | globin promoter | . Site-directed mutagenesis further demonstrated that the enhancer function of o |
| 93204975 | cific nuclear factor-DNA complexes which form at the enhancer ( HS-40 ) and the | globin promoters | . |
| 90376424 | pha RNA in U9-IIIB cells compared with U937 cells, suggesting that HIV-infected | monocytic cells | produced higher levels of TNF-alpha than did normal cells after a secondary vir |
| 90376424 | ts. TNF-alpha was able to increase expression of the HIV LTR in T cells, but in | monocytic cells | , TNF-alpha did not induce the HIV LTR above a constitutive level of activity. T |
| 92052106 | ression in monocytes: role of the 65-kDa plus 50-kDa NF-kappa B dimer. Although | monocytic cells | can provide a reservoir for viral production in vivo, their regulation of human |
| 94254835 | Lipopolysaccharide induction of tissue factor gene expression in | monocytic cells | is mediated by binding of c-Rel / p65 heterodimers to a kappa B-like site. Expo |
| 94254835 | ated by binding of c-Rel / p65 heterodimers to a kappa B-like site. Exposure of | monocytic cells | to bacterial lipopolysaccharide ( LPS ) activates the NF-kappa B / Rel family o |
| 94254835 | e cascades. Here we report the characterization of a nuclear complex from human | monocytic cells | that bound to a kappa B-like site, 5'--3', in the 5'-flanking region of the hum |
| 94254835 | rs to a novel kappa B-like site mediated LPS induction of TF gene expression in | monocytic cells | . |
| 95332324 | Integrin-mediated tyrosine phosphorylation and cytokine message induction in | monocytic cells | . A possible signaling role for the Syk tyrosine kinase. Activation of cytoplasm |
| 95332324 | rosine kinase may be an important component of an integrin signaling pathway in | monocytic cells | , leading to activation of NF-kappa B and to increased levels of cytokine messag |
| 98012705 | e the effects of oxidized LDL ( oxLDL ) on the NF-kappa B system in human THP-1 | monocytic cells | as well as adherent monocytes. Our results demonstrate that short-term incubati |
| 98104459 | are likely to play a dominant role in TNF-alpha-induced ICAM-1 transcription in | monocytic cells | . |
| 99386936 | IKK ) signalsome activation and Ikappa B phosphorylation / proteolysis in human | monocytic cells | and investigated the role of the signalsome proteins IKK-alpha, IKK-beta, NF-ka |
| 90376424 | type 1 ( HIV-1 ) infection and viral RNA production in U937 cells. However, in | Jurkat cells | , TNF-alpha dramatically enhanced the spread of HIV-1 through the cell populatio |
| 94107268 | xpression of the CD45 PTPase and was not observed in CD45-deficient variants of | Jurkat cells | . In the CD45-negative variant, the effect of pervanadate on tyrosine phosphoryl |
| 95000924 | to CD3 were monitored. These parameters were not modified by Nef expression in | Jurkat cells | , whereas stimulation with the same stimuli resulted in partial inhibition of LT |
| 95000924 | with the same stimuli resulted in partial inhibition of LTR activation in Nef+ | Jurkat cells | . This inhibition was not mediated through Nef phosphorylation on Thr-15 or GTP- |
| 96074632 | urther, 1,25 ( OH ) 2D3 inhibited the transcriptional activity of NF-kappa B in | Jurkat cells | transiently transfected with a construct containing four tandem repeats of the |
| 97458245 | ( transmembrane activator and CAML-interactor ) , on the surface of transfected | Jurkat cells | with TACI-specific antibodies led to activation of the transcription factors NF |
| 98230439 | y from the LAI LTR in U-373 MG cells ( an astrocytoma cell line ) as well as in | Jurkat cells | ( a CD4-positive lymphocyte cell line ) . While LTRs which demonstrated the hig |
| 98230439 | trated the highest activities in U-373 MG cells also yielded high activities in | Jurkat cells | , the LTRs were generally more active in Jurkat cells when compared to the LAI L |
| 98230439 | yielded high activities in Jurkat cells, the LTRs were generally more active in | Jurkat cells | when compared to the LAI LTR. Differences in LTR sequence also resulted in diff |
| 98380286 | cell activation, the gene expression of stimulated and nonstimulated Ramos and | Jurkat cells | was studied using cDNA microarray technology. Simultaneous analysis of close to |
| 96322726 | d not inhibit IL-4 receptor alpha-chain and CD69 expression or the induction of | activator protein | 1 transcription factors. cAMP signaling inhibited Stat1 at several different le |
| 97456880 | clear factor of activated T cells ( NFAT ) family proteins as major components. | Activator protein | ( AP ) -1 family proteins interacted with CLE0, P, P2 and P4. NFAT / AP-1 compl |
| 97456880 | vated T cells ( NFAT ) family proteins as major components. Activator protein ( | AP | ) -1 family proteins interacted with CLE0, P, P2 and P4. NFAT / AP-1 complex fo |
| 96184791 | on in T cells. Mutation of the IL-13 P element site significantly reduced IL-13 | promoter activity | in response to T-cell activation. Oligonucleotides containing the IL-13 or IL-4 |
| 96279111 | e pair upstream sequence were demonstrated to play a critical role for the IL-9 | promoter activity | . DNA-protein binding studies indicated that NF-kappa B, c-Jun, and potentially |
| 96279111 | Mutations at different sites within this proximal promoter region abolished the | promoter activity | as well as the DNA binding. Taken together, these results suggest that the coop |
| 97376857 | omplexes encompassing both the CD28RE and the AP-1-binding sites influence IL-2 | promoter activity | in CD28-costimulated T cells. |
| 99005376 | 4, and a novel regulatory element, CPRE ( -- ) at -49/-41, is essential for the | promoter activity | in murine erythroleukemia ( MEL ) cells. In nonerythroid NIH3T3 cells, however, |
| 99083144 | Effect of environmental estrogens on IL-1beta | promoter activity | in a macrophage cell line. Environmental estrogens or estrogen disrupters have |
| 99083144 | porter gene allows us to monitor the effect of estrogenic compounds on IL-1beta | promoter activity | . 17beta-estradiol ( E2 ) markedly enhanced lipopolysaccharide - ( LPS ) induced |
| 99083144 | ounds, with the exception of genistein, synergized with LPS to enhance IL-1beta | promoter activity | . When tested for antiestrogenic activity, the industrial compound 4-octylphenol |
| 97028169 | poiesis via a dual effect hypothetically mediated by interaction with the RAR / | RXR | heterodimer, ie, inhibition of HSC/ primitive HPC proliferation and induction o |
| 98400423 | Retinoid X receptor | and c-cerbA / thyroid hormone receptor regulate erythroid cell growth and diffe | |
| 98400423 | nt regulators of erythroid cell development. Here we investigated the impact of | retinoid X receptor | ( RXR ) , retinoic acid receptor ( RAR ) , and of the c-erbA / thyroid hormone |
| 98400423 | roid cell development. Here we investigated the impact of retinoid X receptor ( | RXR | ) , retinoic acid receptor ( RAR ) , and of the c-erbA / thyroid hormone ( T3 ) |
| 98400423 | an in vitro culture system of stem cell factor-dependent erythroid progenitors. | RXR | , RAR, and c-erbA / TR-specific ligands were found to induce erythroid-specific |
| 98400423 | d c-erbA / TR induces differentiation. Additionally, to determine the impact of | RXR | for erythroid cell development, dominant interfering mutant RXRs, lacking the t |
| 98400423 | erythroid progenitor cells via recombinant retrovirus vectors and analyzed for | RXR | -specific effects. It was found that expression of wild-type RXR and of the RXR |
| 98400423 | nd analyzed for RXR-specific effects. It was found that expression of wild-type | RXR | and of the RXR mutants devoid of AF-1 and / or AF-2 supported a transient outgr |
| 98400423 | RXR-specific effects. It was found that expression of wild-type RXR and of the | RXR | mutants devoid of AF-1 and / or AF-2 supported a transient outgrowth of erythro |
| 98400423 | marked contrast, expression of the dominant interfering deltaDNA-binding domain | RXR | , containing a deletion of the entire DNA-binding domain, was incompatible with |
| 98400423 | incompatible with erythroid cell growth in vitro, suggesting a pivotal role of | RXR | for erythroid cell development. |
| 99369970 | toxin ( SE ) induce a rapid, gradually accumulating, long-lasting tyrosine, and | serine phosphorylation of Stat3 | ( but not Stat5 ) in allogen-specific human CD4+ T cell lines. In contrast, IL- |
| 99369970 | CD4+ T cell lines. In contrast, IL-2 induces a rapid and transient tyrosine and | serine phosphorylation of Stat3 | . Compared with IL-2, CD3 ligation induces a delayed Stat3 binding to oligonucle |
| 99369970 | ow that CD3 ligation by mAb and SE triggers a rapid, PP1-sensitive tyrosine and | serine phosphorylation of Stat3 | in human CD4+ T cells. Moreover, we provide evidence that TCR / CD3 and IL-2 in |
| 95332324 | ytokine message induction in monocytic cells. A possible signaling role for the | Syk tyrosine kinase | . Activation of cytoplasmic tyrosine kinases is an important aspect of signal tr |
| 95332324 | uent to cell adhesion include paxillin, pp125FAK, and the SH2 domain containing | tyrosine kinase Syk | . In contrast, integrin ligation with antibodies induces tyrosine phosphorylatio |
| 95332324 | IL-1 beta message induction is unaffected. These observations indicate that the | Syk tyrosine kinase | may be an important component of an integrin signaling pathway in monocytic cel |
| 91321794 | Inhibition of HIV-1 replication | and NF-kappa B activity by cysteine and cysteine derivatives. HIV-1 proviral DN | |
| 91321794 | N-acetylcysteine ( NAC ) raise the intracellular glutathione ( GSH ) level and | inhibit HIV-1 replication | in persistently infected Molt-4 and U937 cells. However, inhibition of HIV-1 re |
| 91321794 | ibit HIV-1 replication in persistently infected Molt-4 and U937 cells. However, | inhibition of HIV-1 replication | appears not to be directly correlated with GSH levels. Cysteine and NAC also in |
| 97376857 | complex. While several lines of investigation have suggested that NF-kappa B / | Rel family members | make up the CD28 response complex transcription factor, other work has not supp |
| 97376857 | is specific for both the CD28RE and the adjacent AP-1 site. Of the NF-kappa B / | Rel family members | tested, this CD28RE / AP-1-specific complex contains predominantly c-Rel, despi |
| 98104459 | NF-kappa B / | Rel family members | regulating the ICAM-1 promoter in monocytic THP-1 cells. A kappa B-site was ide |
| 94254835 | eceded induction of the TF gene. In vitro binding studies demonstrated that the | TF site | bound translated c-Rel and p65 homodimers but not p50 / p65 heterodimers or p50 |
| 94254835 | ut not p50 / p65 heterodimers or p50 homodimers. Base-pair substitutions in the | TF site | indicated that the presence of a cytosine at position 1 precluded binding of NF |
| 94254835 | tively bound to the TF kappa B-like site. Functional studies indicated that the | TF site | conferred LPS inducibility on a heterologous promoter and was transactivated by |
| 95399771 | Regulation of | granulocyte-macrophage colony | -stimulating factor and E-selectin expression in endothelial cells by cyclospori |
| 95399771 | ressed the induction of NFAT in endothelial cells and inhibited the activity of | granulocyte-macrophage colony | -stimulating factor ( GM-CSF ) gene regulatory elements that use NFAT by 60%. Cs |
| 96329553 | Granulocyte-macrophage colony | -stimulating factor preferentially activates the 94-kD STAT5A and an 80-kD STAT5 | |
| 96329553 | e 94-kD STAT5A and an 80-kD STAT5A isoform in human peripheral blood monocytes. | Granulocyte-macrophage colony | -stimulating factor ( GM-CSF ) induces immediate effects in monocytes by activat |
| 99305241 | or transformed cells and the putative roles in functionality and cell biology. | Granulocyte-macrophage colony | -stimulating factor ( GM-CSF ) and interleukin ( IL ) -3 induced tyrosine phosph |
| 90376424 | ined. Tumor necrosis factor alpha ( TNF-alpha ) mRNA production was analyzed by | polymerase chain reaction | amplification in monocytic U937 cells and in a chronically HIV infected U937 ce |
| 92134262 | the CAGs. After the DNA fragment containing the CAG repeats is amplified by the | polymerase chain reaction | , a primer extension is carried out; the extension of the end-labelled reverse p |
| 98090689 | gulatory elements required for T-cell activation. We used reverse transcriptase- | polymerase chain reaction | to examine both fetal and term neonatal cord bloods for mRNA expression of thre |
| 99155344 | as been shown to correlate with X-inactivation. In this study, we have used the | polymerase chain reaction | ( PCR ) with nested primers to analyze X-inactivation patterns of the HUMARA lo |
| 99155344 | ith X-inactivation. In this study, we have used the polymerase chain reaction ( | PCR | ) with nested primers to analyze X-inactivation patterns of the HUMARA loci in |
| 99356019 | r up to 90 min exposure time ELISA, EMSA ( electromobility shift assay ) and RT- | PCR | were used to measure protein tyrosine kinase activity, protein activity of NF-k |
| 99310627 | GATA-1 and erythropoietin cooperate to promote | erythroid cell survival | by regulating bcl-xL expression. The transcription factor GATA-1 is essential f |
| 99310627 | bcl-2 and mcl-1. Consistent with a role for bcl-xL in mediating GATA-1-induced | erythroid cell survival | , in vitro-differentiated bcl-xL-/- embryonic stem cells fail to generate viable |
| 99310627 | isruption. In addition, we show that erythropoietin, which is also required for | erythroid cell survival | , cooperates with GATA-1 to stimulate bcl-xL gene expression and to maintain ery |
| 96211859 | nse to the different stimuli, whereas the levels of IL-2 produced by stimulated | T cells from other elderly | individuals were equivalent to those observed for stimulated T cells of young s |
| 96211859 | c DNA mobility shift assays showed that decreased IL-2 production by stimulated | T cells of elderly | individuals was closely associated with impairments in the activation of both A |
| 96211859 | s / c-Jun AP-1. The resting and stimulated levels of NF kappa B were reduced in | T cells from certain elderly | individuals; however, alterations of NF kappa B did not correlate with changes |
| 98104459 | B site appeared to bind RelA and c-Rel homodimers as well as heterodimers with | NF-kappa B1 | , but weakly NF-kappa B1 homodimers. In addition, both RelA and c-Rel, but not N |
| 98104459 | RelA and c-Rel homodimers as well as heterodimers with NF-kappa B1, but weakly | NF-kappa B1 | homodimers. In addition, both RelA and c-Rel, but not NF-kappa B1, were shown t |
| 98104459 | 1, but weakly NF-kappa B1 homodimers. In addition, both RelA and c-Rel, but not | NF-kappa B1 | , were shown to transactivate an ICAM-1 kappa B-reporter construct. In monocytic |
| 98104459 | phoretic mobility supershift assay, one of these complexes was shown to contain | NF-kappa B1 | and RelA, and to bind with higher affinity to the consensus kappa B site in the |
| 98104459 | icoid receptor was shown to repress activity of both the RelA homodimer and the | NF-kappa B1 | / RelA heterodimer. We argue that in vivo RelA homodimers are likely to play a |
| 95166251 | g PEBP2 alpha genes in T cells during thymic development. The PEBP2 alpha A and | PEBP2 alpha B | genes encode the DNA-binding subunit of a murine transcription factor, PEBP2, w |
| 95166251 | lated genes share the evolutionarily conserved region encoding the Runt domain. | PEBP2 alpha B | is the murine counterpart of human AML1, which is located at the breakpoints of |
| 95166251 | inent in the thymus. Furthermore, transcripts of PEBP2 alpha A and mouse AML1 / | PEBP2 alpha B | were detected in T lymphocytes in the thymuses from day 16 embryos and newborns |
| 95166251 | at PEBP2 is a T-cell-specific transcription factor. Transcripts of mouse AML1 / | PEBP2 alpha B | were also detected in day 12 fetal hematopoietic liver and in the bone marrow c |
| 95166251 | r and in the bone marrow cells of newborn mice. The implication of mouse AML1 / | PEBP2 alpha B | expression in hematopoietic cells other than those of T-cell lineage is discuss |
| 96303658 | cells with several chemoattractants at physiologically relevant concentrations. | Activation of transcription factors | through these receptors involves G-protein coupling and the activation of prote |
| 98089072 | stigated the effect of ER alpha ( referred to throughout as ER ) on DNA-binding | activities of transcription factors | involved in regulating the expression of erythroid-specific genes, and, in part |
| 98230439 | urally occurring sequence variation impacted transcription factor binding to an | activating transcription factor | / cAMP response element binding ( ATF / CREB ) binding site ( located between t |
| 96388957 | ntly this leukemia was further characterized by an exquisite sensitivity to all- | trans retinoic acid | 's differentiation effect and the production of a fusion gene altering the gene |
| 96388957 | llows strict guidelines related both to the APL cell and the biodisposal of all- | trans retinoic acid | . |
| 97028169 | in FCS- clonogenic culture. On this basis, we have investigated the role of all- | trans retinoic acid | ( ATRA ) and its isomer 9-cis RA in FL hematopoiesis. Both compounds modulate t |
| 99201482 | ivatives of salicylate, triflusal, and its deacetylated metabolite, 2-hydroxy-4- | trifluoromethylbenzoic acid | . The therapeutic potential of drugs that block the induction of cyclooxygenase- |
| 99201482 | been emphasized. When two 4-trifluoromethyl salicylate derivatives [2-acetoxy-4- | trifluoromethyl-benzoic acid | ( triflusal ) and its deacetylated metabolite 2-hydroxy-4-trifluoromethylbenzoi |
| 99201482 | romethyl-benzoic acid ( triflusal ) and its deacetylated metabolite 2-hydroxy-4- | trifluoromethylbenzoic acid | ( HTB ) ] were compared with aspirin and sodium salicylate as cyclooxygenase-2 |
| 95000924 | NA-binding activity of NF-kappa B and AP-1 ( Fos / Jun ) complex in response to | phorbol myristate acetate | , TNF-alpha, or immobilized antibodies to CD3 were monitored. These parameters w |
| 98001571 | ted NF-kappa B, and NFAT DNA-binding activity in T cells stimulated with either | phorbol myristate acetate | plus ionophore or antibodies against the CD3-T-cell receptor complex and simult |
| 99305241 | tional activity by GM-CSF. N-formyl-methionyl-leucyl-phenylalanine ( FMLP ) and | phorbol myristate acetate | ( PMA ) induced tyrosine phosphorylation of 42- and 44-kDa proteins, which were |
| 99408303 | Neutrophil maturation | and the role of retinoic acid. Neutrophil maturation occurs in well defined mor | |
| 99408303 | Neutrophil maturation and the role of retinoic acid. | Neutrophil maturation | occurs in well defined morphological stages that correlate with the acquisition |
| 99408303 | neutrophil function. A variety of factors are known to play a role in terminal | neutrophil maturation | , including the vitamin A derivative, retinoic acid. Retinoic acid can directly |
| 99408303 | n turn, activate transcription of target genes. A role for retinoic acid during | neutrophil maturation | has been suggested from a variety of sources. Here we present a review of the m |
| 99408303 | n and the major evidence showing that normal retinoid signaling is required for | neutrophil maturation | . |
| 94209654 | Activation of a novel serine / | threonine kinase | that phosphorylates c-Fos upon stimulation of T and B lymphocytes via antigen a |
| 94209654 | eus is mediated principally through the action of protein tyrosine and serine / | threonine kinases | . We have identified and characterized a novel serine / threonine kinase that ph |
| 94209654 | rine / threonine kinases. We have identified and characterized a novel serine / | threonine kinase | that phosphorylated the proto-oncogene product, c-Fos, and is termed Fos kinase |
| 94209654 | phorylation. Fos kinase was shown to be distinct from other identified serine / | threonine kinases | , including protein kinase A, protein kinase C, casein kinase II, MAP kinases, p |
| 94254835 | sue factor gene expression in monocytic cells is mediated by binding of c-Rel / | p65 heterodimers | to a kappa B-like site. Exposure of monocytic cells to bacterial lipopolysaccha |
| 94254835 | trated that the TF site bound translated c-Rel and p65 homodimers but not p50 / | p65 heterodimers | or p50 homodimers. Base-pair substitutions in the TF site indicated that the pr |
| 94254835 | nd p65 and the absence of p50 in the TF complex and further showed that c-Rel / | p65 heterodimers | selectively bound to the TF kappa B-like site. Functional studies indicated tha |
| 94254835 | c-Rel or p65. Taken together, our results demonstrated that binding of c-Rel / | p65 heterodimers | to a novel kappa B-like site mediated LPS induction of TF gene expression in mo |
| 97468093 | on of the synthesis and of the hydrolytic activity of phospholipase C gamma 1 ( | PLC gamma | 1 ) in human T lymphocytes by IFN-beta. The increased level of PLC gamma 1 beco |
| 97468093 | ma 1 ( PLC gamma 1 ) in human T lymphocytes by IFN-beta. The increased level of | PLC gamma | 1 becomes evident after 90 min of IFN-beta treatment and is still detectable af |
| 97468093 | er 90 min of IFN-beta treatment and is still detectable after 24 h. Neither the | PLC gamma | 1 overexpression induced by IFN nor the increased hydrolytic activity of the en |
| 97468093 | a can activate other transcription factor ( s ) distinct from ISGF3 to regulate | PLC gamma | 1 expression. In addition, the ability of this enzyme to hydrolyse PIP2, also i |
| 90376424 | y virus infection. The effects of TNF-alpha on gene expression were examined by | transient expression | assays using reporter chloramphenicol acetyltransferase plasmids linked to regu |
| 92135145 | ve inhibitor of NF-kappa B and discuss how these factors may be involved in the | transient expression | of IL-2 and IL-2 alpha genes during the immune response. |
| 93204975 | ent ( HS-40 ) located 40 kb upstream of the zeta 2 globin gene. It was shown by | transient expression | assay that HS-40 behaved as an authentic enhancer for high-level zeta 2 globin |
| 93204975 | id cells. All sequence motifs within the functional core of HS-40, as mapped by | transient expression | analysis, appeared to bind a nuclear factor ( s ) in living K562 cells but not |
| 96279111 | gene expression is controlled, at least in part, by transcriptional activation. | Transient expression | of the luciferase reporter gene linked to serially deleted sequences of the 5'- |
| 98230439 | es ( with respect to the sequence of the LAI LTR ) within the 455-bp U3 region. | Transient expression | analyses in cells of neuroglial and lymphocytic origin demonstrated that some o |
| 90376424 | phoid cells, the inducibility of the different hybrid promoters by TNF-alpha or | phorbol ester | varied in a cell type- and promoter context-specific manner; the levels of gene |
| 90376424 | ity. Although the intact beta interferon promoter was only weakly stimulated by | phorbol ester | or TNF-alpha, multimers of the PRDII NF-kappa B-binding domain were inducible b |
| 94107268 | synergized with signals delivered by T-cell antigen receptor engagement or by a | phorbol ester | to induce interleukin 2 production. Pervanadate activated NF-kappa B, as shown |
| 94209654 | o IL-6 and anti-IgM in the human B cell lines AF10 and Ramos, respectively. The | phorbol ester | , PMA, was also a potent inducer of Fos kinase activity in all of the above popu |
| 98001571 | ) . Accordingly, electrophoretic mobility shift assays ( EMSAs ) indicated that | pyrrolidine DTC | ( PDTC ) prevented NF-kappa B, and NFAT DNA-binding activity in T cells stimula |
| 98001571 | lectrophoretic mobility shift assays ( EMSAs ) indicated that pyrrolidine DTC ( | PDTC | ) prevented NF-kappa B, and NFAT DNA-binding activity in T cells stimulated wit |
| 98001571 | receptor complex and simultaneously activated the binding of AP-1. Furthermore, | PDTC | differentially targeted both NFATp and NFATc family members, inhibiting the tra |
| 98001571 | Strikingly, Western blotting and immunocytochemical experiments indicated that | PDTC | promoted a transient and rapid shuttling of NFATp and NFATc, leading to their a |
| 98001571 | cleus of activated T cells. We propose that the activation of an NFAT kinase by | PDTC | could be responsible for the rapid shuttling of the NFAT, therefore transiently |
| 98038749 | Regulation of Id3 cell cycle function by Cdk-2- | dependent phosphorylation | . The functions of basic helix-loop-helix ( bHLH ) transcription factors in acti |
| 98038749 | gene regulatory ( E box ) sequences. Recently, cyclin E-Cdk2- and cyclin A-Cdk2- | dependent phosphorylation | of a single conserved serine residue ( Ser5 ) in Id2 has been shown to occur du |
| 98038749 | lays an activity significantly greater than that of wild-type Id3 protein. Cdk2- | dependent phosphorylation | therefore provides a switch during late G1-to-S phase that both nullifies an ea |
| 99305241 | . In contrast to neutrophils, p38 was constitutively phosphorylated and agonist- | dependent phosphorylation | and activation was not detected in human monocytes. Superoxide release stimulat |
| 92215726 | y 8 h and approximately 1000 VDR by 24 h. Radiolabeled VDR disappeared from the | nuclear compartment | with a halflife of approximately 30 min if cells were cultured with identical c |
| 92215726 | where VDR halflife was approximately 30 min. No specific translocation into the | nuclear compartment | was seen when isolated nuclei were incubated in [3H]calcitriol. Radiolabeled ho |
| 92215726 | contrast to identical experiments with intact cells-did not disappear from the | nuclear compartment | upon incubation of nuclei with identical concentrations of the unlabeled compou |
| 92215726 | extracts upon translocation of VDR might reflect interaction of both within the | nuclear compartment | , thus initiating DNA-unwinding, a prerequisite of transcription initiation. |
| 96074632 | ffect of the hormone on the levels of p50 was demonstrable in the cytosolic and | nuclear compartments | ; it required between 4 and 8 hr and was specific, as 25-hydroxyvitamin D3 and 2 |
| 93204975 | -40 enhancer region in K562 cells, adult nucleated erythroblasts, and different | nonerythroid cells | . All sequence motifs within the functional core of HS-40, as mapped by transien |
| 93204975 | alysis, appeared to bind a nuclear factor ( s ) in living K562 cells but not in | nonerythroid cells | . On the other hand, only one of the apparently nonfunctional sequence motifs wa |
| 99005376 | ifferential regulation of coproporphyrinogen oxidase gene between erythroid and | nonerythroid cells | . Coproporphyrinogen oxidase ( CPO ) catalyzes the sixth step of the heme biosyn |
| 99005376 | ferential regulation of the promoter function of CPO gene between erythroid and | nonerythroid cells | . Copyright 1998 by The American Society of Hematology |
| 97263762 | ke transcription factor in the activation of serum amyloid A gene in monocyte / | macrophage cells | by lipopolysaccharide. Serum amyloid A ( SAA ) has been linked to atheroscleros |
| 97263762 | study, we investigated the induction mechanism of SAA gene in THP-1 monocyte / | macrophage cells | which play a critical role in the development of atherosclerotic fatty streak a |
| 97263762 | aque formation. We and others have shown that SAA gene is induced in monocyte / | macrophage cells | by lipopolysaccharide ( LPS ) . By promoter function analysis, we show that the |
| 97263762 | . These results demonstrated that LPS-mediated SAA gene induction in monocyte / | macrophage cells | is primarily due to the induction of SAF activity. |
| 92134262 | A novel primer extension method to detect the number of | CAG repeats | in the androgen receptor gene in families with X-linked spinal and bulbar muscu |
| 92134262 | otor neuron disease, was recently reported to be caused by amplification of the | CAG repeats | in the androgen receptor gene. We report here a simple and rapid strategy to de |
| 92134262 | to detect the precise number of the CAGs. After the DNA fragment containing the | CAG repeats | is amplified by the polymerase chain reaction, a primer extension is carried ou |
| 92134262 | ied out; the extension of the end-labelled reverse primer adjacent to 3' end of | CAG repeats | stops at the first T after CAG repeats with the incorporation of dideoxy ATP in |
| 92134262 | led reverse primer adjacent to 3' end of CAG repeats stops at the first T after | CAG repeats | with the incorporation of dideoxy ATP in the reaction mixture. The resultant pr |
| 92134262 | resis and autoradiography. This method could be quite useful to detect not only | CAG repeats | in SBMA but also other polymorphic dinucleotide and trinucleotide repeats. |
| 99386936 | s in human monocytic cells and investigated the role of the signalsome proteins | IKK-alpha | , IKK-beta, NF-kappa B-inducing kinase ( NIK ) , IKK-gamma ( NF-kappa B essentia |
| 99386936 | rapid but short-lived induction of IKK activity with a 3-fold greater effect on | IKK-alpha | than on IKK-beta, peaking at 5 min. In contrast, LPS predominantly stimulated I |
| 99386936 | served at a later time point following LPS stimulation, which consisted of both | IKK-alpha | and -beta activity. The endogenous levels of the signalsome components were una |
| 99386936 | e unaffected by stimulation. Furthermore, our studies showed association of the | IKK-alpha | / beta heterodimer with NIK, Ikappa B-alpha and -epsilon in unstimulated cells. |
| 99386936 | Ikappa B-epsilon disappearance from and reassembly with the signalsome, whereas | IKK-alpha | , IKK-beta, and NIK remained complex-associated. NIK cannot phosphorylate Ikappa |
| 99386936 | stimulus-induced kappa B-dependent transcription more effectively than mutated | IKK-alpha | or -beta. Overexpression of IKK complex-associated protein inhibited stimulus-m |
| 95222739 | l repeat in T lymphocytes. CBF consists of two subunits, a DNA binding subunit, | CBF alpha | , and a second subunit, CBF beta, that stimulates the DNA binding activity of CB |
| 95222739 | ha, and a second subunit, CBF beta, that stimulates the DNA binding activity of | CBF alpha | . One of the genes that encodes a CBF alpha subunit is AML1, also called Cbf alp |
| 95222739 | imulates the DNA binding activity of CBF alpha. One of the genes that encodes a | CBF alpha | subunit is AML1, also called Cbf alpha 2. This locus is rearranged by chromosom |
| 95222739 | F alpha. One of the genes that encodes a CBF alpha subunit is AML1, also called | Cbf alpha | 2. This locus is rearranged by chromosomal translocations in human myeloprolife |
| 95222739 | s in human myeloproliferative disorders and leukemias. An exogenously expressed | Cbf alpha | 2-encoded subunit ( CBF alpha 2-451 ) stimulated transcription from the SL3 enh |
| 95222739 | disorders and leukemias. An exogenously expressed Cbf alpha 2-encoded subunit ( | CBF alpha | 2-451 ) stimulated transcription from the SL3 enhancer in P19 and HeLa cells. A |
| 95222739 | r. The longest form, CBF beta-187, increased the transcriptional stimulation by | CBF alpha | 2-451 twofold in HeLa cells, although it had no effect in P19 cells. Transcript |
| 95222739 | ct in P19 cells. Transcriptional activation by CBF beta required binding to the | CBF alpha | subunit, as a form of CBF beta that lacked binding ability, CBF beta-148, faile |
| 95222739 | transcription in T cells and leukemogenicity of SL3. However, no combination of | CBF alpha | and CBF beta subunits that we tested was able to distinguish the 1-bp differenc |
| 96079922 | ranscription ) pathway. We investigated the ability of PRL and IL-2 to activate | Stat proteins | in different T cell lines. The DNA binding specificities, the reactivities towa |
| 96079922 | proteins in Nb2 and C196 T cell lines were investigated. A comparison with the | Stat proteins | induced by interferon-gamma, PRL, and IL-6 in T47D mammary tumor cells was made |
| 96085174 | oncomitantly, the tyrosine phosphorylation and DNA binding activity of multiple | STAT proteins | . The STAT proteins utilized by IL-7 were identical to those induced by IL-2 and |
| 96085174 | yrosine phosphorylation and DNA binding activity of multiple STAT proteins. The | STAT proteins | utilized by IL-7 were identical to those induced by IL-2 and could be identifie |
| 99168986 | Interferon-alpha activates multiple | STAT proteins | and upregulates proliferation-associated IL-2Ralpha, c-myc, and pim-1 genes in |
| 99168986 | nvolved in the regulation of T-cell mitogenesis. When we analyzed the nature of | STAT proteins | capable of binding to IL-2Ralpha, pim-1, and IRF-1 GAS elements after cytokine |
| 93024468 | ing specificity similar to that of NF-kappa B but is unrelated to this or other | Rel proteins | by functional and biochemical criteria. It can also be distinguished from other |
| 94254835 | stead comigrated with c-Rel / p65 dimers. Antibodies against the NF-kappa B and | Rel proteins | and UV cross-linking studies revealed the presence of c-Rel and p65 and the abs |
| 99146379 | ed in T cells 3 days after activation, coincident with RANTES expression. While | Rel proteins | play the dominant role in RANTES gene expression in fibroblasts, RFLAT-1 is a s |
| 92215726 | Kinetics of | nuclear translocation | and turnover of the vitamin D receptor in human HL60 leukemia cells and periphe |
| 92215726 | yelocytes, can be induced to monocytoid differentiation by calcitriol. Specific | nuclear translocation | of [3H]calcitriol / VDR was examined after exposure of whole cells to 10 ( -9 ) |
| 92215726 | 00-fold excess of unlabeled ligand and subsequent isolation of nuclei. Specific | nuclear translocation | of [3H]calcitriol / VDR was found to be time dependent reaching a maximum of ap |
| 92215726 | 60. No effect was seen in ethanol treated controls. We conclude that a specific | nuclear translocation | mechanism exists for calcitriol in both cell types examined, most likely due to |
| 95332324 | roteins of about 65-75 and 120-125 kDa. In addition, integrin ligation leads to | nuclear translocation | of the p50 and p65 subunits of the NF-kappa B transcription factor, to activati |
| 96075792 | ncreased mRNA stability, the duration of mRNA accumulation was longer following | LPS stimulation | in primed monocytes, in addition to being of greater magnitude. Finally, primed |
| 96075792 | accumulation in unprimed cells, but had no effect on primed monocytes following | LPS stimulation | . |
| 99386936 | , peaking at 30 min. A second peak was observed at a later time point following | LPS stimulation | , which consisted of both IKK-alpha and -beta activity. The endogenous levels of |
| 96329553 | ranulocyte-macrophage colony-stimulating factor preferentially activates the 94- | kD STAT5A | and an 80-kD STAT5A isoform in human peripheral blood monocytes. Granulocyte-ma |
| 96329553 | e colony-stimulating factor preferentially activates the 94-kD STAT5A and an 80- | kD STAT5A | isoform in human peripheral blood monocytes. Granulocyte-macrophage colony-stim |
| 96329553 | lower molecular weight STAT5 isoforms. Freshly isolated monocytes expressed 94- | kD STAT5A | , 92-kD STAT5B, and an 80-kD STAT5A molecule. Whereas 94-kD STAT5A was clearly t |
| 96329553 | rms. Freshly isolated monocytes expressed 94-kD STAT5A, 92-kD STAT5B, and an 80- | kD STAT5A | molecule. Whereas 94-kD STAT5A was clearly tyrosine phosphorylated and bound to |
| 96329553 | expressed 94-kD STAT5A, 92-kD STAT5B, and an 80-kD STAT5A molecule. Whereas 94- | kD STAT5A | was clearly tyrosine phosphorylated and bound to the enhancer element, the gamm |
| 96329553 | o the immobilized GRR element. Macrophages lost their ability to express the 80- | kD STAT5A | protein, but retained their ability to activate STAT5A. STAT5A-STAT5A homodimer |
| 97211823 | re thought to be critical for the transcription of genes involved in immune and | inflammatory responses | . We have reported previously that a nuclear NF-kappa B activity was present in |
| 98001571 | e role of this transcription factor in the regulation of gene expression in the | inflammatory response | , NF-kappa B inhibitors have been suggested as potential therapeutic drugs for i |
| 99118181 | g increasingly apparent that NF-kappa B plays a critical role in regulating the | inflammatory response | . Data obtained from studies in our laboratories demonstrate that the proteasome |
| 99207658 | osteroids are susceptible to modify functions of cells involved in the allergic | inflammatory response | . They are in particular able to inhibit most of the pro-inflammatory functions |
| 95127261 | Alternate | immune system | targets for TCDD: lymphocyte stem cells and extrathymic T-cell development. We |
| 98230439 | LTR-directed gene expression in cells of the central nervous system ( CNS ) and | immune system | , we amplified and cloned LTRs from proviral DNA in HIV-1-infected peripheral bl |
| 98230439 | , which may, in turn, alter the course of viral replication in cells of CNS and | immune system | origin. |
| 99083144 | es. Few, if any, studies have been made on the impact of these compounds on the | immune system | . We sought to determine the activities of various environmental estrogens on th |
| 99294118 | l pathogenic mechanisms. Endogenous and therapeutic steroid hormones affect the | immune system | , and inflammatory diseases are associated with activation of the hypothalamic-p |
| 99357866 | nvolves the production of interleukin-12 ( IL-12 ) , a key signal of the innate | immune system | . Yet, for many pathogens, the molecules that induce IL-12 production by macroph |
| 95036290 | Distinct DNase-I | hypersensitive sites | are associated with TAL-1 transcription in erythroid and T-cell lines. The tal- |
| 95036290 | ranscriptionally inactive alleles in established cell lines. Five major DNase-I | hypersensitive sites | ( HS ) were mapped in the tal-1 locus. HS I, IV, and V were exclusively observe |
| 95036290 | ve alleles in established cell lines. Five major DNase-I hypersensitive sites ( | HS | ) were mapped in the tal-1 locus. HS I, IV, and V were exclusively observed in |
| 95036290 | Five major DNase-I hypersensitive sites ( HS ) were mapped in the tal-1 locus. | HS | I, IV, and V were exclusively observed in the erythroid / megakaryocytic cell l |
| 95036290 | id / megakaryocytic cell lines that express tal-1 from the promoters 1a and 1b. | HS | II was weak in hematopoietic cell lines, absent in Hela, and greatly enhanced i |
| 95036290 | ght be implicated in the cis-activation of tal-1 promoter 1b in this cell line. | HS | III was weak in HEL and Jurkat, and greatly enhanced in DU528, a T-cell line th |
| 95399771 | ndothelial cells were also detected at the chromatin structure level, as DNasel | hypersensitive sites | within both the GM-CSF enhancer and the E-selectin promoter were suppressed by |
| 96239534 | s type 1-infected human T lymphocytes support higher levels of 5S rRNA and tRNA | gene transcription | than chromatin or extracts from uninfected T lymphocytes. The viral protein Tax |
| 96239534 | The viral protein Tax was likely responsible for this higher level of class II | gene transcription | , as purified Tax was found to stimulate both genes when added to the uninfected |
| 96239534 | -component transcription assays and DNA binding assays identified the class III | gene transcription | factor TFIIIB as the principle target of Tax activity. Surprisingly, we find th |
| 96303658 | Gene transcription | through activation of G-protein-coupled chemoattractant receptors. Receptors fo | |
| 96303658 | in-coupled serpentine receptors have been found to transduce signals leading to | gene transcription | and translation in leukocytes. Transcription factors, such as NF kappa B and AP |
| 97211823 | articularly abundant in lymphoid tissues and are thought to be critical for the | transcription of genes | involved in immune and inflammatory responses. We have reported previously that |
| 97303223 | the IL-4Ralpha chain may transduce intracellular signals that lead to Cepsilon | gene transcription | independently of its association with other chains. We show that ligand-induced |
| 97324097 | e E74 site independent of mitogenic signaling. Thus, Elf-1 is able to stimulate | gene transcription | which may be required for the development and activity of lymphocytes. |
| 93204975 | alpha globin regulatory element ( HS-40 ) located 40 kb upstream of the zeta 2 | globin gene | . It was shown by transient expression assay that HS-40 behaved as an authentic |
| 93204975 | or fetal origin. Although sequences located between -559 and -88 of the zeta 2 | globin gene | were dispensable for its expression on enhancerless plasmids, they were require |
| 93204975 | n. These data suggest that transcriptional activation of human embryonic zeta 2 | globin gene | and the fetal / adult alpha globin genes is mediated by erythroid cell-specific |
| 92052106 | pa B heterodimer was preferentially lost. Adding purified NF-kappa B protein to | nuclear extracts | from cells with restricted expression overcomes this lack of binding. In additi |
| 92052106 | cted expression overcomes this lack of binding. In addition, treatment of these | nuclear extracts | with sodium deoxycholate restored their ability to form the heterodimer, sugges |
| 92052106 | the presence of an inhibitor of NF-kappa B activity. Furthermore, treatment of | nuclear extracts | from these cells that had restricted expression with lipopolysaccharide increas |
| 92215726 | ls and peripheral blood lymphocytes-coincident rise of DNA-relaxing activity in | nuclear extracts | . High affinity receptors ( VDR ) for 1,25-dihydroxycholecalciferol ( calcitriol |
| 92215726 | pound. The activity of DNA relaxing enzymes ( e.g. topoisomerases I and II ) in | nuclear extracts | was measured using a PBR 322-relaxation-assay. Enhanced overall enzyme activity |
| 92215726 | using a PBR 322-relaxation-assay. Enhanced overall enzyme activity was found in | nuclear extracts | by 1 h after incubation with calcitriol ( final ethanol concentration 0.0001% v |
| 92215726 | umber of specific nuclear binding sites. Enhanced activity of topoisomerases in | nuclear extracts | upon translocation of VDR might reflect interaction of both within the nuclear |
| 96074632 | eased the abundance of a specific DNA-protein complex formed upon incubation of | nuclear extracts | from activated lymphocytes with a labeled NF-kappa B DNA binding motif. Further |
| 96211859 | ivalent to those observed for stimulated T cells of young subjects. Analyses of | nuclear extracts | by electrophoretic DNA mobility shift assays showed that decreased IL-2 product |
| 98104462 | at is upregulated in LPS toler ant human Mono Mac 6 cells. The same is true for | nuclear extracts | taken from the murine P388D1 macrophage cell line when tested with the -516 mot |
| 94238882 | -1 beta, IL-6 and TNF alpha expression, both at the mRNA and protein level. The | induced expression | of IL-1 beta and TNF alpha mRNA in the monocytic THP-1 cell line increased as q |
| 96279111 | led several positive and negative regulatory elements involved in the basal and | inducible expression | of the IL-9 gene in C5MJ2 cells. An AP-1 site at -146 to -140 was shown to be i |
| 96279111 | on between -46 and -80 was identified as the minimum sequence for the basal and | inducible expression | of the IL-9 gene in C5MJ2 cells. Within this region, an NF-kappa B site at -59 |
| 94107268 | ivation. Moreover, induction of tyrosine phosphorylation appears sufficient per | se | to initiate a complete activation programme. |
| 99081619 | nt CD4 ( + ) T cells into the cell cycle upon stimulation with the superantigen | staphylococcal enterotoxin | B ( SEB ) . IL-10 arrested cells at G0 / G1. IL-10 treatment prevented the down |
| 99369970 | tivation of Stat5 in murine T cells. Here, we show that CD3 ligation by mAb and | Staphylococcal enterotoxin | ( SE ) induce a rapid, gradually accumulating, long-lasting tyrosine, and serin |
| 99369970 | cells. Here, we show that CD3 ligation by mAb and Staphylococcal enterotoxin ( | SE | ) induce a rapid, gradually accumulating, long-lasting tyrosine, and serine pho |
| 99369970 | 3 activation is unaffected. In conclusion, we show that CD3 ligation by mAb and | SE | triggers a rapid, PP1-sensitive tyrosine and serine phosphorylation of Stat3 in |
| 90376424 | Cell-specific differences in activation of NF-kappa B | regulatory elements | of human immunodeficiency virus and beta interferon promoters by tumor necrosis |
| 90376424 | sion assays using reporter chloramphenicol acetyltransferase plasmids linked to | regulatory elements | from the HIV long terminal repeat ( LTR ) and the beta interferon promoter. In |
| 93183827 | This observation directly demonstrates the existence of a Ca2+ signal-dependent | regulatory element | obligatory for expression of some genes in T cells but not in fibroblasts. This |
| 93204975 | Transcriptional activation of human zeta 2 globin promoter by the alpha globin | regulatory element | ( HS-40 ) : functional role of specific nuclear factor-DNA complexes. We studie |
| 93204975 | interaction between human embryonic zeta 2 globin promoter and the alpha globin | regulatory element | ( HS-40 ) located 40 kb upstream of the zeta 2 globin gene. It was shown by tra |
| 94238882 | pon treatment with MDHM. IL-1 beta and IL-6 genes contain AP-1 binding sites as | regulatory elements | , the AP-1 protein being composed of c-jun and c-fos gene products. In THP-1 cel |
| 95036290 | nitiates tal-1 transcription within exon 4. These results suggest that distinct | regulatory elements | are associated with the use of the different tal-1 promoters. |
| 95399771 | he activity of granulocyte-macrophage colony-stimulating factor ( GM-CSF ) gene | regulatory elements | that use NFAT by 60%. CsA similarly mediated a reduction of up to 65% in GM-CSF |
| 96279111 | 5'-flanking region of the IL-9 gene has revealed several positive and negative | regulatory elements | involved in the basal and inducible expression of the IL-9 gene in C5MJ2 cells. |
| 97456880 | rotein-1 family proteins. We previously identified the P sequence as a critical | regulatory element | of the human IL-4 promoter. In the mouse IL-4 promoter, there are five elements |
| 98090689 | natal T-cell activation may be due to lack of expression of the transcriptional | regulatory elements | required for T-cell activation. We used reverse transcriptase-polymerase chain |
| 99005376 | c action between an SP-1-like element at -21/-12, asite at -59/-54, and a novel | regulatory element | , CPRE ( -- ) at -49/-41, is essential for the promoter activity in murine eryth |
| 99083144 | in was a very low-potency agonist, having an EC50 of 1.5 microM. Similar to the | E2 response | , the slope factors for alpha-zearalenol, zearalenone, and genistein were close |
| 99083144 | enic activity, the industrial compound 4-octylphenol was able to antagonize the | response to E2 | ; however, the response was three orders of magnitude less potent than H 1285. N |
| 99083144 | 5. Naringenin, a plant flavonoid, showed little or no ability to antagonize the | response to E2 | . Overall, the results show that some environmental estrogens that display agoni |
| 91190842 | on factor that activates the T-cell receptor C alpha gene enhancer in a context- | dependent manner | . The differentiation of T cells into functionally diverse subpopulations is con |
| 99083144 | olysaccharide - ( LPS ) induced IL-1beta promoter-driven CAT activity in a dose- | dependent manner | . The mycotoxins alpha-zearalenol and zearalenone both exhibited full agonist ac |
| 99083144 | ns H1285 and ICI 182,780 effectively inhibited their agonist activity in a dose- | dependent manner | . Representative environmental estrogenic compounds both from plant and industri |
| 99406845 | t therapeutic concentrations resulted in monocyte apoptosis in a time- and dose- | dependent manner | . Necrosis was excluded by propidium iodide staining. Proinflammatory cytokines |
| 96074632 | -regulation of NF-kappa B protein levels in activated human lymphocytes by 1,25- | dihydroxyvitamin D3 | [published erratum appears in Proc Natl Acad Sci U S A 1996 Jan 9;93 ( 1 ) :524 |
| 96074632 | ppears in Proc Natl Acad Sci U S A 1996 Jan 9;93 ( 1 ) :524] The effect of 1,25- | dihydroxyvitamin D3 | [1,25 ( OH ) 2 ) D3], a steroid hormone with immunomodulating properties, on nu |
| 96074632 | required between 4 and 8 hr and was specific, as 25-hydroxyvitamin D3 and 24,25- | dihydroxyvitamin D3 | were ineffective. Besides p50, 1,25 ( OH ) 2D3 decreased the levels of another |
| 96322726 | er activation. Stimulation of the cAMP signal transduction pathway, which skews | cytokine production | toward a Th2 pattern, resulted in the preferential suppression of Stat1 activit |
| 98090689 | tion. Fetal and neonatal lymphocytes are relatively resistant to activation and | cytokine production | when stimulated either via their T-cell antigen receptors or lectins. The molec |
| 99172186 | ranscription factor NF-kappa B. In parallel, NAC was shown to down-regulate the | production of cytokines | by DC as well as their surface expression of HLA-DR, CD86 ( B7-2 ) , and CD40 m |
| 90140708 | n a complex interplay of ubiquitous and developmentally regulated proteins. Two | complementary DNAs | were isolated that encode proteins, denoted ITF-1 and ITF-2, that are expressed |
| 90140708 | icroE5 / kappa 2 motif found in both heavy and kappa light chain enhancers. The | complementary DNAs | are the products of distinct genes, yet both ITF-1 and ITF-2 are structurally a |
| 96185499 | ylase activity. Both proteins were identified by peptide microsequencing, and a | complementary DNA | encoding the histone deacetylase catalytic subunit ( HD1 ) was cloned from a hu |
| 97303223 | IL-4 receptor ( IL-4R ) in B cells is composed of two chains, the IL-4-binding | IL-4Ralpha chain | , which is shared with the IL-13R, and the IL-2Rgamma ( gammac ) chain, which is |
| 97303223 | lack the gammac chain may involve signaling via the IL-13R. Alternatively, the | IL-4Ralpha chain | may transduce intracellular signals that lead to Cepsilon gene transcription in |
| 97303223 | psilon germline transcripts. These results suggest that homodimerization of the | IL-4Ralpha chain | is sufficient to transduce Jak1-dependent intracellular signals that lead to Ig |
| 94209654 | signal transduction cascades which alter the expression of genes that regulate | cellular proliferation | and differentiation. The transmission of signals from the membrane to the nucle |
| 97054651 | tyrosine kinase ( PTK ) -specific inhibitor herbimycin A dramatically decreased | cellular proliferation | without altering the activity of the human immunodeficiency virus-1 long termin |
| 97054651 | ibited HIV-1 LTR activity at a concentration as low as 100 nM without affecting | cellular proliferation | . Electrophoretic mobility shift assay ( EMSA ) and supershift assay using an NF |
| 90376424 | production was analyzed by polymerase chain reaction amplification in monocytic | U937 cells | and in a chronically HIV infected U937 cell line ( U9-IIIB ) . TNF-alpha RNA wa |
| 90376424 | lly HIV infected U937 cell line ( U9-IIIB ) . TNF-alpha RNA was undetectable in | U937 cells | , whereas a low constitutive level was detected in U9-IIIB cells. Paramyxovirus |
| 90376424 | rease in the steady-state level of TNF-alpha RNA in U9-IIIB cells compared with | U937 cells | , suggesting that HIV-infected monocytic cells produced higher levels of TNF-alp |
| 90376424 | kinetics of de novo HIV type 1 ( HIV-1 ) infection and viral RNA production in | U937 cells | . However, in Jurkat cells, TNF-alpha dramatically enhanced the spread of HIV-1 |
| 91321794 | ( GSH ) level and inhibit HIV-1 replication in persistently infected Molt-4 and | U937 cells | . However, inhibition of HIV-1 replication appears not to be directly correlated |
| 98104462 | or necrosis factor ) gene is only very low, i.e. the cells are tolerant to LPS. | Tolerant cells | still express the CD14 receptor and they can still be activated to mobilize NF- |
| 98104462 | proteins employing the -605 motif of the human TNF promoter () revealed that in | tolerant cells | of the human monocytic cell line Mono Mac 6 there is a predominance of p50p50 o |
| 98104462 | wild type motif gives efficient binding of p50p50 that again is upregulated in | tolerant cells | whereas a mutant with a 3' G shows hardly any binding of p50p50. Conversely, th |
| 98104462 | by a C. These data show that the detection of upregulated p50 homodimers in LPS | tolerant cells | is dependent on subtle differences in the sequence of the DNA binding motif. |
| 92052106 | ive. These differences in gene expression have not been molecularly defined. In | THP-1 cells | with restricted HIV expression, there is an absence of DNA-protein binding comp |
| 94238882 | elements, the AP-1 protein being composed of c-jun and c-fos gene products. In | THP-1 cells | c-jun mRNA expression increased after incubation with MDHM while positive c-fos |
| 94238882 | jun expression was not modulated. c-myc mRNA expression, constitutively high in | THP-1 cells | , was induced in MDHM-stimulated PBMo. In conclusion, MDHM-stimulated induction |
| 94238882 | NA expression was accompanied by different proto-oncogene responses in PBMo and | THP-1 cells | . These differences may represent different regulatory pathways of the two cell |
| 98104459 | NF-kappa B / Rel family members regulating the ICAM-1 promoter in monocytic | THP-1 cells | . A kappa B-site was identified in the promoter of the intercellular adhesion mo |
| 98104459 | were shown to transactivate an ICAM-1 kappa B-reporter construct. In monocytic | THP-1 cells | TNF-alpha induced two nuclear complexes which in vitro bound to the ICAM-1 kapp |
| 92215726 | man leukemia cells and in low numbers in peripheral blood lymphocytes ( PBL ) . | HL60 cells | , expressing some characteristics of promyelocytes, can be induced to monocytoid |
| 92215726 | aximum of approximately 2100 binding sites / nucleus after 3 h of incubation in | HL60 cells | , whereas a maximum of approximately 310 binding sites / nucleus was found after |
| 96437028 | ls peaking after 60 minutes exposure to RA. E3 transcripts were RA-inducible in | HL60 cells | , but not in an RA-resistant subclone, HL60R, that harbors a mutated RAR alpha g |
| 92135145 | two nuclear proteins NF-kappa B ( consisting of subunits p50 an dp65 ) and the | DNA-binding | subunit of NF-kappa B ( p50 ) by itself, also called KBF1, are constitutively e |
| 93024468 | and B lymphocytes but is not found in nonhematopoietic cells. This factor has a | DNA-binding | specificity similar to that of NF-kappa B but is unrelated to this or other Rel |
| 93024468 | t can also be distinguished from other previously described lymphocyte-specific | DNA-binding | proteins. |
| 93321228 | rsistent expression of the c-fos protooncogene, associated to an increased AP-1 | DNA-binding | activity, whereas no variations of CREB or NF-kB were detected. Neither Bt2cAMP |
| 94107268 | ukin 2 production. Pervanadate activated NF-kappa B, as shown by an increase in | DNA-binding | activity of this transcription factor. We thus conclude that PTPases play a cru |
| 95000924 | ssion vector. Secretion of IL-2 and TNF-alpha, surface expression of IL-2R, and | DNA-binding | activity of NF-kappa B and AP-1 ( Fos / Jun ) complex in response to phorbol my |
| 95166251 | during thymic development. The PEBP2 alpha A and PEBP2 alpha B genes encode the | DNA-binding | subunit of a murine transcription factor, PEBP2, which is implicated as a T-cel |
| 95222739 | he viral long terminal repeat in T lymphocytes. CBF consists of two subunits, a | DNA binding | subunit, CBF alpha, and a second subunit, CBF beta, that stimulates the DNA bin |
| 95222739 | binding subunit, CBF alpha, and a second subunit, CBF beta, that stimulates the | DNA binding | activity of CBF alpha. One of the genes that encodes a CBF alpha subunit is AML |
| 95261059 | closely related members of the ets transcription factor family, sharing similar | DNA binding | specificities mediated by similar DNA binding domains. PU.1 and Spi-B have been |
| 95261059 | on factor family, sharing similar DNA binding specificities mediated by similar | DNA binding | domains. PU.1 and Spi-B have been previously described as being predominantly e |
| 96079922 | bility of PRL and IL-2 to activate Stat proteins in different T cell lines. The | DNA binding | specificities, the reactivities toward Stat-specific antisera, and the mol wt o |
| 96079922 | tivities toward Stat-specific antisera, and the mol wt of IL-2 -and PRL-induced | DNA-binding | proteins in Nb2 and C196 T cell lines were investigated. A comparison with the |
| 96085174 | rylation of Jak 1 and Jak 3 and concomitantly, the tyrosine phosphorylation and | DNA binding | activity of multiple STAT proteins. The STAT proteins utilized by IL-7 were ide |
| 96239534 | t or in reconstituted systems. Both limiting-component transcription assays and | DNA binding | assays identified the class III gene transcription factor TFIIIB as the princip |
| 96279111 | in this proximal promoter region abolished the promoter activity as well as the | DNA binding | . Taken together, these results suggest that the cooperation of different transc |
| 96322726 | nking cell surface CD3. Cell activation resulted in a delayed induction of STAT | DNA-binding | activity, which was sustained for several days, was composed predominantly of S |
| 96322726 | signaling inhibited Stat1 at several different levels, including suppression of | DNA binding | and down-regulation of Stat1 protein and mRNA levels. Our results demonstrate t |
| 97064186 | ally involved in IL-12 signaling. Consequently, IL-12 also failed to induce the | DNA-binding | activity of STAT4-containing complexes in the nuclei of these Th2 clones. All T |
| 97162234 | LPS ) . In this study we have investigated the effect of FCM on the LPS-induced | DNA-binding | activity of NF-kappa B, by means of electrophoretic shift assay ( EMSA ) . We p |
| 97207294 | ducers and activators of transcription 6 ( STAT6 ) tyrosine phosphorylation and | DNA binding | activity in X-SCID B cells with a wide range of gammac mutations. However, reco |