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NF-kappaB RelA phosphorylation regulates RelA acetylation
- Mol. Cell. Biol. 2005
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This article cites 35 articles, 17 of which can be accessed free
Steroid receptor coactivator 1 links the steroid and interferon gamma response pathways
- Mol. Endocrinol
, 2003
"... We show here that steroid receptor coactivator 1 (SRC-1) is a coactivator of MHC class II genes that stimulates their interferon (IFN) and class II transactivator (CIITA)-mediated expression. SRC-1 interacts physically with the N-terminal activation domain of CIITA through two regions: one central ..."
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We show here that steroid receptor coactivator 1 (SRC-1) is a coactivator of MHC class II genes that stimulates their interferon (IFN) and class II transactivator (CIITA)-mediated expression. SRC-1 interacts physically with the N-terminal activation domain of CIITA through two regions: one central [extending from amino acids (aa) 360–839] that contains the nuclear receptors binding region and one C-terminal (aa 1138–1441) that contains the activation domain 2. Using chromatin immunopre-cipitation assays we show that SRC-1 recruitment on the class II promoter is enhanced upon IFN stimulation. Most importantly, SRC-1 relieves the inhibitory action of estrogens on the IFN-medi-ated induction of class II genes in transient trans-
Activation of phosphatidylinositol 3-kinase and c-Jun-N-terminal kinase cascades enhances NF-kappaB-dependent gene transcription in BCG-stimulated macrophages through promotion of p65/p300 binding
- J. Leukoc. Biol
, 2004
"... terminal kinase cascades enhances NF-B-dependent gene transcription in BCG-stimulated macrophages through promotion of p65/p300 binding ..."
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terminal kinase cascades enhances NF-B-dependent gene transcription in BCG-stimulated macrophages through promotion of p65/p300 binding
Cell cycle regulation of human interleukin-8 gene expression by the human immunodeficiency virus type 1 Tat protein. J Virol 2001, 75:1736-1743 Publish with BioMed Central and every scientist can read your work free of charge "BioMed Central will be the m
- Sir Paul Nurse, Cancer Research UK Your
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Inhibition of Matrix Metalloproteinase-3 Synthesis in Human Conjunctival Fibroblasts by Interleukin-4 or Interleukin-13
, 2006
"... PURPOSE. Fibroproliferative lesions of the conjunctiva known as giant papillae are a characteristic of vernal keratoconjunctivitis (VKC). The abundance of T helper 2 (Th2) cells and cytokines is increased in the giant papillae and tear fluid of individuals with VKC, and the Th2 cytokines interleuki ..."
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PURPOSE. Fibroproliferative lesions of the conjunctiva known as giant papillae are a characteristic of vernal keratoconjunctivitis (VKC). The abundance of T helper 2 (Th2) cells and cytokines is increased in the giant papillae and tear fluid of individuals with VKC, and the Th2 cytokines interleukin (IL)-4 and IL-13 each stimulate the production of extracellular matrix (ECM) proteins by conjunctival fibroblasts. The role of Th2 cytokines in the development of giant papillae was further examined by determination of the effects of these molecules on the production by conjunctival fibroblasts of matrix metalloproteinase (MMP)-3, a key enzyme in ECM degradation. METHODS. The amount of MMP-3 released into the culture medium by human conjunctival fibroblasts was determined by enzyme-linked immunosorbent assay, and the intracellular abundance of MMP-3 mRNA was quantitated by reverse transcription and real-time polymerase chain reaction analysis. Signaling by the transcription factors NF-B and AP-1 was evaluated by immunoblot and immunofluorescence analyses. RESULTS. Of the Th2 cytokines tested, only IL-4 and -13 inhibited both the basal and IL-1-induced release of MMP-3 by conjunctival fibroblasts. These effects of IL-4 and -13 were inhibited by neutralizing antibodies to the IL-4 receptor complex. IL-4 and -13 also each reduced the basal abundance, as well as inhibited the IL-1-induced upregulation, of MMP-3 mRNA in these cells. Neither IL-4 nor -13 affected the IL-1-induced activation of NF-B or the AP-1 component c-Jun. CONCLUSIONS. IL-4 and -13 each inhibit MMP-3 synthesis in human conjunctival fibroblasts, suggesting that these Th2 cytokines may contribute to the excessive deposition of ECM in giant papillae by preventing matrix degradation mediated by this enzyme. (Invest Ophthalmol Vis Sci.
Expression and Deoxyribonucleic Acid-Binding Activity of the Nuclear Factor �B Family in the Human Myometrium during Pregnancy and Labor
"... In humans, the factors that govern the switch from myometrial quiescence to coordinated contractions at the initiation of labor are not well defined. The onset of parturition is itself associated with increases in a number of proinflammatory factors, many of which are regulated by the nuclear factor ..."
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In humans, the factors that govern the switch from myometrial quiescence to coordinated contractions at the initiation of labor are not well defined. The onset of parturition is itself associated with increases in a number of proinflammatory factors, many of which are regulated by the nuclear factor �B (NF-�B) family of transcription factors. The expression and DNA-binding activity of NF-�B in the myometrium during gestation and parturition were examined. Levels of c-Rel, p50, and p105 NF-�B species were dramatically reduced in pregnant myometrium compared with nonpregnant (NP) controls, whereas expression of the RelA subunit remained uniform. Importantly, during labor, expression of all subunits was observed to be significantly reduced in all myometrial samples DURING FETAL MATURATION, the myometrium must remain in a quiescent state but, at term, be able
Involvement of Different Promoter Elements, Transcription Factors, and Histone
, 2003
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CAPER � Is a Novel Rel-TAD-Interacting Factor That Inhibits Lymphocyte Transformation by the Potent Rel/NF-�B Oncoprotein v-Rel �
, 2008
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These include: This article cites 50 articles, 24 of which can be accessed free at:
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, 2002
"... This article cites 45 articles, 19 of which can be accessed free at: ..."
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The Journal of Immunology Dual Ligand Stimulation of RAW 264.7 Cells Uncovers Feedback Mechanisms That Regulate TLR-Mediated Gene Expression 1,2,3
"... To characterize how signaling by TLR ligands can be modulated by non-TLR ligands, murine RAW 264.7 cells were treated with LPS, IFN-�, 2-methyl-thio-ATP (2MA), PGE 2, and isoproterenol (ISO). Ligands were applied individually and in combination with LPS, for 1, 2, and 4 h, and transcriptional change ..."
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To characterize how signaling by TLR ligands can be modulated by non-TLR ligands, murine RAW 264.7 cells were treated with LPS, IFN-�, 2-methyl-thio-ATP (2MA), PGE 2, and isoproterenol (ISO). Ligands were applied individually and in combination with LPS, for 1, 2, and 4 h, and transcriptional changes were measured using customized oligo arrays. We used nonadditive transcriptional responses to dual ligands (responses that were reproducibly greater or less than the expected additive responses) as a measure of pathway interaction. Our analysis suggests that cross-talk is limited; <24 % of the features with significant responses to the single ligands responded nonadditively to a dual ligand pair. PGE 2 and ISO mainly attenuated, while 2MA enhanced, LPS-induced transcriptional changes. IFN- � and LPS cross-regulated the transcriptional response induced by each other: while LPS preferentially enhanced IFN-�-induced changes in gene expression at 1 h, IFN- � signaling primarily attenuated LPS-induced changes at 4 h. Our data suggest specific cross-talk mechanisms: 1) LPS enhances the expression of IFN-�- response genes by augmenting STAT1 activity and by activating NF-�B, which synergizes with IFN-�-induced transcriptional factors; 2) IFN- � attenuates the late LPS transcriptional response by increasing the expression of suppressor of cytokine signaling 1 and cytokine-inducible SH2-containing protein expression; 3) 2MA modulates LPS secondary transcriptional response by increasing IFN- � and inhibiting IL-10 gene expression; 4) PGE 2 and ISO similarly regulate the LPS transcriptional response. They increase IL-10 transcription, resulting in attenuated expression of known IL-10-suppressed genes. The Journal of Immunology, 2006, 177: 4299–4310.