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these data imply an important role for p300 in the pathophysiology of diabetes.
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Study in a phosphorylation-competent p300 (G442S) knock-in mouse model that ectopically expresses p300 phosphorylation in a homologous site to CREB binding protein Ser436 suggest that a single phosphorylation change in p300 has the capability to modulate hippocampal neurogenesis, Creb binding, and associative fear memory.
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The data indicate that brachyury mediates acetylated H3K27 recruitment through a physical interaction with p300 during the mouse mesoderm development.
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Data suggest a role for CBP/p300 in testis determination mediated by control of histone acetylation at the Sry locus and reveal a novel element in the epigenetic control of Sry and mammalian sex determination.
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Study in mouse model found that liver stiffness activates hepatic stellate cells differentiation into myofibroblasts, which required nuclear accumulation of p300.
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Data (including data from studies in knockout and transgenic mice) suggest that Ep300 and Crebbp are limiting cofactors for pancreatic islet development (including gene expression regulation and cell proliferation), and hence for postnatal glucose homeostasis, with some functional redundancy. (Ep300 = E1A binding protein p300; Crebbp = CREB binding protein)
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Here the authors report a lipopolysaccharide-induced NFkappaB enhanceosome in which TonEBP is required for the recruitment of p300. Increased expression of TonEBP enhances the NFkappaB activity and reduced TonEBP expression lowers it.
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Enhancer-priming by MLL3/MLL4 followed by enhancer-activation by CBP/p300 sequentially shape dynamic enhancer landscapes during cell differentiation
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Data show that LPS induces endoplasmic reticulum (ER) stress and P300 activity via the XBP1/IRE1 pathway.
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Loss of p300 expression is associated with leukemogenesis.
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UTX-MLL4-p300 transcriptional regulatory network establishing an "active enhancer landscape" and defines a detailed mechanism for the joint deposition of H3K4me1 and H3K27ac.
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Acetylation-dependent control of global poly(A) RNA degradation by CBP/p300 and HDAC1-HDAC2 has been described.
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Data, including data from studies in cells from knockout mice, suggest that Prmt1 activity was necessary for c-Myc binding to acetyltransferase p300 in myeloid cells; Prmt1 inhibition decreases p300 recruitment to c-Myc target promoters and increased Hdac1 recruitment. [Prmt1, protein arginine N-methyltransferase 1; c-Myc = Proto-Oncogene Proteins c-myc; Hdac1 = histone deacetylase 1]
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In line with the acetyltransferase activity of p300, H3K27 acetylation was reduced after HDACi and resulted in the formation of heterochromatin in the PTGES1 gene. In conclusion, HDAC activity maintains PTGES1 expression by recruiting p300 to its gene
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ARX positively regulates Wnt/ beta-catenin signaling and the C-terminal domain of ARX interacts with the armadillo repeats in beta-catenin to promote Wnt/beta-catenin signaling. In addition, we found BCL9 and P300 also interact with ARX to modulate Wnt/beta-catenin signaling.
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2-O, 3-O desulfated heparin inhibited HMGB1 release, at least in part, by direct molecular inhibition of p300 HAT activity.
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work shows that helenalin acetate inhibits C/EBPbeta by binding to the N-terminal part of C/EBPbeta, thereby disrupting the cooperation of C/EBPbeta with the co-activator p300.
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STAT6 mediates the CT-induced TIM4 expression in DCs. In conclusion, p300 and STAT6 mediate the microbial product CT-induced TIM4 expression in DCs.
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Findings indicate that E1a-binding protein (p300) is not required for the normal development or functioning of skeletal muscle.
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Hdac3 cooperates with p300 to prime and maintain oligodendrocyte identity