Ignet

Gene Information

Gene symbol: PCAF

Gene name: p300/CBP-associated factor

HGNC ID: 8638

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	CREB1	1 hits
3	CREBBP	1 hits
4	EP300	1 hits
5	GLI2	1 hits
6	GORASP1	1 hits
7	HDAC1	1 hits
8	HDAC9	1 hits
9	HNF1A	1 hits
10	HNF1B	1 hits
11	INS	1 hits
12	MYST2	1 hits
13	NFKB1	1 hits
14	OPN1LW	1 hits
15	PAG1	1 hits
16	PDPK1	1 hits
17	PRKCZ	1 hits
18	PTEN	1 hits
19	PTGS2	1 hits
20	SRA1	1 hits
21	TAF5L	1 hits
22	TMPRSS11D	1 hits
23	TNF	1 hits
24	TRIB3	1 hits

Related Sentences

#	PMID	Sentence
1	11296231	Transcription factor-dependent regulation of CBP and P/CAF histone acetyltransferase activity.
2	11296231	CREB-binding protein (CBP) and CBP-associated factor (P/CAF) are coactivators possessing an intrinsic histone acetyltransferase (HAT) activity.
3	11296231	Here we show that two dominant-negative mutants of hepatocyte nuclear factor-1alpha (HNF-1alpha), P447L and P519L, occurring in maturity onset diabetes of the young (MODY3) patients, exhibit paradoxically stronger interactions than the wild-type protein with either CBP or P/CAF.
4	11296231	However, CBP and P/CAF recruited by these mutants lack HAT activity.
5	11296231	In contrast, wild-type HNF-1alpha and other transcription factors, such as Sp1 or HNF-4, stimulated the HAT activity of CBP.
6	11296231	Transcription factor-dependent regulation of CBP and P/CAF histone acetyltransferase activity.
7	11296231	CREB-binding protein (CBP) and CBP-associated factor (P/CAF) are coactivators possessing an intrinsic histone acetyltransferase (HAT) activity.
8	11296231	Here we show that two dominant-negative mutants of hepatocyte nuclear factor-1alpha (HNF-1alpha), P447L and P519L, occurring in maturity onset diabetes of the young (MODY3) patients, exhibit paradoxically stronger interactions than the wild-type protein with either CBP or P/CAF.
9	11296231	However, CBP and P/CAF recruited by these mutants lack HAT activity.
10	11296231	In contrast, wild-type HNF-1alpha and other transcription factors, such as Sp1 or HNF-4, stimulated the HAT activity of CBP.
11	11296231	Transcription factor-dependent regulation of CBP and P/CAF histone acetyltransferase activity.
12	11296231	CREB-binding protein (CBP) and CBP-associated factor (P/CAF) are coactivators possessing an intrinsic histone acetyltransferase (HAT) activity.
13	11296231	Here we show that two dominant-negative mutants of hepatocyte nuclear factor-1alpha (HNF-1alpha), P447L and P519L, occurring in maturity onset diabetes of the young (MODY3) patients, exhibit paradoxically stronger interactions than the wild-type protein with either CBP or P/CAF.
14	11296231	However, CBP and P/CAF recruited by these mutants lack HAT activity.
15	11296231	In contrast, wild-type HNF-1alpha and other transcription factors, such as Sp1 or HNF-4, stimulated the HAT activity of CBP.
16	11296231	Transcription factor-dependent regulation of CBP and P/CAF histone acetyltransferase activity.
17	11296231	CREB-binding protein (CBP) and CBP-associated factor (P/CAF) are coactivators possessing an intrinsic histone acetyltransferase (HAT) activity.
18	11296231	Here we show that two dominant-negative mutants of hepatocyte nuclear factor-1alpha (HNF-1alpha), P447L and P519L, occurring in maturity onset diabetes of the young (MODY3) patients, exhibit paradoxically stronger interactions than the wild-type protein with either CBP or P/CAF.
19	11296231	However, CBP and P/CAF recruited by these mutants lack HAT activity.
20	11296231	In contrast, wild-type HNF-1alpha and other transcription factors, such as Sp1 or HNF-4, stimulated the HAT activity of CBP.
21	11800161	The recent discovery of estrogen receptor beta as a biological partner with estrogen receptor alpha in mediating the estrogen response has come at precisely the same time as intensive research is revealing the role played by downstream coregulator proteins in linking nuclear hormone receptor activity to general transcription machinery involved in gene transcriptional activation.
22	11800161	In what is a rapidly evolving area of research, findings to date have led to a proposed model of hormonal action, in which a receptor activated by estrogen or cell-membrane-derived phosphorylation-dependent signaling pathways promotes recruitment of selected members of the multifunctional steroid receptor coactivator family and the cointegrators, p300/CBP and P/CAF.
23	11800161	On the other hand, antiestrogen-bound receptors favour the assembly of receptor-corepressor complexes containing the sequence-related corepressors N-CoR (nuclear receptor corepressor) or SMRT (silencing mediator of retinoid and thyroid hormone receptors), localizing histone deacetylase activity to the promoter and leading to transcriptional repression.
24	14976218	Its effects are optimized by various coactivators including histone acetyltransferases (HATs) such as CBP/p300 and p/CAF.
25	14976218	We therefore carried out chromatin immunoprecipitation (ChIP) assays in monocytes to identify 1) chromatin factors bound to the promoters of tumor necrosis factor-alpha (TNF-alpha) and related NF-kappaB-regulated genes under HG or diabetic conditions, 2) specific lysine (Lys (K)) residues on histone H3 (HH3) and HH4 acetylated in this process.
26	14976218	HG treatment of THP-1 monocytes increased the transcriptional activity of NF-kappaB p65, which was augmented by CBP/p300 and p/CAF.
27	14976218	ChIP assays showed that HG increased the recruitment of NF-kappaB p65, CPB, and p/CAF to the TNF-alpha and COX-2 promoters.
28	14976218	Interestingly, ChIP assays also demonstrated concomitant acetylation of HH3 at Lys(9) and Lys(14), and HH4 at Lys(5), Lys(8), and Lys(12) at the TNF-alpha and COX-2 promoters.
29	14976218	Overexpression of histone deacetylase (HDAC) isoforms inhibited p65-mediated TNF-alpha transcription.
30	14976218	Finally, we demonstrated increased HH3 acetylation at TNF-alpha and COX-2 promoters in human blood monocytes from type 1 and type 2 diabetic subjects relative to nondiabetic.
31	14976218	Its effects are optimized by various coactivators including histone acetyltransferases (HATs) such as CBP/p300 and p/CAF.
32	14976218	We therefore carried out chromatin immunoprecipitation (ChIP) assays in monocytes to identify 1) chromatin factors bound to the promoters of tumor necrosis factor-alpha (TNF-alpha) and related NF-kappaB-regulated genes under HG or diabetic conditions, 2) specific lysine (Lys (K)) residues on histone H3 (HH3) and HH4 acetylated in this process.
33	14976218	HG treatment of THP-1 monocytes increased the transcriptional activity of NF-kappaB p65, which was augmented by CBP/p300 and p/CAF.
34	14976218	ChIP assays showed that HG increased the recruitment of NF-kappaB p65, CPB, and p/CAF to the TNF-alpha and COX-2 promoters.
35	14976218	Interestingly, ChIP assays also demonstrated concomitant acetylation of HH3 at Lys(9) and Lys(14), and HH4 at Lys(5), Lys(8), and Lys(12) at the TNF-alpha and COX-2 promoters.
36	14976218	Overexpression of histone deacetylase (HDAC) isoforms inhibited p65-mediated TNF-alpha transcription.
37	14976218	Finally, we demonstrated increased HH3 acetylation at TNF-alpha and COX-2 promoters in human blood monocytes from type 1 and type 2 diabetic subjects relative to nondiabetic.
38	14976218	Its effects are optimized by various coactivators including histone acetyltransferases (HATs) such as CBP/p300 and p/CAF.
39	14976218	We therefore carried out chromatin immunoprecipitation (ChIP) assays in monocytes to identify 1) chromatin factors bound to the promoters of tumor necrosis factor-alpha (TNF-alpha) and related NF-kappaB-regulated genes under HG or diabetic conditions, 2) specific lysine (Lys (K)) residues on histone H3 (HH3) and HH4 acetylated in this process.
40	14976218	HG treatment of THP-1 monocytes increased the transcriptional activity of NF-kappaB p65, which was augmented by CBP/p300 and p/CAF.
41	14976218	ChIP assays showed that HG increased the recruitment of NF-kappaB p65, CPB, and p/CAF to the TNF-alpha and COX-2 promoters.
42	14976218	Interestingly, ChIP assays also demonstrated concomitant acetylation of HH3 at Lys(9) and Lys(14), and HH4 at Lys(5), Lys(8), and Lys(12) at the TNF-alpha and COX-2 promoters.
43	14976218	Overexpression of histone deacetylase (HDAC) isoforms inhibited p65-mediated TNF-alpha transcription.
44	14976218	Finally, we demonstrated increased HH3 acetylation at TNF-alpha and COX-2 promoters in human blood monocytes from type 1 and type 2 diabetic subjects relative to nondiabetic.
45	15509593	The transcriptional impairment of those mutants, whose DNA-binding activity was weakly or not affected, correlated with the loss of association with one of the histone-acetyltransferases CBP or PCAF.
46	15509593	In contrast to wild-type HNF1beta, whose transactivation potential depends on the synergistic action of CBP and PCAF, the activity of these mutants was not increased by the synergistic action of these two coactivators or by treatment with the specific histone-deacetylase inhibitor TSA.
47	15509593	The transcriptional impairment of those mutants, whose DNA-binding activity was weakly or not affected, correlated with the loss of association with one of the histone-acetyltransferases CBP or PCAF.
48	15509593	In contrast to wild-type HNF1beta, whose transactivation potential depends on the synergistic action of CBP and PCAF, the activity of these mutants was not increased by the synergistic action of these two coactivators or by treatment with the specific histone-deacetylase inhibitor TSA.
49	16206511	Our results suggest that the TAF5L gene, encoding TAF5L-like RNA polymerase II p300/CBP associated factor (PCAF)-associated factor, could represent the susceptibility gene for T1D on chromosome 1q42 in Russian affected patients.
50	18385463	Hepatic insulin resistance induced by prenatal alcohol exposure is associated with reduced PTEN and TRB3 acetylation in adult rat offspring.
51	18385463	We performed an intraperitoneal pyruvate tolerance test, determined the phosphorylation status of hepatic phosphoinositide-dependent protein kinase-1 (PDK1), Akt, and PKCzeta before and after intravenous insulin bolus, and measured mRNA and in vivo acetylation of TRB3 (tribbles 3) and PTEN (phosphatase and tensin homolog deleted on chromosome ten) as well as the expression of the histone acetylase (HAT) PCAF (p300/CREB-binding protein-associated factor), histone deacetylase-1 (HDAC1), and HAT and HDAC activities.
52	18385463	In EtOH compared with pair-fed and control offspring, basal and pyruvate-induced blood glucose was increased, insulin-induced PDK1, Akt, and PKCzeta phosphorylation was reduced, and expression of PTEN and TRB3 was increased while their acetylation status was decreased in association with increased HDAC and decreased HAT activities.
53	18385463	Thus female adult rats prenatally exposed to EtOH have increased gluconeogenesis, reduced insulin signaling, and increased PTEN and TRB3 expression in the liver.
54	18385463	In addition, PTEN and TRB3 are hypoacetylated, which can contribute to Akt-inhibiting activity.
55	18385463	These results suggest that hepatic insulin resistance in rats prenatally exposed to EtOH is explained, at least in part, by increased PTEN and TRB3 activity due to both increased gene expression and reduced acetylation.
56	21131905	Histone acetyltransferases (HATs) GCN5 and PCAF (GCN5/PCAF) and CBP and p300 (CBP/p300) are transcription co-activators.
57	21131905	In contrast, CBP/p300 and their HAT activities are essential for ligand-induced Pol II recruitment on, and activation of, NR target genes.