Ignet

Gene Information

Gene symbol: EP300

Gene name: E1A binding protein p300

HGNC ID: 3373

Synonyms: p300, KAT3B

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	BCKDHB	1 hits
3	CCL5	1 hits
4	CREB1	1 hits
5	CREBBP	1 hits
6	EP400	1 hits
7	EXOSC1	1 hits
8	MIRN150	1 hits
9	MYB	1 hits
10	NFKB1	1 hits
11	PAG1	1 hits
12	PAX5	1 hits
13	PBK	1 hits
14	PIK3CA	1 hits
15	RB1	1 hits
16	RBL1	1 hits
17	RBL2	1 hits
18	SPI1	1 hits
19	TLR2	1 hits
20	TRRAP	1 hits

Related Sentences

#	PMID	Sentence
1	16263418	Our results demonstrate: 1) adenovirus infection of MCL cells despite the absence of receptor/coreceptor molecules known to be important for adenovirus infection of other cells types; 2) cytotoxicity of MCL cells after infection with specific adenovirus mutants; 3) a high degree of cytotoxicity after infection of some patient samples with viruses lacking the E1B 19k "antiapoptotic" gene; and 4) cytotoxicity after infection with viruses containing mutations in E1A pRb or p300 binding.
2	18177634	Sphingosine kinase, phosphatidylinositol 3-kinase, Akt, NF-kappaB, and p300 are required for CCL5 production in Mycobacterium bovis Bacillus Calmette-Guérin (BCG)-infected epithelial cells.
3	18177634	Although NF-kappaB has been implicated, signaling cascades involved in CCL5 production by epithelial cells following infection with Mycobacterium bovis BCG are still not defined.
4	18177634	Here we show that using pharmacological inhibition of sphingosine kinase (SPK), striking inhibition of M. bovis BCG-induced CCL5 protein was observed.
5	18177634	Phosphatidylinositol 3-kinase (PI3K) and Akt were also important for CCL5 production by epithelial cells infected with M. bovis BCG.
6	18177634	Moreover, there was increased activation of PI3K, IKK/alphabeta and NF-kappaB in A549 cells infected with M. bovis BCG.
7	18177634	Importantly, the PI3K activation was dependent on SPK.
8	18177634	Together, these studies are the first to show that M. bovis BCG-induced CCL5 secretion is dependent on the SPK/PI3K/Akt/NF-kappaB and p300 signaling pathway.
9	18177634	Sphingosine kinase, phosphatidylinositol 3-kinase, Akt, NF-kappaB, and p300 are required for CCL5 production in Mycobacterium bovis Bacillus Calmette-Guérin (BCG)-infected epithelial cells.
10	18177634	Although NF-kappaB has been implicated, signaling cascades involved in CCL5 production by epithelial cells following infection with Mycobacterium bovis BCG are still not defined.
11	18177634	Here we show that using pharmacological inhibition of sphingosine kinase (SPK), striking inhibition of M. bovis BCG-induced CCL5 protein was observed.
12	18177634	Phosphatidylinositol 3-kinase (PI3K) and Akt were also important for CCL5 production by epithelial cells infected with M. bovis BCG.
13	18177634	Moreover, there was increased activation of PI3K, IKK/alphabeta and NF-kappaB in A549 cells infected with M. bovis BCG.
14	18177634	Importantly, the PI3K activation was dependent on SPK.
15	18177634	Together, these studies are the first to show that M. bovis BCG-induced CCL5 secretion is dependent on the SPK/PI3K/Akt/NF-kappaB and p300 signaling pathway.
16	19150725	The identification of Rb as an E1A and LT interacting protein quickly led to the cloning of p107, p130, p300, CBP, p400 and TRRAP and the concept that viral transformation was due, at least in part, to the perturbation of the function of normal cellular proteins.
17	21677314	HTLV-1 replication is positively regulated by Tax and Rex and negatively regulated by the p30 and HBZ proteins.
18	21677314	The p13 protein directly binds Tax, decreases Tax binding to the CBP/p300 transcriptional coactivator, and, by reducing Tax transcriptional activity, suppresses viral expression.
19	22593239	Several genes, including CREB1, EP300, MYB, PAX5, and SPI1/PU.1, were sequenced from FPS-affected and unaffected foals.
20	26391398	Ac2PIM-responsive miR-150 and miR-143 target receptor-interacting protein kinase 2 and transforming growth factor beta-activated kinase 1 to suppress NOD2-induced immunomodulators.
21	26391398	While Ac2PIM treatment of macrophages compromised their ability to induce NOD2-dependent immunomodulators like cyclooxygenase (COX)-2, suppressor of cytokine signaling (SOCS)-3, and matrix metalloproteinase (MMP)-9, no change in the NOD2-responsive NO, TNF-α, VEGF-A, and IL-12 levels was observed.
22	26391398	Further, genome-wide microRNA expression profiling identified Ac2PIM-responsive miR-150 and miR-143 to target NOD2 signaling adaptors, RIP2 and TAK1, respectively.
23	26391398	Interestingly, Ac2PIM was found to activate the SRC-FAK-PYK2-CREB cascade via TLR2 to recruit CBP/P300 at the promoters of miR-150 and miR-143 and epigenetically induce their expression.
24	26391398	Loss-of-function studies utilizing specific miRNA inhibitors establish that Ac2PIM, via the miRNAs, abrogate NOD2-induced PI3K-PKCδ-MAPK pathway to suppress β-catenin-mediated expression of COX-2, SOCS-3, and MMP-9.