Ignet

Gene Information

Gene symbol: ATF3

Gene name: activating transcription factor 3

HGNC ID: 785

Related Genes

#	Gene Symbol	Number of hits
1	ATF4	1 hits
2	CASP3	1 hits
3	CDK4	1 hits
4	EP300	1 hits
5	GCK	1 hits
6	HMX1	1 hits
7	IL12A	1 hits
8	INS	1 hits
9	IRF6	1 hits
10	ITGA1	1 hits
11	KDR	1 hits
12	LDLR	1 hits
13	MMP13	1 hits
14	PDX1	1 hits
15	PMAIP1	1 hits
16	SERPINE1	1 hits
17	SOD3	1 hits
18	STAT1	1 hits
19	XBP1	1 hits

Related Sentences

#	PMID	Sentence
1	15131119	These alterations exhibited 10 defined patterns and occurred in response to two distinct regulatory effects. 63 genes were identified as changed in expression depending primarily upon adipocyte size, including C/EBP-alpha, C/EBP-delta, superoxide dismutase 3, and the platelet-derived growth factor receptor. 48 genes were regulated primarily by impairment of insulin signaling, including transforming growth factor beta, interferon gamma, insulin-like growth factor I receptor, activating transcription factor 3, aldehyde dehydrogenase 2, and protein kinase Cdelta.
2	16246168	ATF4 also enhances the expression of additional transcription factors, ATF3 and CHOP (CCAAT/enhancer-binding protein homologous protein)/GADD153 (growth arrest and DNA-damage-inducible protein), that assist in the regulation of genes involved in metabolism, the redox status of the cells and apoptosis.
3	16428460	While ATF3 failed to induce expressions of VEGF and VEGFR, it regulated those of CDK2, CDK4, p8, plasminogen activator inhibitor 1, integrin alpha1, subunit and matrix metalloprotease MMP13.
4	17785797	Activating transcription factor-3 (ATF3) is rapidly induced by LPS in mouse macrophages and regulates TLR4 responses.
5	17785797	In primary macrophages from mice with a targeted deletion of the atf3 gene (ATF3-knockout (KO)), TLR-stimulated levels of IL-12 and IL-6 were elevated relative to responses in wild-type macrophages.
6	18334611	In normal, healthy human subjects insulin increased the mRNAs of a number of inflammatory genes (CCL2, CXCL2 and THBD) and transcription factors (ATF3, BHLHB2, HES1, KLF10, JUNB, FOS, and FOSB).
7	19164757	We show that ATF3 and ATF4 form a complex capable of binding to the NOXA promoter, which is required for NOXA activation.
8	19647793	Furthermore, GST pull-down and co-IP assay showed that STAT1 bound to C-terminal domain of ATF3.
9	20519332	We also used INS-1 beta-cells and primary islets to analyze the roles of ATF3 in beta-cell function, including insulin gene expression and glucose-induced insulin secretion.
10	20855893	Specific blockade of ATF3 using siRNA or C-terminally deleted ATF3(?C) attenuated ethanol-induced pancreatic ?-cell apoptosis or dysfunction and restored the down-regulation of glucokinase (GCK), insulin, and pancreatic duodenal homeobox-1 induced by ethanol.
11	20600850	Here, we investigated whether activating transcription factor 3 (ATF3) affects STAT1-mediated beta-cell dysfunction and apoptosis in streptozotocin-treated mice.
12	20600850	The STZ induction of ATF3 was completely depleted in IFN-gamma(-/-) mice, but not in STAT1(-/-) mice.
13	20600850	Furthermore, STAT1 did not affect ATF3 expression, but STAT1 depletion or its inactivation inhibited STZ-induced ATF3 nuclear translocation and beta-cell apoptosis.
14	20600850	Interestingly, ATF3 also increased STAT1 transcription by directly binding to a putative binding region (-116 to -96 bp) in the STAT1 promoter.
15	20349223	In vivo, Atf3 KO islets performed better than WT islets after transplantation, as evidenced by better glucose homeostasis in the recipients and the reduction of the following variables in the KO grafts: caspase 3 activation, macrophage infiltration and expression of the above apoptotic and immunomodulatory genes.
16	21294679	Serial deletion studies revealed that the LDLR promoter region within -234 bp was involved in the repression of LDLR by ATF3.
17	21294679	Transfection of ATF3-specific siRNA rescued LDLR expression under organelle stress, indicating that ATF3 was mainly responsible for the repression of LDLR by these stressors.
18	21294679	Additionally, chromatin immunoprecipitation revealed that ATF3 directly binds to the LDLR promoter in a stress-dependent manner.
19	21821004	Both thapsigargin treatment, an inducer of ER stress, and ATF3 expression decreased PDX-1 expression in pancreatic ?-cells, MIN6N8.
20	21986529	Previously, we showed that ATF3 downregulates PDX-1 gene expression in MIN6N8 pancreatic ?-cells.
21	21986529	Here, we investigated another role of ATF3 on the regulation of PDX-1 activity.
22	21986529	ATF3 significantly inhibited PDX-1-stimulated transactivation of reporter plasmid containing promoters for PDX-1 binding element and the PDX-1 target gene glucokinase, which is dependent on C-terminal domain of ATF3.
23	21986529	ATF3 interacted with PDX-1, and effectively inhibited p300-mediated transcriptional coactivation of the PBE-containing promoter, whereas C-terminal domain-deleted ATF3 did not inhibit the transcoactivation of p300.
24	21986529	ATF3 decreased the interaction of p300 with PDX-1 in MIN6N8 cells coexpressing PDX-1 and ATF3.
25	21986529	In addition, chromatin immunoprecipitation analysis demonstrated that both tunicamycin treatment and ATF3 overexpression inhibited the recruitment of p300 to PDX-1 on the insulin promoter in MIN6N8 cells.
26	21986529	Taken together, these results suggest that ATF3 inhibits PDX-1-mediated transactivation through the inhibition of p300-stimulated coactivation, which may lead to ?-cell dysfunction by ER stress.
27	22033410	The glucose sensitivity of Atf3(-/-) and WT islets for the stimulation of insulin secretion and Xbp1 mRNA splicing during 18h culture was similar, demonstrating that glucose metabolism was unaffected by Atf3 deletion.