Ignet

Gene Information

Gene symbol: ETS1

Gene name: v-ets erythroblastosis virus E26 oncogene homolog 1 (avian)

HGNC ID: 3488

Synonyms: FLJ10768, ETS-1

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	BAX	1 hits
3	BCL2	1 hits
4	C11orf6	1 hits
5	CBX1	1 hits
6	CD3D	1 hits
7	CDKN2A	1 hits
8	EGFR	1 hits
9	EP300	1 hits
10	ERBB2	1 hits
11	ERBB3	1 hits
12	ETV7	1 hits
13	FGFR2	1 hits
14	FGFR3	1 hits
15	FLII	1 hits
16	FOS	1 hits
17	HRAS	1 hits
18	INS	1 hits
19	IRF1	1 hits
20	JUN	1 hits
21	KLF2	1 hits
22	LDLR	1 hits
23	MAPK1	1 hits
24	MIRN192	1 hits
25	MKI67	1 hits
26	MMP9	1 hits
27	MYC	1 hits
28	MZF1	1 hits
29	NRAS	1 hits
30	PPARG	1 hits
31	PTK2B	1 hits
32	SMAD2	1 hits
33	SMAD7	1 hits
34	SP1	1 hits
35	STAT3	1 hits
36	STAT6	1 hits
37	TBPL1	1 hits
38	TERT	1 hits
39	THY1	1 hits
40	TP53	1 hits
41	TRA	1 hits
42	TRB	1 hits
43	TRG	1 hits
44	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	1686010	The HLA of 56 unrelated Japanese with insulin-dependent diabetes mellitus (IDDM) was investigated and reconfirmed their role in the pathogenesis by restriction fragment length polymorphism (RFLP).
2	1686010	Furthermore, several non-HLA genes, the polymorphism in the genes encoding the alpha (A), beta (B) and gamma (G) chains of the T-cell receptor (TCRA, TCRB and TCRG), insulin gene (INS) and three closely linked polymorphic genes on chromosome 11q23; Thy-1 (THY1), T3-D (CD3D) and c-ets proto oncogene (ETS1) were analyzed.
3	1686010	Only the EST1 gene showed a significant association with IDDM by AvaII-polymorphic fragment (P less than 0.03).
4	1982251	Non-HLA genetic factors and insulin dependent diabetes mellitus in the Japanese: TCRA, TCRB and TCRG, INS, THY1, CD3D and ETS1.
5	1982251	Polymorphism of the genes encoding the alpha, beta, and gamma chains of the human T-cell receptor (TCRA, TCRB, and TCRG), insulin gene (INS), and three closely linked polymorphic genes on chromosome 11q23, Thy-1 (THY1), T3-D (CD3D), and c-ets proto oncogene (ETS1) were investigated among 56 unrelated patients with insulin-dependent diabetes mellitus (IDDM) and 48 healthy controls.
6	1982251	Only eight of the 17 enzymes examined revealed restriction fragment length polymorphism (RFLP), with the use of TCRA, TCRB, and TCRG.
7	1982251	THY1 and CD3D genes were polymorphic after MspI digestion but no significant association was observed.
8	1982251	Non-HLA genetic factors and insulin dependent diabetes mellitus in the Japanese: TCRA, TCRB and TCRG, INS, THY1, CD3D and ETS1.
9	1982251	Polymorphism of the genes encoding the alpha, beta, and gamma chains of the human T-cell receptor (TCRA, TCRB, and TCRG), insulin gene (INS), and three closely linked polymorphic genes on chromosome 11q23, Thy-1 (THY1), T3-D (CD3D), and c-ets proto oncogene (ETS1) were investigated among 56 unrelated patients with insulin-dependent diabetes mellitus (IDDM) and 48 healthy controls.
10	1982251	Only eight of the 17 enzymes examined revealed restriction fragment length polymorphism (RFLP), with the use of TCRA, TCRB, and TCRG.
11	1982251	THY1 and CD3D genes were polymorphic after MspI digestion but no significant association was observed.
12	2576007	Genetic outcross and backcross analysis of nonobese diabetic (NOD/Lt) mice with a related but diabetes-resistant strain, nonobese normal (NON/Lt), has demonstrated that susceptibility to insulin-dependent diabetes mellitus is controlled in a recessive fashion by multiple genetic loci, including one (Idd-1s) associated with H-2 on chromosome 17 and another (Idd-2s) associated with Thy-1b/Apoa-1b (formerly Alp-1) on chromosome 9.
13	2576007	Severe insulitis and concomitant high diabetes incidences occurred in all genotypic classes of congenic mice carrying Thy-1/Apoa-1 linkage markers for either NOD or NON alleles at Idd-2.
14	2576007	Restriction-fragment-length polymorphism analysis of two polymorphic markers proximal to Thy-1, low-density lipoprotein receptor Ldlr and Ets-1, a protooncogene, confirmed a recombinant chromosome 9, because homozygosity for NOD genomic fragments was found centromeric to an NON congenic segment of at least 20 centiMorgans spanning the Thy-1 and Mod-1 loci.
15	9754812	Candidate genes for Tlf are Ets1 and Fli1, proximally and Igif distally.
16	16543722	High ambient glucose levels modulates the production of MMP-9 and alpha5(IV) collagen by cultured podocytes.
17	16543722	The activity of 92-kDa (MMP-9) gelatinase, but not of 72 kDa (MMP-2), in an HG medium significantly increased during incubation of 2 to 3 days and decreased during incubation of more than 5 days revealed by Gelatin zymography.
18	16543722	Opposite to the increases in MMP-9 activity, HG medium produced significant decreases in the protein levels of alpha5(IV) collagen.
19	16543722	HG medium rapidly activated ERK1/2 MAPK in podocytes.
20	16543722	Moreover, ERK1/2 activation was required for HG-induced enhancement of MMP-9 activity and a decrease in the level of alpha5(IV) collagen.
21	16543722	Blocking the ERK pathway suppressed HG-induced expression and nuclear accumulation of transcriptional factor Ets-1, and MMP-9 mRNA expression.
22	16543722	We suggest that short- or long-term exposure to HG concentrations increases or decreases MMP-9 production and alpha5(IV) collagen expression in podocytes, this may contribute to the GBM abnormality caused by an imbalance in extracellular matrix (ECM) synthesis and degradation, and may play a critical role in the pathogenesis of proteinuria in diabetic nephropathy.
23	16556873	Activation of the peroxisome proliferator-activated receptor (PPAR) gamma, the molecular target for insulin sensitizing thiazolidinediones used in patients with type 2 diabetes, inhibits vascular smooth muscle cell (VSMC) proliferation and prevents atherosclerosis and neointima formation.
24	16556873	Telomerase reverse transcriptase (TERT) confers the catalytic activity of telomerase, and PPARgamma ligands inhibit TERT expression through a receptor-dependent suppression of the TERT promoter. 5'-deletion analysis, site-directed mutagenesis, and transactivation studies using overexpression of Ets-1 revealed that suppression of TERT transcription by PPARgamma is mediated through negative cross-talk with Ets-1-dependent transactivation of the TERT promoter.
25	16556873	Chromatin immunoprecipitation assays further demonstrated that PPARgamma ligands inhibit Ets-1 binding to the TERT promoter, which is mediated at least in part through an inhibition of Ets-1 expression by PPARgamma ligands.
26	16556873	In VSMCs overexpressing TERT, the efficacy of PPARgamma ligands to inhibit cell proliferation is lost, indicating that TERT constitutes an important molecular target for the antiproliferative effects of PPARgamma ligands.
27	16556873	Activation of the peroxisome proliferator-activated receptor (PPAR) gamma, the molecular target for insulin sensitizing thiazolidinediones used in patients with type 2 diabetes, inhibits vascular smooth muscle cell (VSMC) proliferation and prevents atherosclerosis and neointima formation.
28	16556873	Telomerase reverse transcriptase (TERT) confers the catalytic activity of telomerase, and PPARgamma ligands inhibit TERT expression through a receptor-dependent suppression of the TERT promoter. 5'-deletion analysis, site-directed mutagenesis, and transactivation studies using overexpression of Ets-1 revealed that suppression of TERT transcription by PPARgamma is mediated through negative cross-talk with Ets-1-dependent transactivation of the TERT promoter.
29	16556873	Chromatin immunoprecipitation assays further demonstrated that PPARgamma ligands inhibit Ets-1 binding to the TERT promoter, which is mediated at least in part through an inhibition of Ets-1 expression by PPARgamma ligands.
30	16556873	In VSMCs overexpressing TERT, the efficacy of PPARgamma ligands to inhibit cell proliferation is lost, indicating that TERT constitutes an important molecular target for the antiproliferative effects of PPARgamma ligands.
31	17708355	Diabetes increases both N-ras and ets-1 expression during rat oral oncogenesis resulting in enhanced cell proliferation and metastatic potential.
32	18225590	The expression of EGFR, erbB2, erbB3, FGFR-2, FGFR-3, c-myc, N-ras, ets-1, H-ras, c-fos and c-jun, the tumor suppressor genes p53 and p16, apoptosis markers Bax and Bcl-2, and the cell proliferation marker Ki-67 in the sequential stages of rat oral oncogenesis was investigated.
33	18225590	Diabetes seems to promote the activation of the Ras/Raf/MAPK signal transduction pathway mainly by induction of erbB2 and erbB3 receptors, leading to increased cell proliferation, while there was no difference in apoptosis levels during oncogenesis.
34	19787252	Regulation of protein tyrosine kinases in tumour cells by the transcription factor Ets-1.
35	19787252	We investigated the role of Ets-1 in transcriptional regulation of a panel of 89 PTKs in epithelial HeLa tumour cells.
36	19787252	In this study, HeLa cells stably overexpressing and underexpressing Ets-1 were used for real-time PCR analysis of all known human PTKs.
37	19787252	Transcription of most PTKs was found to be increased by Ets-1.
38	19787252	In contrast Ets-1 seems to act as a transcriptional repressor of other PTKs.
39	19787252	Regulation of protein tyrosine kinases in tumour cells by the transcription factor Ets-1.
40	19787252	We investigated the role of Ets-1 in transcriptional regulation of a panel of 89 PTKs in epithelial HeLa tumour cells.
41	19787252	In this study, HeLa cells stably overexpressing and underexpressing Ets-1 were used for real-time PCR analysis of all known human PTKs.
42	19787252	Transcription of most PTKs was found to be increased by Ets-1.
43	19787252	In contrast Ets-1 seems to act as a transcriptional repressor of other PTKs.
44	19787252	Regulation of protein tyrosine kinases in tumour cells by the transcription factor Ets-1.
45	19787252	We investigated the role of Ets-1 in transcriptional regulation of a panel of 89 PTKs in epithelial HeLa tumour cells.
46	19787252	In this study, HeLa cells stably overexpressing and underexpressing Ets-1 were used for real-time PCR analysis of all known human PTKs.
47	19787252	Transcription of most PTKs was found to be increased by Ets-1.
48	19787252	In contrast Ets-1 seems to act as a transcriptional repressor of other PTKs.
49	19787252	Regulation of protein tyrosine kinases in tumour cells by the transcription factor Ets-1.
50	19787252	We investigated the role of Ets-1 in transcriptional regulation of a panel of 89 PTKs in epithelial HeLa tumour cells.
51	19787252	In this study, HeLa cells stably overexpressing and underexpressing Ets-1 were used for real-time PCR analysis of all known human PTKs.
52	19787252	Transcription of most PTKs was found to be increased by Ets-1.
53	19787252	In contrast Ets-1 seems to act as a transcriptional repressor of other PTKs.
54	19787252	Regulation of protein tyrosine kinases in tumour cells by the transcription factor Ets-1.
55	19787252	We investigated the role of Ets-1 in transcriptional regulation of a panel of 89 PTKs in epithelial HeLa tumour cells.
56	19787252	In this study, HeLa cells stably overexpressing and underexpressing Ets-1 were used for real-time PCR analysis of all known human PTKs.
57	19787252	Transcription of most PTKs was found to be increased by Ets-1.
58	19787252	In contrast Ets-1 seems to act as a transcriptional repressor of other PTKs.
59	20970311	The addition of NSs to the media increased the expression and activity of the TFs CCAAT displacement protein (CUX1), v-ets avian erythroblastosis virus E26 oncogene homolog 1 (ETS1) and SMAD family member 2.
60	20970311	In contrast, NS addition decreased the expression and activity of the general upstream stimulatory factor 1 (USF1), glucocorticoid receptor (NR3C1), NFKB and tumor protein p53.
61	21953375	Analysis of mRNA sequencing data identified that treatment of keratinocytes with 20 μM hydroxytyrosol results in the upregulation of numerous antioxidant proteins and enzymes, including heme oxygenase-1 (15.46-fold upregulation), glutaredoxin (1.65) and glutathione peroxidase (1.53).
62	21953375	These include changes in the expression of STAT3, STAT6, SMAD7 and ETS-1.
63	22242005	MAPK/ERK signaling regulates insulin sensitivity to control glucose metabolism in Drosophila.
64	22242005	The insulin/IGF-activated AKT signaling pathway plays a crucial role in regulating tissue growth and metabolism in multicellular animals.
65	22242005	Components of the MAPK/ERK pathway were identified as modifiers of cellular insulin responsiveness.
66	22242005	Insulin resistance was due to downregulation of insulin-like receptor gene expression following persistent MAPK/ERK inhibition.
67	22242005	The MAPK/ERK pathway acts via the ETS-1 transcription factor Pointed.
68	23133314	Transcription factors Sp1, Ets1, Mzf1, Klf2, and Irf1 bind to and transactivate the L-selectin promoter.
69	23542713	Activation of a retinoic acid receptor pathway by thiazolidinediones induces production of vascular endothelial growth factor/vascular permeability factor in OP9 adipocytes.
70	23542713	TGZ induced the expression of VEGF but not interleukin-6 and monocyte chemoattractant protein-1. 2-chloro-5-nitrobenzanilide (GW9662) blocked both the differentiation and the production of VEGF induced by TGZ. 15-deoxy-Δ(12,14)-Prostaglandin J2, a natural ligand of PPARγ, and another PPARγ agonist, ginkgolic acid, also induced an increase in the expression of VEGE as well as the differentiation of OP9 cells.
71	23542713	Although VEGF expression was enhanced under hypoxic conditions, the expression of hypoxia inducible factor and Ets-1 was down-regulated during the TGZ-induced differentiation.
72	23542713	These findings suggested that the major adipocyte-derived vascular permeability factor produced in response to TGZ was VEGF, and a RAR pathway was involved in the production.
73	23737551	TGF-β induces acetylation of chromatin and of Ets-1 to alleviate repression of miR-192 in diabetic nephropathy.
74	23737551	MicroRNAs (miRNAs), such as miR-192, mediate the actions of transforming growth factor-β1 (TGF-β) related to the pathogenesis of diabetic kidney diseases.
75	23737551	We found that the biphasic induction of miR-192 expression by TGF-β in mouse renal glomerular mesangial cells initially involved the Smad transcription factors, followed by sustained expression that was promoted by acetylation of the transcription factor Ets-1 and of histone H3 by the acetyltransferase p300, which was activated by the serine and threonine kinase Akt.
76	23737551	In mesangial cells from Ets-1-deficient mice or in cells in which Ets-1 was knocked down, basal amounts of miR-192 were higher than those in control cells, but sustained induction of miR-192 by TGF-β was attenuated.
77	23737551	Furthermore, inhibition of Akt or ectopic expression of dominant-negative histone acetyltransferases decreased p300-mediated acetylation and Ets-1 dissociation from the miR-192 promoter and prevented miR-192 expression in response to TGF-β.
78	23737551	Activation of Akt and p300 and acetylation of Ets-1 and histone H3 were increased in glomeruli from diabetic db/db mice compared to nondiabetic db/+ mice, suggesting that this pathway may contribute to diabetic nephropathy.
79	23737551	TGF-β induces acetylation of chromatin and of Ets-1 to alleviate repression of miR-192 in diabetic nephropathy.
80	23737551	MicroRNAs (miRNAs), such as miR-192, mediate the actions of transforming growth factor-β1 (TGF-β) related to the pathogenesis of diabetic kidney diseases.
81	23737551	We found that the biphasic induction of miR-192 expression by TGF-β in mouse renal glomerular mesangial cells initially involved the Smad transcription factors, followed by sustained expression that was promoted by acetylation of the transcription factor Ets-1 and of histone H3 by the acetyltransferase p300, which was activated by the serine and threonine kinase Akt.
82	23737551	In mesangial cells from Ets-1-deficient mice or in cells in which Ets-1 was knocked down, basal amounts of miR-192 were higher than those in control cells, but sustained induction of miR-192 by TGF-β was attenuated.
83	23737551	Furthermore, inhibition of Akt or ectopic expression of dominant-negative histone acetyltransferases decreased p300-mediated acetylation and Ets-1 dissociation from the miR-192 promoter and prevented miR-192 expression in response to TGF-β.
84	23737551	Activation of Akt and p300 and acetylation of Ets-1 and histone H3 were increased in glomeruli from diabetic db/db mice compared to nondiabetic db/+ mice, suggesting that this pathway may contribute to diabetic nephropathy.
85	23737551	TGF-β induces acetylation of chromatin and of Ets-1 to alleviate repression of miR-192 in diabetic nephropathy.
86	23737551	MicroRNAs (miRNAs), such as miR-192, mediate the actions of transforming growth factor-β1 (TGF-β) related to the pathogenesis of diabetic kidney diseases.
87	23737551	We found that the biphasic induction of miR-192 expression by TGF-β in mouse renal glomerular mesangial cells initially involved the Smad transcription factors, followed by sustained expression that was promoted by acetylation of the transcription factor Ets-1 and of histone H3 by the acetyltransferase p300, which was activated by the serine and threonine kinase Akt.
88	23737551	In mesangial cells from Ets-1-deficient mice or in cells in which Ets-1 was knocked down, basal amounts of miR-192 were higher than those in control cells, but sustained induction of miR-192 by TGF-β was attenuated.
89	23737551	Furthermore, inhibition of Akt or ectopic expression of dominant-negative histone acetyltransferases decreased p300-mediated acetylation and Ets-1 dissociation from the miR-192 promoter and prevented miR-192 expression in response to TGF-β.
90	23737551	Activation of Akt and p300 and acetylation of Ets-1 and histone H3 were increased in glomeruli from diabetic db/db mice compared to nondiabetic db/+ mice, suggesting that this pathway may contribute to diabetic nephropathy.
91	23737551	TGF-β induces acetylation of chromatin and of Ets-1 to alleviate repression of miR-192 in diabetic nephropathy.
92	23737551	MicroRNAs (miRNAs), such as miR-192, mediate the actions of transforming growth factor-β1 (TGF-β) related to the pathogenesis of diabetic kidney diseases.
93	23737551	We found that the biphasic induction of miR-192 expression by TGF-β in mouse renal glomerular mesangial cells initially involved the Smad transcription factors, followed by sustained expression that was promoted by acetylation of the transcription factor Ets-1 and of histone H3 by the acetyltransferase p300, which was activated by the serine and threonine kinase Akt.
94	23737551	In mesangial cells from Ets-1-deficient mice or in cells in which Ets-1 was knocked down, basal amounts of miR-192 were higher than those in control cells, but sustained induction of miR-192 by TGF-β was attenuated.
95	23737551	Furthermore, inhibition of Akt or ectopic expression of dominant-negative histone acetyltransferases decreased p300-mediated acetylation and Ets-1 dissociation from the miR-192 promoter and prevented miR-192 expression in response to TGF-β.
96	23737551	Activation of Akt and p300 and acetylation of Ets-1 and histone H3 were increased in glomeruli from diabetic db/db mice compared to nondiabetic db/+ mice, suggesting that this pathway may contribute to diabetic nephropathy.
97	23737551	TGF-β induces acetylation of chromatin and of Ets-1 to alleviate repression of miR-192 in diabetic nephropathy.
98	23737551	MicroRNAs (miRNAs), such as miR-192, mediate the actions of transforming growth factor-β1 (TGF-β) related to the pathogenesis of diabetic kidney diseases.
99	23737551	We found that the biphasic induction of miR-192 expression by TGF-β in mouse renal glomerular mesangial cells initially involved the Smad transcription factors, followed by sustained expression that was promoted by acetylation of the transcription factor Ets-1 and of histone H3 by the acetyltransferase p300, which was activated by the serine and threonine kinase Akt.
100	23737551	In mesangial cells from Ets-1-deficient mice or in cells in which Ets-1 was knocked down, basal amounts of miR-192 were higher than those in control cells, but sustained induction of miR-192 by TGF-β was attenuated.
101	23737551	Furthermore, inhibition of Akt or ectopic expression of dominant-negative histone acetyltransferases decreased p300-mediated acetylation and Ets-1 dissociation from the miR-192 promoter and prevented miR-192 expression in response to TGF-β.
102	23737551	Activation of Akt and p300 and acetylation of Ets-1 and histone H3 were increased in glomeruli from diabetic db/db mice compared to nondiabetic db/+ mice, suggesting that this pathway may contribute to diabetic nephropathy.