Ignet

Gene Information

Gene symbol: STAT2

Gene name: signal transducer and activator of transcription 2, 113kDa

HGNC ID: 11363

Synonyms: STAT113

Related Genes

#	Gene Symbol	Number of hits
1	ADAM33	1 hits
2	C19orf10	1 hits
3	CISH	1 hits
4	CXCL10	1 hits
5	CXCL11	1 hits
6	CXCL9	1 hits
7	F9	1 hits
8	IFI27	1 hits
9	IFI6	1 hits
10	IFNA1	1 hits
11	IFNA13	1 hits
12	IFNAR2	1 hits
13	IFNG	1 hits
14	IL27	1 hits
15	IRF9	1 hits
16	ISG15	1 hits
17	JAK1	1 hits
18	JAK2	1 hits
19	MX1	1 hits
20	NFKBIA	1 hits
21	OAS2	1 hits
22	SOCS1	1 hits
23	SOCS2	1 hits
24	STAT1	1 hits
25	STAT3	1 hits
26	STAT4	1 hits
27	STAT5A	1 hits
28	STAT5B	1 hits
29	STAT6	1 hits
30	TGFBR1	1 hits
31	TYK2	1 hits

Related Sentences

#	PMID	Sentence
1	25921106	Association Study of Single-Nucleotide Polymorphisms of STAT2/STAT3/IFN-γ Genes in Cervical Cancer in Southern Chinese Han Women.
2	22121102	JAK/STAT/SOCS-signaling pathway and colon and rectal cancer.
3	22121102	JAK/STAT/SOCS-signaling pathway and colon and rectal cancer.
4	22121102	We evaluated the association between genetic variation in JAK1 (10 SNPs), JAK2 (9 SNPs), TYK2 (5 SNPs), suppressors of cytokine signaling (SOCS)1 (2 SNPs), SOCS2 (2 SNPs), STAT1 (16 SNPs), STAT2 (2 SNPs), STAT3 (6 SNPs), STAT4 (21 SNPs), STAT5A (2 SNPs), STAT5B (3 SNPs), STAT6 (4 SNPs) with risk of colorectal cancer.
5	22121102	We evaluated the association between genetic variation in JAK1 (10 SNPs), JAK2 (9 SNPs), TYK2 (5 SNPs), suppressors of cytokine signaling (SOCS)1 (2 SNPs), SOCS2 (2 SNPs), STAT1 (16 SNPs), STAT2 (2 SNPs), STAT3 (6 SNPs), STAT4 (21 SNPs), STAT5A (2 SNPs), STAT5B (3 SNPs), STAT6 (4 SNPs) with risk of colorectal cancer.
6	22121102	JAK2, SOCS2, STAT1, STAT3, STAT5A, STAT5B, and STAT6 were associated with colon cancer; STAT3, STAT4, STAT6, and TYK2 were associated with rectal cancer.
7	22121102	JAK2, SOCS2, STAT1, STAT3, STAT5A, STAT5B, and STAT6 were associated with colon cancer; STAT3, STAT4, STAT6, and TYK2 were associated with rectal cancer.
8	22121102	Given the biological role of the JAK/STAT-signaling pathway and cytokines, we evaluated interaction with IFNG, TNF, and IL6; numerous statistically significant associations after adjustment for multiple comparisons were observed.
9	22121102	Given the biological role of the JAK/STAT-signaling pathway and cytokines, we evaluated interaction with IFNG, TNF, and IL6; numerous statistically significant associations after adjustment for multiple comparisons were observed.
10	22121102	The following statistically significant interactions were observed: TYK2 with aspirin/NSAID use; STAT1, STAT4, and TYK2 with estrogen status; and JAK2, STAT2, STAT4, STAT5A, STAT5B, and STAT6 with smoking status and colon cancer risk; JAK2, STAT6, and TYK2 with aspirin/NSAID use; JAK1 with estrogen status; STAT2 with cigarette smoking and rectal cancer.
11	22121102	The following statistically significant interactions were observed: TYK2 with aspirin/NSAID use; STAT1, STAT4, and TYK2 with estrogen status; and JAK2, STAT2, STAT4, STAT5A, STAT5B, and STAT6 with smoking status and colon cancer risk; JAK2, STAT6, and TYK2 with aspirin/NSAID use; JAK1 with estrogen status; STAT2 with cigarette smoking and rectal cancer.
12	22121102	JAK2, SOCS1, STAT3, STAT5, and TYK2 were associated with colon cancer survival (hazard rate ratio (HRR) of 3.3 95% CI 2.01,5.42 for high mutational load).
13	22121102	JAK2, SOCS1, STAT3, STAT5, and TYK2 were associated with colon cancer survival (hazard rate ratio (HRR) of 3.3 95% CI 2.01,5.42 for high mutational load).
14	22121102	JAK2, SOCS1, STAT1, STAT4, and TYK2 were associated with rectal cancer survival (HRR 2.80 95% CI 1.63,4.80).
15	22121102	JAK2, SOCS1, STAT1, STAT4, and TYK2 were associated with rectal cancer survival (HRR 2.80 95% CI 1.63,4.80).
16	19258923	We show that genetic factors in innate immune genes (IFNA13, IFNAR2, STAT2, IL27, NFKBIA, C3, IL1RN, TLR5), in innate and adaptive immunity (IFNG), and in airway remodeling genes (ADAM33 and TGFBR1), affect disease susceptibility to a different extent in preterm children, born with underdeveloped lungs, than in term children.
17	15661146	The most noteworthy changes in gene expression mainly affected the transcriptional network regulated by interferons (IFNs), including both IFN-alpha/beta-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, MX1) and IFN-gamma-inducible genes (CXCL9, CXCL10, CXCL11).
18	15661146	Interesting, upregulation of IFN-alpha/beta-inducible genes (but not IFN-gamma-inducible genes) was independent of histological scores (grade and stage of fibrosis) and HCV characteristics (hepatic HCV mRNA levels and the HCV genotype), and was specific to HCV (as compared to hepatitis B virus (HBV)).
19	15661146	Other genes dysregulated in F1-CH-C, albeit less markedly than IFN-alpha/beta- and IFN-gamma-inducible genes, were mainly involved in the activation of lymphocytes infiltrating the liver (IFNG, TNF, CXCL6, IL6, CCL8, CXCR3, CXCR4, CCR2), cell proliferation (p16/CDKN2A, MKI67, p14/ARF), extracellular matrix remodeling (MMP9, ITGA2), lymphangiogenesis (XLKD1/LYVE), oxidative stress (CYP2E1), and cytoskeleton microtubule organization (STMN2/SCG10).
20	15187113	We hypothesized that IL-12 pretreatments would result in endogenous IFN-gamma production, and that this, in turn, would up-regulate levels of Janus kinase-STAT signaling intermediates and lead to increased expression of genes regulated by IFN-alpha.
21	15187113	Pretreatment of PBMCs and tumor cells with IFN-gamma-containing supernatants from IL-12-stimulated PBMCs led to up-regulation of STAT1, STAT2, and IFN regulatory factor 9 (IRF9) and potentiated IFN-alpha-induced STAT signaling within PBMCs and tumor cells.
22	15187113	Pretreatment of HT144 melanoma cells and PBMCs with IFN-gamma or IFN-gamma-containing supernatants enhanced the actions of IFN-alpha at the transcriptional level, as measured by real-time RT PCR analysis of the IFN-stimulated gene 15.
23	15187113	Experiments in wild-type C57BL/6 and IFN-gamma receptor knockout (B6.129S7-Ifngr(tm1Agt)) mice demonstrated that a regimen of IL-12 pretreatment, followed by IFN-alpha, could cure mice of i.p.
24	15187113	However, this treatment regimen did not significantly prolong the survival of IFN-gamma-deficient (B6.129S7-Ifng(tm1Ts)) mice compared with mice treated with IFN-alpha alone.
25	15187113	These results suggest that the response to IFN-alpha immunotherapy can be significantly enhanced by IL-12 pretreatment, and this effect is dependent upon endogenous IFN-gamma production and its actions on melanoma cells.