Ignet

Gene Information

Gene symbol: SOCS6

Gene name: suppressor of cytokine signaling 6

HGNC ID: 16833

Synonyms: CIS4, SSI4, HSPC060, STATI4, STAI4, Cish4

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	CISH	1 hits
3	IFNG	1 hits
4	IL12A	1 hits
5	IL23A	1 hits
6	INS	1 hits
7	IRS1	1 hits
8	LEP	1 hits
9	MAPK1	1 hits
10	MAPK3	1 hits
11	MAPK8	1 hits
12	RPS27A	1 hits
13	SOCS1	1 hits
14	SOCS3	1 hits
15	SOCS7	1 hits
16	STAT1	1 hits

Related Sentences

#	PMID	Sentence
1	11342531	Cytokines, such as tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6, and hormones, such as growth hormone, are known to cause insulin resistance, but the mechanisms by which they inhibit the cellular response to insulin have not been elucidated.
2	11342531	SOCS proteins are therefore attractive candidates as mediators of cytokine-induced insulin resistance.
3	11342531	We have found that SOCS-1 and SOCS-6 interact with the IR when expressed in human hepatoma cells (HepG2) or in rat hepatoma cells overexpressing the human IR.
4	11342531	In SOCS-1-expressing cells, insulin treatment increases the extent of interaction with the IR, whereas in SOCS-6-expressing cells the association with the IR appears to require insulin treatment.
5	11342531	SOCS-1 and SOCS-6 do not inhibit insulin-dependent IR autophosphorylation, but both proteins inhibit insulin-dependent activation of ERK1/2 and protein kinase B in vivo and IR-directed phosphorylation of IRS-1 in vitro.
6	11342531	These results suggest that SOCS proteins may be inhibitors of IR signaling and could mediate cytokine-induced insulin resistance and contribute to the pathogenesis of type II diabetes.
7	11342531	Cytokines, such as tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6, and hormones, such as growth hormone, are known to cause insulin resistance, but the mechanisms by which they inhibit the cellular response to insulin have not been elucidated.
8	11342531	SOCS proteins are therefore attractive candidates as mediators of cytokine-induced insulin resistance.
9	11342531	We have found that SOCS-1 and SOCS-6 interact with the IR when expressed in human hepatoma cells (HepG2) or in rat hepatoma cells overexpressing the human IR.
10	11342531	In SOCS-1-expressing cells, insulin treatment increases the extent of interaction with the IR, whereas in SOCS-6-expressing cells the association with the IR appears to require insulin treatment.
11	11342531	SOCS-1 and SOCS-6 do not inhibit insulin-dependent IR autophosphorylation, but both proteins inhibit insulin-dependent activation of ERK1/2 and protein kinase B in vivo and IR-directed phosphorylation of IRS-1 in vitro.
12	11342531	These results suggest that SOCS proteins may be inhibitors of IR signaling and could mediate cytokine-induced insulin resistance and contribute to the pathogenesis of type II diabetes.
13	11994496	We examined the expression of IFN-gamma, a characteristic Th1 cytokine, and IL-4, a characteristic Th2 cytokine, in islet infiltrates of female and male NOD mice at various ages.
14	11994496	IFN-gamma was significantly higher in young females, whereas IL-4 was higher in young males.
15	11994496	CD4(+) T cells isolated from lymph nodes of female mice and activated with anti-CD3 and anti-CD28 Abs produced more IFN-gamma, but less IL-4, as compared with males.
16	11994496	Treatment of CD4(+) T cells with estrogen significantly increased, whereas testosterone treatment decreased the IL-12-induced production of IFN-gamma.
17	11994496	We then examined whether the change in IL-12-induced IFN-gamma production by treatment with sex hormones was due to the regulation of STAT4 activation.
18	11994496	We found that estrogen treatment increased the phosphorylation of STAT4 in IL-12-stimulated T cells.
19	11994496	We conclude that the increased susceptibility of female NOD mice to the development of autoimmune diabetes could be due to the enhancement of the Th1 immune response through the increase of IL-12-induced STAT4 activation by estrogen.
20	11994496	We examined the expression of IFN-gamma, a characteristic Th1 cytokine, and IL-4, a characteristic Th2 cytokine, in islet infiltrates of female and male NOD mice at various ages.
21	11994496	IFN-gamma was significantly higher in young females, whereas IL-4 was higher in young males.
22	11994496	CD4(+) T cells isolated from lymph nodes of female mice and activated with anti-CD3 and anti-CD28 Abs produced more IFN-gamma, but less IL-4, as compared with males.
23	11994496	Treatment of CD4(+) T cells with estrogen significantly increased, whereas testosterone treatment decreased the IL-12-induced production of IFN-gamma.
24	11994496	We then examined whether the change in IL-12-induced IFN-gamma production by treatment with sex hormones was due to the regulation of STAT4 activation.
25	11994496	We found that estrogen treatment increased the phosphorylation of STAT4 in IL-12-stimulated T cells.
26	11994496	We conclude that the increased susceptibility of female NOD mice to the development of autoimmune diabetes could be due to the enhancement of the Th1 immune response through the increase of IL-12-induced STAT4 activation by estrogen.
27	11994496	We examined the expression of IFN-gamma, a characteristic Th1 cytokine, and IL-4, a characteristic Th2 cytokine, in islet infiltrates of female and male NOD mice at various ages.
28	11994496	IFN-gamma was significantly higher in young females, whereas IL-4 was higher in young males.
29	11994496	CD4(+) T cells isolated from lymph nodes of female mice and activated with anti-CD3 and anti-CD28 Abs produced more IFN-gamma, but less IL-4, as compared with males.
30	11994496	Treatment of CD4(+) T cells with estrogen significantly increased, whereas testosterone treatment decreased the IL-12-induced production of IFN-gamma.
31	11994496	We then examined whether the change in IL-12-induced IFN-gamma production by treatment with sex hormones was due to the regulation of STAT4 activation.
32	11994496	We found that estrogen treatment increased the phosphorylation of STAT4 in IL-12-stimulated T cells.
33	11994496	We conclude that the increased susceptibility of female NOD mice to the development of autoimmune diabetes could be due to the enhancement of the Th1 immune response through the increase of IL-12-induced STAT4 activation by estrogen.
34	17010638	Attenuation of leptin and insulin signaling by SOCS proteins.
35	17010638	Leptin and insulin are key hormones involved in the regulation of energy balance and glucose homeostasis.
36	17010638	Specific members of the suppressor of cytokine signaling (SOCS) family of proteins are now thought to have a role in the development of leptin and insulin resistance owing to their ability to inhibit leptin and insulin signaling pathways.
37	17010638	In the case of leptin, current evidence suggests that SOCS3 appears to be of particular importance in the development of leptin resistance, whereas the ability to diminish insulin action has been described for several SOCS proteins (SOCS1, SOCS3, SOCS6 and SOCS7).
38	19120275	In an effort to discover non-HLA genes affecting susceptibility to type 1 diabetes (T1D), we have investigated the association of polymorphisms in STAT4, an important signaling molecule of IL-12, gammaIFN, and IL-23, in a sample of 389 T1D patients and 152 nondiabetic controls in Korea.
39	19661066	Berberine differentially modulates the activities of ERK, p38 MAPK, and JNK to suppress Th17 and Th1 T cell differentiation in type 1 diabetic mice.
40	19661066	We found that berberine inhibited Th17 differentiation by activating ERK1/2 and inhibited Th1 differentiation by inhibiting p38 MAPK and JNK activation.
41	19661066	Berberine down-regulated the activity of STAT1 and STAT4 through the suppression of p38 MAPK and JNK activation, and it controlled the stability of STAT4 through the ubiquitin-proteasome pathway.
42	19661066	This study revealed a novel role of ERK in Th17 differentiation through down-regulation of STAT3 phosphorylation and RORgamma t expression.