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Gene Review

Socs1  -  suppressor of cytokine signaling 1

Rattus norvegicus

Synonyms: Cish1, SOCS-1, Socs-1, Suppressor of cytokine signaling 1
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Disease relevance of Socs1

  • On the other hand overexpression of SOCS1 or SOCS3 inhibited both CT-1-induced STAT3 phosphorylation and cell hypertrophy [1].
  • We further demonstrate that the protein inhibitor of activated Stat3 (PIAS3) and the suppressor of cytokine signaling (SOCS-1) were up-regulated early after induction of liver failure (6-12 h) [2].
  • Considering the ability of these SOCS to inhibit the JAK-STAT pathway induced by GH, these results suggest that the overexpression of SOCS-3 and CIS mRNAs induced by IL-1beta and TNFalpha or by endotoxin in vivo may play a role in the GH resistance induced by sepsis [3].
  • Induction of nephritis in mice with a deficiency in the FcgammaR gamma-chain (gamma(-/-) mice) resulted in a decrease in the renal expression of SOCS-3 and SOCS-1 [4].
  • SOCS1/JAB likely mediates the protective effect of cardiotrophin-1 against lipopolysaccharide-induced left ventricular dysfunction in vivo [5].

High impact information on Socs1

  • In conclusion, CRF causes a postreceptor defect in GH signal transduction characterized by impaired phosphorylation and nuclear translocation of GH-activated STAT proteins, which is possibly mediated, at least in part, by overexpression of SOCS proteins [6].
  • Similar kinetics was observed for SOCS-1, whereas SOCS-2 expression was very low [4].
  • 15d-PGJ2 and rosiglitazone suppress Janus kinase-STAT inflammatory signaling through induction of suppressor of cytokine signaling 1 (SOCS1) and SOCS3 in glia [7].
  • 15d-PGJ(2) and rosiglitazone rapidly induce the transcription of suppressor of cytokine signaling (SOCS) 1 and 3, which in turn inhibit JAK activity in activated glial cells [7].
  • Systemic Ang II infusion for 3 d increased the renal mRNA expression of SOCS-3 and SOCS-1 [8].

Biological context of Socs1


Anatomical context of Socs1

  • In nonpregnant female rats, acute treatment with ovine prolactin markedly increased levels of SOCS-1 and -3 and cytokine-inducible SH2-containing protein mRNA in arcuate nucleus micropunches [9].
  • On the other hand, the inhibitory actions of SOCS1, 2, and -3 on GH-induced STAT5 reporter activity were partially blocked by disruption of the cytoskeleton [12].
  • In this study we sought to explore the relationships between endoplasmic reticulum stress, GH-induced JAK2/STAT5 activity and SOCS expression [13].
  • CONCLUSIONS/INTERPRETATION: This study suggests that there is an unexpected cross-talk between the SOCS/IFN and the IL-1beta pathways of signalling in pancreatic beta cells, which could lead to a novel perspective of blocking two important proapoptotic pathways in pancreatic beta cells by influencing a single signalling molecule, namely SOCS-3 [14].
  • Northern analysis on whole hypothalamus showed that CIS (cytokine-inducible SH2 domain-containing protein), but not SOCS1 or SOCS3, mRNA expression was significantly (P < 0.01) up-regulated in suckled lactating rats [15].

Associations of Socs1 with chemical compounds

  • In d 19 pregnant rats, cloprostenol, a PGF(2alpha) analog, rapidly induced transcripts for SOCS-3 and, to a lesser extent, SOCS-1 [16].
  • Both GH and lipopolysaccharide induced the three SOCS messenger RNAs (mRNAs) in vivo [3].
  • To determine whether ovarian steroids directly alter SOCS mRNA levels, estrogen- and/or progesterone-treated ovariectomized nonpregnant rats were acutely injected with prolactin (300 microg sc) or vehicle [17].

Regulatory relationships of Socs1

  • Forced expression of SOCS1 significantly inhibited iNOS transcription induced by LPS, tumor necrosis factor-alpha or interferon-gamma [5].
  • BACKGROUND: Suppressor of cytokine signaling 1 (SOCS1) is a negative regulator of cytokine signaling whose expression is induced in the rat heart by cardiotrophin-1 (CT-1) [5].

Other interactions of Socs1


Analytical, diagnostic and therapeutic context of Socs1

  • CIS (cytokine-inducible SH2 protein), SOCS (suppressor of cytokine signaling), or SSI (signal transducers and activators of transcription [STAT]-induced STAT inhibitor) proteins are a family of cytokine-inducible negative regulators of cytokine signaling via Janus kinase (JAK)-STAT pathways [18].
  • METHODS: STAT3-activated cells and SOCS1-positive cells were identified by immunohistochemistry after a two-thirds PH in rats [19].


  1. Hypertrophic responses to cardiotrophin-1 are not mediated by STAT3, but via a MEK5-ERK5 pathway in cultured cardiomyocytes. Takahashi, N., Saito, Y., Kuwahara, K., Harada, M., Tanimoto, K., Nakagawa, Y., Kawakami, R., Nakanishi, M., Yasuno, S., Usami, S., Yoshimura, A., Nakao, K. J. Mol. Cell. Cardiol. (2005) [Pubmed]
  2. Inhibition of signal transducer and activator transcription factor 3 in rats with acute hepatic failure. Kamohara, Y., Sugiyama, N., Mizuguchi, T., Inderbitzin, D., Lilja, H., Middleton, Y., Neuman, T., Demetriou, A.A., Rozga, J. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
  3. Potentiation of growth hormone-induced liver suppressors of cytokine signaling messenger ribonucleic acid by cytokines. Colson, A., Le Cam, A., Maiter, D., Edery, M., Thissen, J.P. Endocrinology (2000) [Pubmed]
  4. Suppressors of cytokine signaling regulate Fc receptor signaling and cell activation during immune renal injury. Gómez-Guerrero, C., López-Franco, O., Sanjuán, G., Hernández-Vargas, P., Suzuki, Y., Ortiz-Muñoz, G., Blanco, J., Egido, J. J. Immunol. (2004) [Pubmed]
  5. SOCS1/JAB likely mediates the protective effect of cardiotrophin-1 against lipopolysaccharide-induced left ventricular dysfunction in vivo. Tanimoto, K., Saito, Y., Hamanaka, I., Kuwahara, K., Harada, M., Takahashi, N., Kawakami, R., Nakagawa, Y., Nakanishi, M., Adachi, Y., Shirakami, G., Fukuda, K., Yoshimura, A., Nakao, K. Circ. J. (2005) [Pubmed]
  6. Impaired JAK-STAT signal transduction contributes to growth hormone resistance in chronic uremia. Schaefer, F., Chen, Y., Tsao, T., Nouri, P., Rabkin, R. J. Clin. Invest. (2001) [Pubmed]
  7. 15d-PGJ2 and rosiglitazone suppress Janus kinase-STAT inflammatory signaling through induction of suppressor of cytokine signaling 1 (SOCS1) and SOCS3 in glia. Park, E.J., Park, S.Y., Joe, E.H., Jou, I. J. Biol. Chem. (2003) [Pubmed]
  8. Suppressors of cytokine signaling regulate angiotensin II-activated Janus kinase-signal transducers and activators of transcription pathway in renal cells. Hernández-Vargas, P., López-Franco, O., Sanjuán, G., Rupérez, M., Ortiz-Muñoz, G., Suzuki, Y., Aguado-Roncero, P., Pérez-Tejerizo, G., Blanco, J., Egido, J., Ruiz-Ortega, M., Gómez-Guerrero, C. J. Am. Soc. Nephrol. (2005) [Pubmed]
  9. Suppression of Prolactin-Induced Signal Transducer and Activator of Transcription 5b Signaling and Induction of Suppressors of Cytokine Signaling Messenger Ribonucleic Acid in the Hypothalamic Arcuate Nucleus of the Rat during Late Pregnancy and Lactation. Anderson, G.M., Beijer, P., Bang, A.S., Fenwick, M.A., Bunn, S.J., Grattan, D.R. Endocrinology (2006) [Pubmed]
  10. SOCS-1, -2, -3: selective targets and functions downstream of the prolactin receptor. Tomic, S., Chughtai, N., Ali, S. Mol. Cell. Endocrinol. (1999) [Pubmed]
  11. Involvement of SOCS-1, the suppressor of cytokine signaling, in the prevention of prolactin-responsive gene expression in decidual cells. Barkai, U., Prigent-Tessier, A., Tessier, C., Gibori, G.B., Gibori, G. Mol. Endocrinol. (2000) [Pubmed]
  12. Downregulation of the growth hormone-induced Janus kinase 2/signal transducer and activator of transcription 5 signaling pathway requires an intact actin cytoskeleton. Rico-Bautista, E., Negrín-Martínez, C., Novoa-Mogollón, J., Fernández-Perez, L., Flores-Morales, A. Exp. Cell Res. (2004) [Pubmed]
  13. Endoplasmic reticulum stress prolongs GH-induced Janus kinase (JAK2)/signal transducer and activator of transcription (STAT5) signaling pathway. Flores-Morales, A., Fernández, L., Rico-Bautista, E., Umana, A., Negrín, C., Zhang, J.G., Norstedt, G. Mol. Endocrinol. (2001) [Pubmed]
  14. Suppressor of cytokine signalling (SOCS)-3 protects beta cells against IL-1beta-mediated toxicity through inhibition of multiple nuclear factor-kappaB-regulated proapoptotic pathways. Karlsen, A.E., Heding, P.E., Frobøse, H., Rønn, S.G., Kruhøffer, M., Orntoft, T.F., Darville, M., Eizirik, D.L., Pociot, F., Nerup, J., Mandrup-Poulsen, T., Billestrup, N. Diabetologia (2004) [Pubmed]
  15. Mechanisms underlying the diminished sensitivity to prolactin negative feedback during lactation: reduced STAT5 signaling and up-regulation of cytokine-inducible SH2 domain-containing protein (CIS) expression in tuberoinfundibular dopaminergic neurons. Anderson, S.T., Barclay, J.L., Fanning, K.J., Kusters, D.H., Waters, M.J., Curlewis, J.D. Endocrinology (2006) [Pubmed]
  16. A prostaglandin f(2alpha) analog induces suppressors of cytokine signaling-3 expression in the corpus luteum of the pregnant rat: a potential new mechanism in luteolysis. Curlewis, J.D., Tam, S.P., Lau, P., Kusters, D.H., Barclay, J.L., Anderson, S.T., Waters, M.J. Endocrinology (2002) [Pubmed]
  17. Hormonal regulation of suppressors of cytokine signaling (SOCS) messenger ribonucleic acid in the arcuate nucleus during late pregnancy. Steyn, F.J., Anderson, G.M., Grattan, D.R. Endocrinology (2008) [Pubmed]
  18. Induction of JAB/SOCS-1/SSI-1 and CIS3/SOCS-3/SSI-3 is involved in gp130 resistance in cardiovascular system in rat treated with cardiotrophin-1 in vivo. Hamanaka, I., Saito, Y., Yasukawa, H., Kishimoto, I., Kuwahara, K., Miyamoto, Y., Harada, M., Ogawa, E., Kajiyama, N., Takahashi, N., Izumi, T., Kawakami, R., Masuda, I., Yoshimura, A., Nakao, K. Circ. Res. (2001) [Pubmed]
  19. Activation of signal transducer and activator transcription 3 and expression of suppressor of cytokine signal 1 during liver regeneration in rats. Sakuda, S., Tamura, S., Yamada, A., Miyagawa, J., Yamamoto, K., Kiso, S., Ito, N., Imanaka, K., Wada, A., Naka, T., Kishimoto, T., Kawata, S., Matsuzawa, Y. J. Hepatol. (2002) [Pubmed]
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