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

• On gestation d 22, SOCS-1 and SOCS-3 mRNA levels were 10-fold that on G20 [9].
• SOCS-1 and -3 and cytokine-inducible SH2-containing protein mRNA levels were also elevated on lactation d 7 [9].
• Using transient overexpression system the role of SOCS proteins in regulating prolactin receptor intracellular mediators leading to gene activation was analyzed [10].
• Involvement of SOCS-1, the suppressor of cytokine signaling, in the prevention of prolactin-responsive gene expression in decidual cells [11].
• These findings suggest that after massive hepatocyte loss, an early and rapid rise in blood IL-6 levels may weaken the hepatic regenerative response through up-regulation of Stat3 inhibitors PIAS3 and SOCS-1 [2].

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

• SOCS-1, -2, -3: selective targets and functions downstream of the prolactin receptor [10].
• However, we discovered a profound difference in the expression of SOCS-1, an inhibitor of the Jak/Stat pathway [11].

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].

References