ID:SOCS2_HUMAN DESCRIPTION: RecName: Full=Suppressor of cytokine signaling 2; Short=SOCS-2; AltName: Full=Cytokine-inducible SH2 protein 2; Short=CIS-2; AltName: Full=STAT-induced STAT inhibitor 2; Short=SSI-2; FUNCTION: SOCS family proteins form part of a classical negative feedback system that regulates cytokine signal transduction. SOCS2 appears to be a negative regulator in the growth hormone/IGF1 signaling pathway. Probable substrate recognition component of a SCF-like ECS (Elongin BC-CUL2/5-SOCS-box protein) E3 ubiquitin- protein ligase complex which mediates the ubiquitination and subsequent proteasomal degradation of target proteins. PATHWAY: Protein modification; protein ubiquitination. SUBUNIT: Interacts with IGF1 receptor, prolactin receptor and growth hormone (GH) receptor. Associates with the Elongin BC complex. INTERACTION: P19235:EPOR; NbExp=3; IntAct=EBI-617737, EBI-617321; TISSUE SPECIFICITY: High expression in heart, placenta, lung, kidney and prostate. INDUCTION: By a subset of cytokines, including EPO/erythropoietin and CSF2/GM-CSF. DOMAIN: The SOCS box domain mediates the interaction with the Elongin BC complex, an adapter module in different E3 ubiquitin ligase complexes. SIMILARITY: Contains 1 SH2 domain. SIMILARITY: Contains 1 SOCS box domain. WEB RESOURCE: Name=Atlas of Genetics and Cytogenetics in Oncology and Haematology; URL="http://atlasgeneticsoncology.org/Genes/SOCS2ID44123ch12q21.html";
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on O14508
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.