Principal Names - SOCS3; CIS3; Cish3; SSI-3; SOCS-3; suppressor of cytokine signaling 3; STAT induced STAT inhibitor 3; cytokine-induced SH2 protein 3
Official Gene Symbol - SOCS3
GenBank Accession Number – NP_003946
LocusLink ID - 9021 (human); 12702 (mouse); 89829 (rat)
Gene Ontology terms - protein kinase inhibitor; JAK-STAT cascade; anti-apoptosis
Size - 225 aa
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Western Blot - Approx 24kDa band seen in MOLT-4 lysate. Recommended for use at 4.0-6.0µg/ml. Block membrane in 2.5% skimmed milk in TBST (TBS + 0.05% Tween). Incubate primary antibody for 1 hour at room temperature with agitation.
SOCS family proteins form part of a classical negative feedback system that regulates cytokine signal transduction. SOCS3 is involved in negative regulation of cytokines that signal through the JAK/STAT pathway. Inhibits cytokine signal transduction by binding to tyrosine kinase receptors including gp130, LIF, erythropoietin, insulin, IL12, GCSF and leptin receptors. Binding to JAK2 inhibits its kinase activity. Suppresses fetal liver erythropoiesis. Regulates onset and maintenance of allergic responses mediated by T-helper type 2 cells. Regulates IL-6 signaling in vivo (By similarity). 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. Seems to recognize IL6ST.
Widely expressed with high expression in heart, placenta, skeletal muscle, peripheral blood leukocytes, fetal and adult lung, and fetal liver and kidney. Lower levels in thymus.
Protein modification; protein ubiquitination.
Note=There is some evidence that SOCS3 may be a susceptibility gene for atopic dermatitis linked to 17q25. SOCS3 messenger RNA is significantly more highly expressed in skin from patients with atopic dermatitis than in skin from healthy controls. Furthermore, a genetic association between atopic dermatitis and a haplotype in the SOCS3 gene has been found in two independent groups of patients.
The ESS and SH2 domains are required for JAK phosphotyrosine binding. Further interaction with the KIR domain is necessary for signal and kinase inhibition. The SOCS box domain mediates the interaction with the Elongin BC complex, an adapter module in different E3 ubiquitin ligase complexes.
Phosphorylated on tyrosine residues after stimulation by the cytokines, IL-2, EPO or IGF1.