High impact information on Socs2

• The expression of the suppressor of cytokine signaling-2 (SOCS-2) was increased twofold in GH-treated CRF animals, and SOCS-3 mRNA levels were elevated by 60% in CRF, independent of GH treatment [1].
• Our findings suggest that SOCS2 regulates EGFR phosphorylation, leading to regulation of neurite outgrowth through a novel pathway that is distinct from GH [2].
• SOCS2 binds to the GH receptor and inhibits GH signaling, including attenuation of STAT5 activation [2].
• The overexpressed SOCS2 bound to the EGFR, which was constitutively phosphorylated at Tyr845, the Src binding site [2].
• SOCS2 expression also resulted in a modest 30% decrease in phosphorylation of STAT5b at Tyr699, which is the primary site on STAT5 phosphorylated by GH; however, total tyrosine phosphorylation of STAT5 was decreased by 75-80% under basal and epidermal growth factor-stimulated conditions [2].

Biological context of Socs2

• SOCS-2 displayed a relatively higher level of basal expression, particularly in CA3, and a mild and transient downregulation by 24 h [3].
• Furthermore, cotransfection studies in the rat liver cell line, BRL-4, revealed that constitutive expression of Cis, but not Socs-2, inhibited the GH-induced transactivation of a Stat5-responsive reporter gene construct [4].

Anatomical context of Socs2

• SOCS2 induces neurite outgrowth by regulation of epidermal growth factor receptor activation [2].
• Here we demonstrate that Socs-2 and Cis mRNA expression in rat liver is dependent on the presence of growth hormone (GH), and that GH induce Cis mRNA expression in cultures of primary rat hepatocytes [4].

Other interactions of Socs2

• SOCS2 mRNA and cytokine-inducible SH2-containing protein (CIS) mRNA were detected at the same levels for both sham and burn at all time points in the liver [5].
• Overexpression of SOCS2 in central nervous system neurons promoted neurite outgrowth, and in PC12 cells, neurite outgrowth was induced under nondifferentiating conditions, leading to inhibition of the neurite-inhibitory GTPase Rho and activation of the neurite-promoting GTPase Rac1 [2].
• For comparison, we also examined SOCS-2, which is involved in insulin-like growth factor signaling [3].

References