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 ligase complex which mediates the ubiquitination and subsequent proteasomal degradation of target proteins (By similarity). Protein modification; protein ubiquitination. Interacts with IGF1R (By similarity). Associates with the Elongin BC complex (By similarity). Interacts with AREL1 and PRKCA (PubMed:31578312). Interacts with DCUN1D1 (By similarity). Expressed primarily in the testis, some expression in liver and lung. In the developing brain, expressed at relatively high levels from 10 dpc stages to young adulthood (P25) with peak levels from 14 dpc to P8. Levels of SOCS2 increase dramatically between 10 dpc and 12 dpc. At 12 dpc, high expression found in the olfactory epithelium with moderate expression in the neuroepithelium of the neocortex, presumptive striatum, hippocampus and septum. Low expression in the retina. At 14 dpc, in the cortical wall, levels increase in the cortical plate and decrease in the intermediate zone. High expression also in the hippocampus, fimbria, thalamic neuroepithelium and innermost layer of the retina. At P8, high expression in the neurons of the hippocampus. Lower levels found in the dentate gyrus. Levels of expression decrease between P8 and P15 and remain constant until P25. In adulthood, levels decrease. In the peripheral nervous system, expression found at low levels at 14 dpc in a subpopulation of neurons in the dorsal root ganglion. The SOCS box domain mediates the interaction with the Elongin BC complex, an adapter module in different E3 ubiquitin ligase complexes. Ubiquitinated; mediated by AREL1 and leading to its subsequent proteasomal degradation (PubMed:31578312). Ubiquitination is dependent on phosphorylation at Ser-52, by PKC and is stimulated by LPS (PubMed:31578312). Phosphorylation at Ser-52 by PKC facilitates its ubiquitination and proteosomal degradation. Mice deficient in SOCS2 exhibit considerable weight increase (30-40% more than normal) after 3 weeks of age. This is attributable to increase in visceral organ weight, carcass weight, long bone length and body length. In addition there is a thickening of the dermis due to excess collagen accumulation.