Regulates signaling cascades probably through protein ubiquitination and/or sequestration. Functions in insulin signaling and glucose homeostasis through IRS1 ubiquitination and subsequent proteasomal degradation. Inhibits also prolactin, growth hormone and leptin signaling by preventing STAT3 and STAT5 activation, sequestering them in the cytoplasm and reducing their binding to DNA. May be a substrate recognition component of a SCF-like E3 ubiquitin-protein ligase complex which mediates the ubiquitination and subsequent proteasomal degradation of target proteins (By similarity). Protein modification; protein ubiquitination. Interacts with phosphorylated IRS4 and PIK3R1. Interacts, via the third proline-rich region, with the second SH3 domain of the adapter protein NCK1. Also interacts with GRB2, INSR, IRS1, PLCG1, SORBS3/vinexin and phosphorylated STAT3 and STAT5 (By similarity). Interacts with SEPT6 (By similarity). Mostly cytoplasmic, but shuttles between the cytoplasm and the nucleus. Rapidly relocalizes to the nucleus after UV irradiation. Cytoplasmic location depends upon SEPT7 presence (By similarity). Widely expressed with higher expression in brain and testis where it is expressed by spermatocytes and early spermatids. Also significantly expressed in spleen, skeletal muscle and kidney. Ubiquitously expressed at low level in 12.5 dpc and 15.5 dpc embryos. More significantly expressed in the nervous system at 12.5 dpc and the cortical plate at 15.5 dpc. Expressed in the brain postnatally in particular in the hippocampal formation and the medial habenular nuclei at P7. Low-level expression in other brain areas was present at P7 and was reduced to very low levels at P14 and P21. The hippocampal granule cell layer and the cerebellar granular layer maintained moderate expression levels at P7, P14, and P21. The SOCS box domain is required for IRS1 ubiquitination and subsequent proteasomal degradation. The SOCS box domain mediates the interaction with the Elongin BC complex, an adapter module in different E3 ubiquitin ligase complexes. Mice are smaller and half of them develop fatal hydrocephalus between 3 to 15 weeks of age. They display subtle alterations in glucose homeostasis with an enhanced response to insulin which causes hypoglycemia. Pancreatic islets become progressively larger.