Insulin Receptor Beta Antibody (YA5878),MedChemexpress,HY-P86186

CD220 is a receptor tyrosine kinase that mediates the pleiotropic actions of insulin. Insulin binding triggers phosphorylation of intracellular substrates such as insulin receptor substrates (IRS1, IRS2, IRS3, IRS4), SHC, GAB1, CBL, and other signaling intermediates. These phosphorylated proteins serve as docking platforms for SH2 domain-containing signaling proteins like the p85 regulatory subunit of PI3K and SHP2, activating two major pathways: the PI3K-AKT/PKB pathway (responsible for most metabolic effects of insulin) and the Ras-MAPK pathway (regulating gene expression and cooperating with PI3K to control cell growth/differentiation). PI3K recruitment to phospho-IRS1 generates phosphatidylinositol-(3,4,5)-trisphosphate (PIP3), activating PDPK1 and AKT/PKB to promote GLUT4 translocation for glucose uptake. Activated AKT also exerts anti-apoptotic effects via BAD phosphorylation and regulates gluconeogenic/lipogenic enzymes through FOX transcription factors. The PI3K-AKT axis additionally modulates mTORC1 signaling to integrate insulin-dependent growth/metabolic responses, with AKT phosphorylating TSC2 to activate mTORC1-mediated protein synthesis. The Ras/RAF/MAP2K/MAPK cascade, initiated by GRB2/SOS recruitment to phospho-IRS1, primarily mediates insulin's mitogenic/differentiation effects. Beyond insulin, CD220 binds IGF1/IGF2, with the Short isoform showing higher IGF2 affinity. Hybrid receptors with IGF1R exhibit variant ligand specificity: IGF1R-Long hybrids respond strongly to IGF1 but weakly to IGF2/insulin, while IGF1R-Short hybrids are activated by all three ligands (though some studies report similar IGF1 preference and low insulin affinity for both hybrids). In adipocytes, it suppresses lipolysis (by similar).

Insulin receptor; IR; CD antigen CD220; [Cleaved into: Insulin receptor subunit alpha; Insulin receptor subunit beta]