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    Insulin Receptor alpha Antibody, ALEXA FLUOR® 350 Conjugated

    Overview
    Catalog # bs-0047R-A350
    Product Name Insulin Receptor alpha Antibody, ALEXA FLUOR® 350 Conjugated
    Applications FCM, IF(IHC-P)
    Reactivity Human, Mouse, Rat
    Specifications
    Conjugation ALEXA FLUOR® 350
    Host Rabbit
    Source KLH conjugated synthetic peptide derived from human Insulin Receptor alpha
    Immunogen Range 700-750/1382
    Clonality Polyclonal
    Isotype IgG
    Concentration 1ug/ul
    Purification Purified by Protein A.
    Storage Aqueous buffered solution containing 1% BSA, 50% glycerol and 0.09% sodium azide. Store at 4°C for 12 months.
    Target
    Gene ID 3643
    Swiss Prot P06213
    Subcellular location Extracellular
    Synonyms HHF5; CD220; Insulin receptor; IR; INSR; Insulin receptor subunit alpha; PRO_0000016687
    Background Receptor tyrosine kinase which mediates the pleiotropic actions of insulin. Binding of insulin leads to phosphorylation of several intracellular substrates, including, insulin receptor substrates (IRS1, 2, 3, 4), SHC, GAB1, CBL and other signaling intermediates. Each of these phosphorylated proteins serve as docking proteins for other signaling proteins that contain Src-homology-2 domains (SH2 domain) that specifically recognize different phosphotyrosines residues, including the p85 regulatory subunit of PI3K and SHP2. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway, which is responsible for most of the metabolic actions of insulin, and the Ras-MAPK pathway, which regulates expression of some genes and cooperates with the PI3K pathway to control cell growth and differentiation. Binding of the SH2 domains of PI3K to phosphotyrosines on IRS1 leads to the activation of PI3K and the generation of phosphatidylinositol-(3, 4, 5)-triphosphate (PIP3), a lipid second messenger, which activates several PIP3-dependent serine/threonine kinases, such as PDPK1 and subsequently AKT/PKB. The net effect of this pathway is to produce a translocation of the glucose transporter SLC2A4/GLUT4 from cytoplasmic vesicles to the cell membrane to facilitate glucose transport. Moreover, upon insulin stimulation, activated AKT/PKB is responsible for: anti-apoptotic effect of insulin by inducing phosphorylation of BAD; regulates the expression of gluconeogenic and lipogenic enzymes by controlling the activity of the winged helix or forkhead (FOX) class of transcription factors. Another pathway regulated by PI3K-AKT/PKB activation is mTORC1 signaling pathway which regulates cell growth and metabolism and integrates signals from insulin. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 thereby activating mTORC1 pathway.