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Anti-Insulin Receptor Antibody (PE)

  • Product Information
  • Description
Catalog: C-FC-3360A
Product Type: FCM Antibody
Size: 25 Tests/100 Tests
Concentration: 10 μl/Test, 0.1 mg/ml
Reactivity: Human
Specificity: Human Insulin Receptor
Analysis mode: FCM
Host: Mouse
Clonality: Monoclonal
Isotype: IgG1
Alternate names: insulin receptor
Form: Liquid
Shipping: This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
Storage: This antibody can be stored at 2℃-8℃ for twelve months without detectable loss of activity. Protected from prolonged exposure to light. Do not freeze ! Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
Purification method: Protein A
Conjugation: PE
Immunogen: Recombinant Human Insulin Receptor/INSR/CD220 Protein
Buffer: Aqueous solution containing 0.5% BSA and 0.09% sodium azide
Application: Receptor Tyrosine Kinases (RTKs)

INSR (Insulin receptor), also known as CD22, is a transmembrane receptor that is activated by insulin. INSR belongs to the protein kinase superfamily and exists as a tetramer consisting of two alpha subunits and two beta subunits linked by disulfide bonds. The alpha and beta subunits are encoded by a single INSR gene, and the beta subunits pass through the cellular membrane. As the receptor for insulin with tyrosine-protein kinase activity, INSR associates with downstream mediators upon binding to insulin, including IRS1 (insulin receptor substrate 1) and phosphatidylinositol 3'-kinase (PI3K). IRS-1 binding and phosphorylation eventually lead to an increase in the high-affinity glucose transporter (Glut4) molecules on the outer membrane of insulin-responsive tissues. INSR isoform long and isoform short are expressed in the peripheral nerve, kidney, liver, striated muscle, fibroblasts and skin, and is found as a hybrid receptor with IGF1R which also binds IGF1 in muscle, heart, kidney, adipose tissue, skeletal muscle, hepatoma, fibroblasts, spleen, and placenta. Defects in Insulin Receptor/INSR are the cause of Rabson-Mendenhall syndrome (Mendenhall syndrome), insulin resistance (Ins resistance), leprechaunism (Donohue syndrome), and familial hyperinsulinemic hypoglycemia 5 (HHF5). It may also be associated with noninsulin-dependent diabetes mellitus (NIDDM).

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