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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