Recombinant Human Insulin Receptor/INSR Protein (His & GST Tag) (PKSH030373)
For research use only.
| Synonyms | CD220, HHF5, Insulin Receptor |
| Species | Human |
| Expression Host | Baculovirus-Insect Cells |
| Sequence | Gly 989-Ser 1382 |
| Accession | NP_000199.2 |
| Calculated Molecular Weight | 72.3 kDa |
| Observed Molecular Weight | 70 kDa |
| Tag | N-His-GST |
| Bio-activity | The specific activity was determined to be 45 nmol/min/mg using Poly(Ala, Glu, Lys, Tyr)6:2:5:1 as substrate. |
| Purity | > 92 % as determined by reducing SDS-PAGE. |
| Endotoxin | < 1.0 EU per μg of the protein as determined by the LAL method. |
| Storage | Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles. |
| Shipping | This product is provided as liquid. It is shipped at frozen temperature with blue ice/gel packs. Upon receipt, store it immediately at < - 20°C. |
| Formulation | Supplied as sterile 50mM Tris, 100mM NaCI, pH 7.5, 25% glycerol, 1mM TCEP,0.5mM GSH |
| Reconstitution | Not Applicable |
| Background | INSR (Insulin receptor), also known as CD220, is a transmembrane receptor that is activated by insulin. INSR belongs to theprotein 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 leads 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, fibrobasts, 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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