|Datasheet||Specific References||Reviews||Related Products||Protocols|
|CD220, HHF5, INSR|
|A DNA sequence encoding the human INSR isoform long (NP_000199.2) cytoplasmic domain (Gly 989-Ser 1382) was fused with the N-terminal polyhistidine-tagged GST tag at the N-terminus.|
|Kinases are highly recommended to be shipped at frozen temperature with blue ice or dry ice.|
Shipment made at ambient temperature may seriously affect the activity of the ordered products.
|> 92 % as determined by SDS-PAGE|
|The specific activity was determined to be 45 nmol/min/mg using Poly(Ala,Glu,Lys,Tyr)6:2:5:1 as substrate.|
|< 1.0 EU per μg of the protein as determined by the LAL method|
|Samples are stable for up to twelve months from date of receipt at -70℃|
|The recombinant human INSR (989-1382)/GST chimera consists of 631 amino acids and has a calculated molecular mass of 72.3 KDa. It migrates as an approximately 70 KDa band in SDS-PAGE under reducing conditions.|
|Supplied as sterile 50mM Tris, 100mM NaCl, pH 7.4, 20% gly, 0.3mM DTT|
1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
2. Please contact us for any concerns or special requirements.
|Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.|
|A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.|
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).