Insulin Receptor / INSR / CD220 (989-1382) Protein (GST Tag)

Insulin receptor Protein Datasheet

Insulin Receptor / INSR / CD220 Protein Product Information

• Synonym: CD220, HHF5, INSR
• Protein Construction: 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.
• Source: Human
• Expression Host: Baculovirus-Insect cells

Insulin Receptor / INSR / CD220 Protein QC Testing

• Purity: >92 % as determined by SDS-PAGE.
• Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method
• Stability: Samples are stable for up to twelve months from date of receipt at -70℃
• Predicted N terminal: Met
• Molecular Mass: 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.
• Formulation: Lyophilized from sterile 50mM Tris, 100mM NaCl, pH 7.4, 20%gly, 0.3 mM 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.
• SDS-PAGE: Insulin Receptor / INSR / CD220 protein

Insulin Receptor / INSR / CD220 Protein Usage Guide

• Storage: Store it under sterile conditions at -70℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
• Reconstitution: A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.

INSR / CD220 Protein Description

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).

References

1. Kadowaki T. et al., 1990, J Biol Chem. 265:19143-50.
2. Kan M. et al., 1995, Diabetes. 44: 1081-6.
3. Duckworth WC. et al., 1998, Endocr Rev. 19 (5): 608-24.
4. Maddux B A. et al., 2000, Diabetes. 49 (1): 13-9.
5. Longo N. et al., 2002, Hum Mol Genet. 11 (12): 1465-75.
6. Ward CW. et al., 2009, Bioessays. 31 (4): 422-34.