Insulin Receptor / CD220 / INSR Antibody (Antigen Affinity Purified)

Insulin Receptor / CD220 / INSR Antibody ( Antigen Affinity Purified ) Datasheet

Insulin Receptor / CD220 / INSR Antibody Product Information

• Immunogen: Recombinant Human Insulin Receptor / CD220 / INSR protein (Catalog#11081-H08H)
• Antibody Type: Rabbit Polyclonal Antibody ( Antibody Purification Platform )
• Ig Type: Rabbit IgG
• Formulation: 0.2 μm filtered solution in PBS with 5% trehalose
• Preparation: Produced in rabbits immunized with purified, recombinant Human Insulin Receptor / CD220 / INSR (rh Insulin Receptor / CD220 / INSR; Catalog#11081-H08H; NP_000199.2; Met 1-Lys 956). Insulin Receptor / CD220 / INSR specific IgG was purified by Human Insulin Receptor / CD220 / INSR affinity chromatography.

Insulin Receptor / CD220 / INSR Antibody Usage Guide

• Specificity: Human Insulin Receptor / CD220 / INSR
• Immunochemistry: IHC-P: 1-3 μg/mL

  

  Immunochemical staining of human INSR in human kidney with rabbit polyclonal antibody (15μ g/mL, formalin-fixed paraffin embedded sections).

  Immunochemical staining of human INSR in human pancreas with rabbit polyclonal antibody (15 μg/mL, formalin-fixed paraffin embedded sections).

• Direct ELISA: This antibody can be used at 0.5-1 μg/mL with the appropriate secondary reagents to detect Human INSR. The detection limit for Human INSR is approximately 0.00245 ng/well.
• Storage: This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free.
  Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.

Insulin Receptor / CD220 / INSR Antibody 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).

References

1. Kadowaki, T. et al., 1990, J. Biol. Chem. 265:19143-19150.
2. Kan, M. et al., 1995, Diabetes. 44: 1081-1086.
3. Duckworth, WC. et al., 1998,Endocr. Rev.19 (5): 608-624.
4. Maddux, B A. et al., 2000, Diabetes. 49 (1): 13-9.
5. Longo, N. et al., 2002, Hum. Mol. Genet.11 (12): 1465-1475.
6. Ward, CW. et al., 2009, Bioessays. 31 (4): 422-434.