R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
Insulin Receptor β (E9L5V) XP® Rabbit mAb #23413
Filter:
- WB
- IP
- IHC
- IF
- F
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 95, 220 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IHC-Immunohistochemistry
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
| IHC Leica Bond | 1:50 - 1:200 |
| Immunohistochemistry (Paraffin) | 1:50 - 1:200 |
| Immunofluorescence (Frozen) | 1:50 - 1:200 |
| Immunofluorescence (Immunocytochemistry) | 1:50 - 1:200 |
| Flow Cytometry (Fixed/Permeabilized) | 1:50 - 1:200 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
For a carrier free (BSA and azide free) version of this product see product #98649.
For a carrier free (BSA and azide free) version of this product see product #98649.
Protocol
Specificity / Sensitivity
Insulin Receptor β (E9L5V) XP® Rabbit mAb recognizes endogenous levels of total insulin receptor β. The 50 kDa band(s) seen on western blot is a probable partial degradation product of insulin receptor β.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu1374 of human insulin receptor.
Background
Insulin receptor (InsR) is a heterodimeric membrane receptor tyrosine kinase. It is composed of an extracellular α-subunit containing the ligand binding domain, a β-subunit containing an extracellular domain, a transmembrane domain, and a cytoplasmic tyrosine kinase domain (1). Binding of insulin to InsR results in receptor autophosphorylation and subsequent tyrosine kinase activation (2). This provides a docking site for various adaptor molecules, including insulin receptor substrate (IRS), Gab, and Shc, phosphorylation of which promotes subsequent activation of multiple downstream signaling pathways, including MAPK, PI3K, and TC10 (3,4). These events lead to increased glucose uptake and metabolism, and can promote cell growth. Loss-of-function mutation or desensitization of the InsR are two major contributors to insulin resistance and Type 2 diabetes (5).
- Yip, C.C. and Ottensmeyer, P. (2003) J Biol Chem 278, 27329-32.
- Hubbard, S.R. (2013) Cold Spring Harb Perspect Biol 5, a008946.
- Saltiel, A.R. and Pessin, J.E. (2002) Trends Cell Biol 12, 65-71.
- Zick, Y. (2001) Trends Cell Biol 11, 437-41.
- Boucher, J. et al. (2014) Cold Spring Harb Perspect Biol 6, pii: a009191. doi: 10.1101/cshperspect.a009191.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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