Insulin Receptor β (E9L5V) XP® Rabbit mAb (BSA and Azide Free) #98649
- WB
- IHC
- IF
- F
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 95, 220 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
Formulation
Storage
Specificity / Sensitivity
Insulin Receptor β (E9L5V) XP® Rabbit mAb (BSA and Azide Free) 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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