Cell Signaling Technology

Product Pathways - Metabolism

IGF-I Receptor β Antibody #3027

Applications Reactivity Sensitivity MW (kDa) Source
W IP IHC-P H M R Mk Endogenous 95 Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation  IHC-P=Immunohistochemistry (Paraffin)
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

IGF-I Receptor beta Antibody detects endogenous levels of IGF-IR beta. It does not cross-react with insulin receptor.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the carboxy-terminal residues of human IGF-IR beta. Antibodies are purified by protein A andd peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of various cell extracts using IGF-I Receptor beta antibody.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human breast tumor section showing membrane and cytoplasmic staining, using IGF-I Receptor b Antibody.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human prostate carcinoma using IGF-I Receptor b Antibody.


Background

Type I insulin-like growth factor receptor (IGF-IR) is a transmembrane receptor tyrosine kinase that is widely expressed in many cell lines and cell types within fetal and postnatal tissues (1-3). Receptor autophosphorylation follows binding of the IGF-I and IGF-II ligands. Three tyrosine residues within the kinase domain (Tyr1131, Tyr1135, and Tyr1136) are the earliest major autophosphorylation sites (4). Phosphorylation of these three tyrosine residues is necessary for kinase activation (5,6). Insulin receptors (IRs) share significant structural and functional similarity with IGF-I receptors, including the presence of an equivalent tyrosine cluster (Tyr1146/1150/1151) within the kinase domain activation loop. Tyrosine autophosphorylation of IRs is one of the earliest cellular responses to insulin stimulation (7). Autophosphorylation begins with phosphorylation at Tyr1146 and either Tyr1150 or Tyr1151, while full kinase activation requires triple tyrosine phosphorylation (8).

  1. Adams, T.E. et al. (2000) Cell. Mol. Life Sci. 57, 1050-1093.
  2. Baserga, R. et al. (2000) Oncogene 19, 5574-5581.
  3. Scheidegger, K.J. et al. (2000) J. Biol. Chem. 275, 38921-38928.
  4. Hernandez-Sanchez, C. et al. (1995) J. Biol. Chem. 270, 29176-29181.
  5. Lopaczynski, W. et al. (2000) Biochem. Biophys. Res. Commun. 279, 955-960.
  6. Baserga, R. et al. (1999) Exp. Cell Res. 253, 1-6.
  7. White, M.F. et al. (1985) J. Biol. Chem. 260, 9470-9478.
  8. White, M.F. et al. (1988) J. Biol. Chem. 263, 2969-2980.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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