Background:  Elucidation of the mechanism by which receptor tyrosine kinases (RTKs) modulate cellular physiology in response to stimuli is critical to the understanding of growth regulation. Miscues in RTK signaling pathways can result in cellular transformation and ultimately in cancer. Two novel EGF receptor substrates designated EGF-receptor pathway substrates 8 and 15, or Eps8 and Eps15, have been described. Eps8 and Eps15 become tyrosine phosphorylated subsequent to EGF stimulation. Overexpression of Eps15 in NIH/3T3 cells causes cellular transformation, implying involvement in the regulation of cell proliferation. Eps15 is capable of binding the amino-terminal portion of Crk via a conserved proline-rich domain, characteristic of all Crk binding proteins. Over-expression of Eps8 in both fibroblasts and hematopoietic cells results in an increased mitogenic response to EGF. Eps8 has been shown to associate with the EGF receptor despite its lack of a functional SH2 domain. Further characterization suggests the protein has both a PH domain and a SH3 domain, the functional significance of which are not yet known.

Description: Rabbit polyclonal to EPS8

Immunogen: KLH conjugated synthetic peptide derived from EPS8

Specificity:  ·Reacts with Human, Mouse, Pig, Dog and Rat.

·Isotype: IgG

Application:  ·Western blotting: 1/100-500. Predicted Mol wt: 92 kDa;

·Immunohistochemistry (Paraffin/frozen tissue section): 1/50-200;

·Immunocytochemistry/Immunofluorescence: 1/100;

·Immunoprecipitation: 1/50;

·ELISA: 1/500;

·Optimal working dilutions must be determined by the end user.