Background:  Crkl is a 34kDa adaptor protein which has been shown to activate the RAS and JUN kinase signalling pathways and transforms fibroblasts in a RAS dependant manner. Crkl is a substitute of BCR ABL tyrosine kinase. In addition, Crkl has oncogenic potential. SH2 and SH3 (Src homology) domains were originally identified as critical functional domains within non-receptor proteins with tyrosine kinase activity. A subset of these proteins appears to exist predominately of SH2/SH3 domains in the absence of detectable catalytic domains. One of the first members of the family to be identified, Crk, is a transformation-specific protein that induces elevation of cellular phosphotyrosine levels, but lacks tyrosine kinase activity itself. A second protein, Nck, consists solely of three SH3 domains and one SH2 domain, while GRB2 contains an SH2 domain flanked on both sides by SH3 domains. A member of this protein class, Crk-L, is encoded by a gene located on chromosome 22, band 11, centromeric of the chronic myelogenous leukemia breakpoint region. Crk-L encodes a 303 amino acid protein with one SH2 and two SH3 domains.

Description: Rabbit polyclonal to Crkl

Immunogen: KLH conjugated synthetic peptide derived from Crkl

Specificity:  ·Reacts with Human, Mouse and Rat.

·Isotype: IgG

Application:  ·Western blotting: 1/100-500. Predicted Mol wt: 34 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.