epitope mapping at the C-terminus of R-Ras of human origin
recommended for detection of R-Ras p23 of mouse, rat and human origin of WB, IP, IF, IHC(P) and ELISA; also reactive with additional species, including equine, canine and bovine
R-Ras Background Information H-, K- and N-Ras represent the prototype members of a family of small G proteins that are frequently activated to an oncogenic state in a wide variety of human tumors. Activation is due to point mutations at either position 12 or 61 within their coding sequence. Such mutations cause these proteins to be constitutively converted to their active, rather than the inactive, GDP-bound state. The related human R-Ras gene was initially cloned by low stringency hybridization methods. The R-Ras protein has been shown to interact with the Bcl-2 gene product involved in a signaling pathway that intervenes with apoptosis. Positions 38 and 87 (analogous to positions 12 and 61 in H-Ras) mutants of R-Ras have been shown to be capable of activating oncogenic function. Data has been obtained indicating that R-Ras may exert its biological effect by means of modulating the activity of the Raf-1 kinase on its direct downstream effectors.
R-Ras (C-19): sc-523. Western blot analysis of R-Ras expression in CCD-1064Sk (A) and Hs68 (B) whole cell lysates.
R-Ras (C-19): sc-523. Western blot analysis of R-Ras expression in non-transfected: sc-117752 (A) and human R-Ras transfected: sc-111894 (B) 293T whole cell lysates.
R-Ras (C-19): sc-523. Immunoperoxidase staining of formalin fixed, paraffin-embedded human heart muscle tissue showing cytoplasmic staining of myocytes at high magnification. Kindly provided by The Swedish Human Protein Atlas (HPA) program.
