H-Ras, K-Ras 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.

Oncogene RRAS; p23; R Ras; Ras related Protein; Ras related protein R Ras; Ras-related protein R-Ras; related RAS viral (r ras) oncogene homolog; RRAS; RRAS_HUMAN.

Human,Mouse,Rat,Dog,Pig,Cow,Sheep

IHC,IF,ICC

IHC 1:100-500
IF 1:100-500
ICC 1:100-1:400

23kD

6237

P10301

https://www.uniprot.org/uniprotkb/P10301

Cell membrane; Lipid-anchor; Cytoplasmic side (By similarity). Note=Inner surface of plasma membrane possibly with attachment requiring acylation of the C-terminal cysteine (By similarity with RAS).

KLH conjugated synthetic peptide derived from human RRAS

Rabbit

Polyclonal

IgG

affinity purified by Protein A

Liquid

0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.