RRAS Human
Description
Product Specs
Product Science Overview
The Related RAS Viral (r-ras) Oncogene Homolog, commonly referred to as RRAS, is a member of the Ras superfamily of small GTP-binding proteins. These proteins play a crucial role in various cellular processes, including cell growth, differentiation, and survival. The RRAS gene is located on chromosome 19q13.33 in humans .
The RRAS gene was first isolated by Lowe et al. in 1987 through low-stringency hybridization with a Harvey-ras probe . The predicted RRAS protein consists of 218 amino acids and has an amino-terminal extension of 26 residues compared to HRAS p21. The human RRAS protein shares 55% sequence identity with HRAS p21 .
RRAS is a plasma membrane-associated GTP-binding protein with intrinsic GTPase activity. It cycles between an active GTP-bound state and an inactive GDP-bound state at the cytoplasmic face of the plasma membrane . RRAS is involved in promoting cell adhesion and neurite outgrowth. It has been implicated in various cellular signaling pathways, including those mediated by the semaphorin-4D (SEMA4D) receptor plexin B1 .
RRAS is primarily expressed in vascular smooth muscle cells in small arterioles and major arteries, as well as in endothelial cells of lung capillaries . Lower levels of RRAS are found in smooth muscle cells of veins, renal glomeruli, and venous endothelium of the spleen. In smooth muscle cells, RRAS is distributed along the plasma membrane .
RRAS has been implicated in the pathogenesis of various human cancers. It is known to transduce growth inhibitory signals across the cell membrane, exerting its effect through an effector shared with other Ras proteins . Downregulation of RRAS activity by the plexin B1/RND1 complex is essential for SEMA4D-induced growth cone collapse in hippocampal neurons .
Studies on Rras-null mice have shown that these mice are viable and fertile with no obvious abnormalities. However, they exhibit exaggerated neointimal thickening in response to arterial injury and increased angiogenesis in implanted tumors . Overexpression of activated RRAS suppresses mitogenic and invasive activities of growth factor-stimulated vascular cells .
