MOUSE ANTI HUMAN H-Ras

H-Ras

Purified IgG prepared by affinity chromatography on Protein A

Specifically recognises human H-Ras otherwise known as p21Ras a ubiquitously expressed lipid-anchored GTPase and member of the Ras superfamily of small GTPases which acts as a molecular signal transduction on/off switch on the inner surface of the plasma membrane and endomembranes. H-Ras N-Ras and K-Ras4A/4B are highly related RAS genes which regulate pathways involved in cell differentiation proliferation adhesion migration and apoptosis and are known proto-oncogenes. Mutations in the H-Ras gene are responsible for the rare condition known as Costello syndrome characterized by facial cardiovascular and musculoskeletal abnormalities and mental retardation. Recommended Secondary Antibodies: Rabbit Anti Mouse IgGGoat Anti Mouse IgGGoat Anti Mouse IgG (H/L)Goat Anti Mouse IgG IgA IgMHuCAL Anti Mouse IgG1Goat Anti Mouse IgG (Fc)Sheep Anti Mouse IgG (H/L)

Shuttles between the plasma membrane and the Golgi apparatus. Ref. 22Post-translational modificationPalmitoylated by the ZDHHC9-GOLGA7 complex. A continuous cycle of de- and re-palmitoylation regulates rapid exchange between plasma membrane and Golgi. Ref. 22Ref. 16Ref. 17Ref. 21S-nitrosylated; critical for redox regulation. Important for stimulating guanine nucleotide exchange. No structural perturbation on nitrosylation. Involvement in diseaseDefects in HRAS are the cause of Costello syndrome [MIM:218040]; also known as faciocutaneoskeletal syndrome. Costello syndrome is a rare condition characterized by prenatally increased growth postnatal growth deficiency mental retardation distinctive facial appearance cardiovascular abnormalities (typically pulmonic stenosis hypertrophic cardiomyopathy and/or atrial tachycardia) tumor predisposition skin and musculoskeletal abnormalities. Defects in HRAS are the cause of congenital myopathy with excess of muscle spindles (CMEMS) [MIM:218040]. CMEMS is a variant of Costello syndrome. Ref. 41Defects in HRAS may be a cause of susceptibility to Hurthle cell thyroid carcinoma [MIM:607464]; also known as Hurthle cell thyroid neoplasia. Hurthle cell thyroid carcinoma accounts for approximately 3% of all thyroid cancers. Although they are classified as variants of follicular neoplasms they are more often multifocal and somewhat more aggressive and are less likely to take up iodine than are other follicular neoplasms. Ref. 36Note=Mutations which change positions 12 13 or 61 activate the potential of HRAS to transform cultured cells and are implicated in a variety of human tumors. Defects in HRAS are a cause of susceptibility to bladder cancer (BLC) [MIM:109800]. A malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and at different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences. Note=Defects in HRAS are the cause of oral squamous cell carcinoma (OSCC). Ref. 35Sequence similaritiesBelongs to the small GTPase superfamily. Ras family. Mass spectrometryMolecular mass is 6223& plusmn; 2 Da from positions 112 - 166. Determined by ESI. Ref. 18Molecular mass is 6253& plusmn; 2 Da from positions 112 - 166. Determined by ESI. Includes one nitric oxide molecule. Ref. 18