% SDS-PAGE. Protein preparation is 100% GDP-loaded, measured by HPLC.
ab90766 comprises the first 166 residues of Ras that are sufficient for binding guanine nucleotides and hydrolysis of GTP, but lacks the C-terminal CaaX motif necessary for membrane localization of Ras.
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Preparation and Storage
Stability and Storage
Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.
This product is an active protein and may elicit a biological response in vivo, handle with caution.
c H ras
C HA RAS1
c has/bas p21 protein
c ras Ki 2 activated oncogene
GTP and GDP binding peptide B
GTPase HRas, N-terminally processed
H Ras 1
Ha Ras1 proto oncoprotein
Harvey rat sarcoma viral oncogene homolog
Harvey rat sarcoma viral oncoprotein
p19 H RasIDX protein
Ras family small GTP binding protein H Ras
Transformation gene oncogene HAMSV
Transforming protein p21
v Ha ras Harvey rat sarcoma viral oncogene homolog
FunctionRas proteins bind GDP/GTP and possess intrinsic GTPase activity.
Involvement in diseaseDefects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS) [MIM:218040]. 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. Defects in HRAS may be a cause of susceptibility to Hurthle cell thyroid carcinoma (HCTC) [MIM:607464]. 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. Note=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).
Sequence similaritiesBelongs to the small GTPase superfamily. Ras family.
Post-translational modificationsPalmitoylated by the ZDHHC9-GOLGA7 complex. A continuous cycle of de- and re-palmitoylation regulates rapid exchange between plasma membrane and Golgi. S-nitrosylated; critical for redox regulation. Important for stimulating guanine nucleotide exchange. No structural perturbation on nitrosylation.
Cellular localizationCell membrane. Golgi apparatus membrane. The active GTP-bound form is localized most strongly to membranes than the inactive GDP-bound form (By similarity). Shuttles between the plasma membrane and the Golgi apparatus.