Recombinant Human GTPase HRAS (mutated S17 N) protein (ab90767)



  • NatureRecombinant
  • SourceEscherichia coli
  • Amino Acid Sequence
    • SpeciesHuman


Our Abpromise guarantee covers the use of ab90767 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

  • Applications


  • Purity> 95 % SDS-PAGE.
    Protein preparation is 95% GDP- and 5% GTP-loaded, measured by HPLC.
  • FormLiquid
  • Additional notes

    ab90767 lacks the C-terminus with the CaaX recognition sequence necessary for anchoring Ras into the plasma membrane. The mutation S17N results in a 40-fold increase in the affinity for GTP without affecting its affinity for GDP.

  • Concentration information loading...

Preparation and Storage

  • Stability and Storage

    Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.

    Preservative: None
    Constituents: 64mM Tris HCl, 5mM DTE (1, 4-Dithioerythritol), 10mM Magnesium chloride, pH 7.2

General Info

  • Alternative names
    • C BAS/HAS
    • c H ras
    • C HA RAS1
    • c has/bas p21 protein
    • c ras Ki 2 activated oncogene
    • c-H-ras
    • CTLO
    • GTP and GDP binding peptide B
    • GTPase HRas, N-terminally processed
    • H Ras 1
    • H RASIDX
    • H-Ras-1
    • Ha Ras
    • Ha Ras1 proto oncoprotein
    • Ha-Ras
    • HAMSV
    • Harvey rat sarcoma viral oncogene homolog
    • Harvey rat sarcoma viral oncoprotein
    • HRAS
    • HRAS1
    • K ras
    • N ras
    • p19 H RasIDX protein
    • p21ras
    • Ras family small GTP binding protein H Ras
    • RASH1
    • Transformation gene oncogene HAMSV
    • Transforming protein p21
    • v Ha ras Harvey rat sarcoma viral oncogene homolog
    • VH Ras
    • vHa RAS
    see all
  • 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
    Palmitoylated 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.
  • Information by UniProt

References for Recombinant Human GTPase HRAS (mutated S17 N) protein (ab90767)

ab90767 has not yet been referenced specifically in any publications.

Product Wall

There are currently no Abreviews or Questions for ab90767.
Please use the links above to contact us or submit feedback about this product.