Description

  • Product name

    Recombinant human H-Ras (G12V) (mutated G12 V) protein
    See all H-Ras (G12V) proteins and peptides
  • Purity

    > 95 % Densitometry.

  • Expression system

    Escherichia coli
  • Accession

  • Protein length

    Full length protein
  • Animal free

    No
  • Nature

    Recombinant
    • Species

      Human
    • Sequence

      TEYKLVVVGA VGVGKSALTI QLIQNHFVDE YDPTIEDSYR KQVVIDGETC LLDILDTAGQ EEYSAMRDQY MRTGEGFLCV FAINNTKSFE DIHQYREQIK RVKDSDDVPM VLVGNKCDLA ARTVESRQAQ DLARSYGIPY IETSAKTRQG VEDAFYTLVR EIRQHKLRKL NPPDESGPGC MSCKC
    • Predicted molecular weight

      23 kDa including tags
    • Amino acids

      2 to 186
    • Tags

      His tag N-Terminus
    • Additional sequence information

      Genbank Number: NM_ 005343 Full length mature protein, without the initiator methionine or the propeptide.

Specifications

Our Abpromise guarantee covers the use of ab140571 in the following tested applications.

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

  • Applications

    Western blot

    SDS-PAGE

  • Form

    Liquid
  • Additional notes

    The mutation G12V leads to elimination of the intrinsic GTPase activity.

  • Concentration information loading...

Preparation and Storage

  • Stability and Storage

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

    pH: 7.00
    Preservative: 1.02% Imidazole
    Constituents: 0.00174% PMSF, 0.82% Sodium phosphate, 0.00385% DTT, 25% Glycerol, 1.74% Sodium chloride

    This product is an active protein and may elicit a biological response in vivo, handle with caution.

General Info

  • Alternative names

    • c-H-ras
    • CBAS/HAS
    • CHARAS1
    • cHras
    • CTLO
    • GTPase HRas
    • H-Ras-1
    • Ha-Ras
    • HAMSV
    • HaRas
    • HRAS
    • HRas1
    • HRASIDX
    • KRAS
    • N-terminally processed
    • NRAS
    • p21ras
    • RASH_HUMAN
    • RASH1
    • Transforming protein p21
    • vHaras Harvey rat sarcoma viral oncogene homolog
    see all
  • Function

    Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
  • Tissue specificity

    Widely expressed.
  • Involvement in disease

    Defects 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 similarities

    Belongs to the small GTPase superfamily. Ras family.
  • Post-translational
    modifications

    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.
    The covalent modification of cysteine by 15-deoxy-Delta12,14-prostaglandin-J2 is autocatalytic and reversible. It may occur as an alternative to other cysteine modifications, such as S-nitrosylation and S-palmitoylation.
  • Cellular localization

    Cell membrane. Cell membrane. Golgi apparatus. 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 and Nucleus. Cytoplasm. Cytoplasm > perinuclear region. Colocalizes with GNB2L1 to the perinuclear region.
  • Information by UniProt

Images

  • SDS-PAGE analysis of ab140571

References

ab140571 has not yet been referenced specifically in any publications.

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