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H-Ras (G12V) protein (Active) (ab90627)

Overview

  • Product nameH-Ras (G12V) protein (Active)See all H-Ras (G12V) proteins and peptides ...
  • Protein descriptionRecombinant full length, proprietary tagged, Human H-Ras (G12V) protein. 189 amino acids; Predicted MWt 47 kDa. UniProt ID = P01112.
  • Expression hostE. coli
  • Properties

  • Purity> 95 % by SDS-PAGE
  • Biological activityab90627 is effective in activation of PI3K and PKB
  • FormLiquid
  • Storage instructionsShipped 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.
  • Storage bufferPreservative: None
    Constituents: 5mM Magnesium chloride, 5mM Beta mercaptoethanol, 25mM Tris HCl, 150mM Sodium chloride, pH 7.5
  • Concentration information loading...
  • Research Areas
  • Applications

    Our Abpromise guarantee covers the use of ab90627 in the following tested applications.

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

    Application Notes
    SDS-PAGE
    Functional Studies
  • Application notesFuncS: Use at an assay dependent dilution.
    SDS-PAGE: Use at an assay dependent dilution.


    Not yet tested in other applications.
    Optimal dilutions/concentrations should be determined by the end user.
  • Protein info

    • Alternative names
        c-H-rasCBAS/HASCHARAS1
        cHrasCTLOGTPase HRasH-Ras-1Ha-RasHAMSVHaRasHRASHRas1HRASIDXKRASN-terminally processedNRASp21rasRASH_HUMANRASH1Transforming protein p21vHaras Harvey rat sarcoma viral oncogene homolog
      see all
  • FunctionRas proteins bind GDP/GTP and possess intrinsic GTPase activity.
  • Tissue specificityWidely expressed.
  • 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
    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 localizationCell 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.
  • Target information above from: UniProt accession P01112 The UniProt Consortium
    The Universal Protein Resource (UniProt) in 2010
    Nucleic Acids Res. 38:D142-D148 (2010) .

    Information by UniProt

    References for H-Ras (G12V) protein (Active) (ab90627)

    ab90627 has not yet been referenced specifically in any publications.

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    Thank you for contacting us.

    The ab90765 and ab90768 are also active proteins and can be used in functional assays.

    ab96817 is not an active protein.

    Please note that we haven't tried these proteins in functional assay so th...

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    Thank you for contacting us.

    We are not sure what sort of transfection method you will be using. However the protein datasheets which say the protein can be used in functional assay will bea good choice e.g. ab90627.

    I hope this info...

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    Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"