Overview

  • Product name

    H-Ras Activation Assay Kit
  • Sample type

    Tissue, Adherent cells, Suspension cells
  • Species reactivity

    Reacts with: Mouse, Rat, Human
  • Product overview

    H-Ras Activation Assay Kit (ab211158) uses Raf-1 RBD agarose beads to selectively isolate and pull-down the active form of Ras from cell or tissue lysates. The precipitated GTP-Ras is subsequently detected by western blot analysis using an anti-H-Ras specific rabbit polyclonal antibody, which reacts with the human, mouse and rat protein.


    Features: 1) non radioactive assay format; 2) fast results: 1 hour assay plus electrophoresis/blotting time; 3) includes Cdc42 positive control; 4) pink colored agarose beads for easy identification during washing and aspiration steps.

  • Notes

    Small GTP-binding proteins (or GTPases) are a family of proteins that serve as molecular regulators in signaling transduction pathways.

    Ras, a 21 kD protein, regulates a variety of biological response pathways that include cell growth, cell transformation and tumor invasion. Like other small GTPases, Ras regulates molecular events by cycling between an inactive GDP-bound form and an active GTP-bound form. In its active GTP-bound state, Ras binds specifically to the Ras-binding domain (RBD)of Raf1 to control downstream signaling cascades. Since defects in Ras signaling may result in malignant transformation, the activation of Ras proteins is tightly controlled in normal cells.

    The 3 Ras genes in human are H-Ras, N-Ras and K-Ras – it is estimated now that approximately 20% – 25% of all human tumors have activating mutations in one of the Ras genes.

    H-Ras (Harvey Rat Sarcome Viral Oncogene Homolog), also known as transforming protein p21, is associated with Costello Syndrome and phakomatosis pigmentokeratotica.

Properties

  • Storage instructions

    Store at -20°C. Please refer to protocols.
  • Components 20 tests 5 tests
    100X GDP 1 x 50µl 1 x 20µl
    100X GTPyS 1 x 50µl 1 x 20µl
    5X Assay/Lysis Buffer 1 x 30ml 4 x 2ml
    Anti-H-Ras Rabbit polyclonal antibody 1 x 40µl 1 x 10µl
    H-Ras Immunoblot Positive Control 1 x 100µl 1 x 100µl
    ab211176 - Raf-1 RBD Agarose Beads 1 x 800µl 1 x 200µl
  • Research areas

  • Function

    Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
  • 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.
  • Cellular localization

    Cell 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
  • 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
    • RASH_HUMAN
    • RASH1
    • Transformation gene oncogene HAMSV
    • Transforming protein p21
    • v Ha ras Harvey rat sarcoma viral oncogene homolog
    • VH Ras
    • vHa RAS
    see all
  • Database links

Associated products

Images

  • Dot blot that demonstrates specificity of anti-H-Ras rabbit antibody.

Protocols

References

ab211158 has not yet been referenced specifically in any publications.

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