|Other Names||GTPase HRas, H-Ras-1, Ha-Ras, Transforming protein p21, c-H-ras, p21ras, GTPase HRas, N-terminally processed, HRAS, HRAS1|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP7764c was selected from the Center region of human HRAS. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml DI water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.|
|Cellular Location||Cell membrane. Cell membrane; Lipid-anchor; Cytoplasmic side. Golgi apparatus. Golgi apparatus membrane; Lipid-anchor. Note=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.|
|Tissue Location||Widely expressed.|
email@example.com, and receive a free "I Love Antibodies" mug.
Provided below are standard protocols that you may find useful for product applications.
HRAS belongs to the Ras oncogene family, whose members are related to the transforming genes of mammalian sarcoma retroviruses. These proteins function in signal transduction pathways. They can bind GTP and GDP, and they have intrinsic GTPase activity. HRAS undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. Mutations in this gene cause Costello syndrome, a disease characterized by increased growth at the prenatal stage, growth deficiency at the postnatal stage, predisposition to tumor formation, mental retardation, skin and musculoskeletal abnormalities, distinctive facial appearance and cardiovascular abnormalities. Defects in the HRAS gene are implicated in a variety of cancers, including bladder cancer, follicular thyroid cancer, and oral squamous cell carcinoma.
Winter-Vann,A.M., Proc. Natl. Acad. Sci. U.S.A. 100 (11), 6529-6534 (2003)Coats,S.G., Biochemistry 38 (39), 12926-12934 (1999)Sakai,E., Int. J. Cancer 52 (6), 867-872 (1992)
If you have any additional inquiries please email technical services at firstname.lastname@example.org.