|Application ||WB, IHC|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||21298 Da|
|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||A synthetic peptide corresponding to residues in the C-terminus of human H-Ras was used as an immunogen. The antibody does not cross-react with other Ras family member.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||H-Ras Antibody (C-term) is for research use only and 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.|
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Provided below are standard protocols that you may find useful for product applications.
Ras, a signal transducer, was first characterized as the transforming genes of Harvey & Kristen sarcoma virus (1). The Ras family (H-Ras, N-Ras, and K-Ras) regulates cell growth, differentiation and apoptosis (2). Switching from an active or resting state, Ras can either bind GTP or GDP respectively. In the triphosphate conformation, Ras will interact with GTPase activating protein (GAP) to increase its activity (3). Mutations in any of the three isoforms can convert these proteins into active oncogenes. Additionally, Ras mutations are found in 30 % of all human cancer (4).
1. Ellis RW, et al. Nature. 1981 Aug 6; 292(5823):506
2. Campbell, S. L., (1998) Oncogene 17, 1395-1413
3. heng, Y., and Quilliam, L. A. (2003) EMBO Rep 4, 463-468
4. Bos JL. Cancer Res. 1989; 49:4682
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