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|Tested species reactivity||Human|
|Host / Isotype||Mouse / IgG2b|
|Immunogen||Recombinant human protein purified from E.coli(His-R-Ras)|
|Purification||Ammonium sulfate precipitation|
|Storage buffer||HEPES with 0.15M NaCl, 0.01% BSA, 50% glycerol|
|Contains||0.03% sodium azide|
|Tested Applications||Dilution *|
|Western Blot (WB)||1:2000|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
A suggested positive control for this product is HeLa cells.
The Ras superfamily of small GTPases includes the Ras, Rho, Arf, Rab, and Ran families. Ras-regulated signal pathways control such as actin cytoskeletal integrity, proliferation, differentiation, cell adhesion, apoptosis, and cell migration. These GTPases function as molecular switches that control eukaryotic cell function by cycling between two interconvertible forms, a GDP-bound inactive form and a GTP-bound active form. The binding of GTP leads to a conformational change in the downstream effector-binding domain of the G-protein. The small GTPases are monomeric G-proteins with molecular masses over the range 20-30 kDa. Ras is attached to the cell membrane by prenylation. Mutations in the Ras family of proto-oncogenes (comprising H-Ras, N-Ras and K-Ras) are very common, being found in 20% to 30% of all human tumours. The frequency of RAS mutations is among the highest for any gene in human cancer. K-ras mutations occur frequently in non-small-cell lung, colorectal, and pancreatic carcinomas; H-ras mutations are common in bladder, kidney, and thyroid carcinomas; N-ras mutations are found in melanoma, hepatocellular carcinoma, and hematologic malignancies.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
Oncogene RRAS; p23; ras family small GTP binding protein R-Ras; ras-related protein R-Ras