Harvey rat sarcoma viral oncogene homolog, residues 1-166
human, recombinant, E. coli
| Cat. No. | Amount | Price (EUR) | Buy / Note |
|---|---|---|---|
| PR-202 | 50 μg | 271,40 | Add to Basket/Quote Add to Notepad |
For general laboratory use.
Shipping: shipped on dry ice
Storage Conditions: store at -80 °C
avoid freeze/thaw cycles
Shelf Life: 12 months
Molecular Weight: 19.5 kDa (171 amino acids)
Accession number: NP_005334
Purity: > 90 % (SDS-PAGE)
Form: liquid (Supplied in 64 mM Tris-HCl pH 7.2, 10 mM MgCl2 and 5 mM DTE)
Description:
Ras proteins are members of the superfamily of small GTP-binding proteins that function as molecular switches controlling a variety of signaling and transport pathways. H-Ras is one of the classic human Ras proteins (H-, N-, K-Ras4A, and K-Ras4B). H-Ras ΔC (aa 1 - 171) lacks the C-terminus with the CaaX recognition sequence necessary for anchoring Ras into the plasma membrane. The mutation S17N results in a 40-fold increase in the affinity for GTP without affecting its affinity for GDP. Protein preparation is 95% GDP- and 5% GTP-loaded, measured by HPLC.
BIOZ Product Citations:
Selected References:
Nassar et al. (2010) Structure of the Dominant Negative S17N Mutant of Ras. Biochemistry 49:1970.
Sasazuki et al. (2005) Transformation by Oncogenic RAS Sensitizes Human Colon Cells to TRAIL-induced Apoptosis by Up-regulating Death Receptor 4 and Death Receptor 5 through a MEK-dependent Pathway. J Biol. Chem. 280:22856.
Wittinghofer et al. (2000) Ras - a molecular switch involved in tumor formation. Angew. Chem. Int. Ed. 39:4192.
Feig et al. (1988) Inhibition of NIH 3T3 cell proliferation by a mutant ras protein with preferential affinity for GDP. Mol. Cell. Biol. 8:3235.
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