Recombinant NRAS G12D protein with the N-terminal AviTag™ peptide and His-tag is produced in E. coli cells and site-specifically biotinylated at AviTag with BirA enzyme.

Catalog # NRAS12D-B-301-1

NRAS mutations have a very similar effect on cancer cells as KRAS mutations. However, they are much less common. A wild-type NRAS (or normal) protein acts as an “on-and-off switch” involved in controlling cell growth, division, and survival. Mutated NRAS protein acts as an “on switch” resulting in uncontrollable cell growth and division, which can lead to cancer.

Activating mutations in the NRAS gene occur in approximately 2-3% of colorectal carcinomas, 20% of melanomas, and a variety of other human cancers. NRAS mutations are predominantly single nucleotide substitutions, occurring most frequently within exons 2 and 3 at codons 12, 13, and 61. These NRAS mutations are associated with poor clinical response to epidermal growth factor receptor (EGFR) targeted therapies in patients with colorectal cancer. 

The most common NRAS mutations are G12D, G12V, G12C, G12S, G12A, G12R, Q61K, and Q61R. There are currently no approved treatments directly targeting NRAS mutations.

For Research Use Only (RUO). This product is for research use only. It is not intended for diagnostic or therapeutic use in humans or animals.