Neuroblastoma RAS viral oncogene homolog (NRAS) (NRAS)

Neuroblastoma RAS viral oncogene homolog (NRAS) is a member of the RAS family of small GTPases that play a critical role in cellular signal transduction. It functions as a molecular switch, cycling between an active GTP-bound state and an inactive GDP-bound state to regulate pathways such as MAPK/ERK and PI3K/AKT, which govern cell growth, differentiation, and survival [1][2]. Mutations in the NRAS gene, particularly at codons 12, 13, and 61, lead to constitutive activation of the protein, driving oncogenesis in various malignancies including melanoma, acute myeloid leukemia, and thyroid carcinoma [3][4]. While NRAS was historically considered "undruggable" due to its high affinity for GTP and lack of deep binding pockets, current therapeutic strategies focus on inhibiting downstream effectors like MEK or exploring mRNA-targeted approaches and covalent inhibitors [5][6]. Targeting NRAS mRNA specifically involves the use of antisense oligonucleotides or RNA interference to prevent the translation of the oncogenic protein [7].

Other names

NRASGTPase NRasN-rasNRAS1Transforming protein N-RasNeuroblastoma RAS viral oncogene homolog mRNA

Inhibition of downstream MAPK/ERK signaling pathway, prevention of post-translational membrane localization, or degradation of target mRNA via RNA interference.