The Neuroblastoma RAS Viral Oncogene Homolog (NRAS) is a member of the Ras gene family, which plays a crucial role in cell signaling pathways that control cell growth and differentiation. The NRAS gene is located on chromosome 1 in humans and chromosome 3 in mice . It was initially identified in human neuroblastoma cells, hence the name .
NRAS encodes a protein that is part of the Ras family of GTPases. These proteins are involved in transmitting signals within cells (signal transduction). The NRAS protein binds to GTP and GDP and has intrinsic GTPase activity, which is essential for its role as a molecular switch in various signaling pathways . The normal function of NRAS is to regulate cell growth, differentiation, and survival by activating downstream signaling pathways such as the MAPK/ERK pathway .
Mutations in the NRAS gene can lead to uncontrolled cell growth and cancer. NRAS mutations are found in various types of cancer, including melanoma, colorectal cancer, and hematologic malignancies . These mutations often result in the protein being permanently activated, leading to continuous cell proliferation and survival signals .
Mouse models are invaluable for studying the role of NRAS in cancer. Genetically engineered mouse models (GEMMs) have been developed to mimic human cancers driven by NRAS mutations . These models help researchers understand the mechanisms of tumor initiation, progression, and metastasis. They also serve as platforms for testing new therapies and understanding drug resistance .
Research on NRAS has significant implications for cancer therapy. Understanding the molecular mechanisms underlying NRAS-driven cancers can lead to the development of targeted therapies. For instance, inhibitors targeting the MAPK/ERK pathway are being explored as potential treatments for cancers with NRAS mutations . Additionally, mouse models of NRAS-driven cancers are used to identify and validate new therapeutic targets .