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NRAS gene
Reviewed by Medicinsk Expert•Last updated: 2026-10-22•Gene

NRAS gene

The NRAS gene provides instructions for making a protein involved in regulating cell division and signal transduction, and mutations in this gene are linked to various cancers and developmental conditions.

Normal Function

The NRAS gene provides instructions for making a protein called N-Ras that is involved primarily in regulating cell division. Through a process known as signal transduction, the protein relays signals from outside the cell to the cell's nucleus. These signals instruct the cell to grow and divide (proliferate) or to mature and take on specialized functions (differentiate).

The N-Ras protein is a GTPase, which means it converts a molecule called GTP into another molecule called GDP. The N-Ras protein acts like a switch, and it is turned on and off by the GTP and GDP molecules. To transmit signals, the N-Ras protein must be turned on by attaching (binding) to a molecule of GTP. The N-Ras protein is turned off (inactivated) when it converts the GTP to GDP. When the protein is bound to GDP, it does not relay signals to the cell's nucleus.

The NRAS gene belongs to a class of genes known as oncogenes. When mutated, oncogenes have the potential to cause normal cells to become cancerous. The NRAS gene is in the Ras family of oncogenes, which also includes two other genes: HRAS and KRAS. The proteins produced from these three genes are GTPases. These proteins play important roles in cell division, cell differentiation, and the self-destruction of cells (apoptosis).

Health Conditions Related to Genetic Changes

Giant congenital melanocytic nevus

At least two mutations in the NRAS gene have been found to cause giant congenital melanocytic nevus. This condition is characterized by a large, noncancerous patch of abnormally dark skin that is present from birth and an increased risk of a type of skin cell cancer called melanoma.

  • The NRAS gene mutations that cause this condition are somatic, meaning that they occur during a person's lifetime and are present only in certain cells.
  • The mutations occur during embryonic development in cells that will develop into pigment-producing skin cells (melanocytes).
  • The mutations replace the amino acid glutamine at position 61 with either lysine or arginine (written as Gln61Lys or Q61K and Gln61Arg or Q61R).
  • These mutations lead to production of an N-Ras protein that is constantly turned on (constitutively active), directing cells to grow and divide constantly.

Cancers

Somatic mutations in the NRAS gene are involved in the development of several types of cancer. These mutations lead to an N-Ras protein that is constitutively active and can direct cells to grow and divide without control. Studies suggest that NRAS gene mutations are common in the aggressive skin cancer melanoma. Mutations in the NRAS gene have also been found in other types of cancer.

For reasons that are unclear, inherited mutations in the NRAS gene do not appear to increase the risk of cancer in people with Noonan syndrome.

Other Names for This Gene

  • GTPase NRas
  • GTPase NRas precursor
  • N-ras
  • N-ras protein part 4
  • neuroblastoma RAS viral (v-ras) oncogene homolog
  • neuroblastoma RAS viral oncogene homolog
  • NRAS1
  • NS6
  • RASN_HUMAN
  • transforming protein N-Ras
  • v-ras neuroblastoma RAS viral oncogene homolog

Frequently Asked Questions

In giant congenital melanocytic nevus, the NRAS mutation is usually a somatic mutation, meaning it occurs after conception in a specific cluster of cells during fetal development. This is distinct from germline mutations, which are present in every cell of the body and can be inherited from a parent. Because it is somatic, the condition is generally not inherited, though the risk of developing melanoma is higher in individuals with large nevi.
Inheritance of NRAS mutations is rare and depends on the specific condition. Most cancer-associated NRAS mutations are acquired (somatic) and are not inherited. However, in rare cases of familial conditions or if a parent has a germline mutation, genetic counseling is recommended. Clinicians typically use genetic testing to determine if a mutation is present in all cells (germline) or only in the tumor tissue (somatic) to assess recurrence risk and family implications.
NRAS mutations typically cause the N-Ras protein to become permanently "stuck" in its active state. Normally, the protein switches off by converting GTP to GDP, but the mutation prevents this switch-off mechanism. As a result, the cell continuously receives signals to divide and grow even when it should stop, leading to uncontrolled proliferation and tumor formation.
NRAS is one of three genes in the Ras family of oncogenes, alongside KRAS and HRAS. All three produce GTPase proteins that function as molecular switches for cell division and differentiation. While they share similar functions, mutations in each gene are associated with different patterns of cancer; for example, KRAS mutations are very common in pancreatic and lung cancers, while NRAS mutations are frequently found in melanoma, colorectal cancer, and thyroid cancer.
Source: MedlinePlus, National Library of Medicine

MedlinePlus brings together authoritative health information from the National Library of Medicine (NLM), the National Institutes of Health (NIH), and other government agencies and health-related organizations.

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