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The official name of this gene is “neuroblastoma RAS viral (v-ras) oncogene homolog.”
NRAS is the gene's official symbol. The NRAS gene is also known by other names, listed below.
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).
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 that cause this condition affect a single protein building block (amino acid) in the N-Ras protein. Specifically, 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). Instead of triggering cell growth in response to particular signals from outside the cell, the overactive protein directs cells to grow and divide constantly. The uncontrolled cell growth of early melanocytes leads to a large patch of darkly pigmented skin characteristic of giant congenital melanocytic nevus. Uncontrolled cell growth of melanocytes after birth contributes to the risk of developing melanoma in people with giant congenital melanocytic nevus.
At least four mutations in the NRAS gene have been found to cause Noonan syndrome. These mutations are inherited and are present in both copies of the NRAS gene in essentially all of the body's cells. The mutations that cause Noonan syndrome replace single amino acids in the N-Ras protein and lead to the production of altered N-Ras proteins that are constitutively active and relaying signals. During embryonic development, the overactive N-Ras protein disrupts the normal growth and maturation of certain tissues. Researchers believe that increased N-Ras activation leading to defective cell movement and differentiation could play a role in the signs and symptoms of Noonan syndrome, including short stature, heart defects, and skeletal abnormalities.
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, including individuals without giant congenital melanocytic nevus (described above). 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.
Cytogenetic Location: 1p13.2
Molecular Location on chromosome 1: base pairs 114,704,463 to 114,716,893
The NRAS gene is located on the short (p) arm of chromosome 1 at position 13.2.
More precisely, the NRAS gene is located from base pair 114,704,463 to base pair 114,716,893 on chromosome 1.
See How do geneticists indicate the location of a gene? (http://ghr.nlm.nih.gov/handbook/howgeneswork/genelocation) in the Handbook.
You and your healthcare professional may find the following resources about NRAS helpful.
You may also be interested in these resources, which are designed for genetics professionals and researchers.
See How are genetic conditions and genes named? (http://ghr.nlm.nih.gov/handbook/mutationsanddisorders/naming) in the Handbook.
acids ; acute ; acute myeloid leukemia ; amino acid ; apoptosis ; arginine ; autoimmune ; cancer ; cell ; cell division ; class ; congenital ; differentiation ; embryonic ; gene ; glutamine ; GTP ; inherited ; leukemia ; lysine ; melanocytes ; melanoma ; molecule ; myeloid ; nucleus ; oncogene ; pigment ; precursor ; proliferate ; protein ; RAS ; short stature ; signal transduction ; stature ; syndrome ; transduction
You may find definitions for these and many other terms in the Genetics Home Reference Glossary (http://ghr.nlm.nih.gov/glossary).
The resources on this site should not be used as a substitute for professional medical care or advice. Users seeking information about a personal genetic disease, syndrome, or condition should consult with a qualified healthcare professional. See How can I find a genetics professional in my area? (http://ghr.nlm.nih.gov/handbook/consult/findingprofessional) in the Handbook.