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NRAS / N-Ras  Protein, Antibody, ELISA Kit, cDNA Clone

Expression host: E. coli  
12073-H07E-20
12073-H07E-100
20 µg 
100 µg 
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NRAS / N-Ras Related Area

NRAS / N-Ras Related Pathways

NRAS / N-Ras Related Protein, Antibody, cDNA Gene, and ELISA Kits

NRAS / N-Ras Related Protein, Antibody, cDNA Gene, and ELISA Kits

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NRAS / N-Ras Summary & Protein Information

NRAS / N-Ras Background

Enzyme regulation: ENZYME REGULATION: Alternates between an inactive form bound to GDP and an active form bound to GTP. Activated by a guanine nucleotide-exchange factor (GEF) and inactivated by a GTPase-activating protein (GAP).
Subunit structure: Interacts (active GTP-bound form preferentially) with RGS14 (By similarity). Interacts (active GTP-bound form) with RASSF7. {ECO:0000250, ECO:0000269|PubMed:21278800}.
Subcellular location: Cell membrane {ECO:0000269|PubMed:15705808}; Lipid-anchor {ECO:0000269|PubMed:15705808}; Cytoplasmic side {ECO:0000269|PubMed:15705808}. Golgi apparatus membrane {ECO:0000269|PubMed:15705808}; Lipid-anchor {ECO:0000269|PubMed:15705808}. Note=Shuttles between the plasma membrane and the Golgi apparatus.
Post-translational: Palmitoylated by the ZDHHC9-GOLGA7 complex. A continuous cycle of de- and re-palmitoylation regulates rapid exchange between plasma membrane and Golgi. {ECO:0000269|PubMed:15705808, ECO:0000269|PubMed:16000296, ECO:0000269|PubMed:2661017}.; Acetylation at Lys-104 prevents interaction with guanine nucleotide exchange factors (GEFs). {ECO:0000250}.
Involvement in disease: DISEASE: Leukemia, juvenile myelomonocytic (JMML) [MIM:607785]: An aggressive pediatric myelodysplastic syndrome/myeloproliferative disorder characterized by malignant transformation in the hematopoietic stem cell compartment with proliferation of differentiated progeny. Patients have splenomegaly, enlarged lymph nodes, rashes, and hemorrhages. Note=The disease is caused by mutations affecting the gene represented in this entry.; DISEASE: Noonan syndrome 6 (NS6) [MIM:613224]: A form of Noonan syndrome, a disease characterized by short stature, facial dysmorphic features such as hypertelorism, a downward eyeslant and low-set posteriorly rotated ears, and a high incidence of congenital heart defects and hypertrophic cardiomyopathy. Other features can include a short neck with webbing or redundancy of skin, deafness, motor delay, variable intellectual deficits, multiple skeletal defects, cryptorchidism, and bleeding diathesis. Individuals with Noonan syndrome are at risk of juvenile myelomonocytic leukemia, a myeloproliferative disorder characterized by excessive production of myelomonocytic cells. {ECO:0000269|PubMed:19966803}. Note=The disease is caused by mutations affecting the gene represented in this entry.; DISEASE: RAS-associated autoimmune leukoproliferative disorder (RALD) [MIM:614470]: A disorder of apoptosis, characterized by chronic accumulation of non-malignant lymphocytes, defective lymphocyte apoptosis, and an increased risk for the development of hematologic malignancies. {ECO:0000269|PubMed:17517660}. Note=The disease is caused by mutations affecting the gene represented in this entry.; DISEASE: Melanocytic nevus syndrome, congenital (CMNS) [MIM:137550]: A syndrome characterized by congenital pigmentary skin lesions which can occur at any site and can cover most of the body surface. These lesions may or may not be hairy. Congenital melanocytic nevi are associated with neuromelanosis (the presence of melanin-producing cells within the brain parenchyma or leptomeninges). Less commonly they are associated with malignant melanoma in childhood, both in the skin and the central nervous system. CMNS patients also tend to have a characteristic facial appearance, including wide or prominent forehead, periorbital fullness, small short nose with narrow nasal bridge, round face, full cheeks, prominent premaxilla, and everted lower lip. {ECO:0000269|PubMed:18633438, ECO:0000269|PubMed:23392294}. Note=The disease is caused by mutations affecting the gene represented in this entry.; DISEASE: Melanosis, neurocutaneous (NCMS) [MIM:249400]: A rare congenital disease characterized by the presence of giant or multiple melanocytic nevi on the skin, foci of melanin-producing cells within the brain parenchyma, and infiltration of leptomeninges by abnormal melanin deposits. Neurologic abnormalities include seizures, hydrocephalus, arachnoid cysts, tumors, and syringomyelia. Some patients may develop malignant melanoma. {ECO:0000269|PubMed:23392294}. Note=The disease is caused by mutations affecting the gene represented in this entry.; DISEASE: Keratinocytic non-epidermolytic nevus (KNEN) [MIM:162900]: Epidermal nevi of the common, non-organoid and non-epidermolytic type are benign skin lesions and may vary in their extent from a single (usually linear) lesion to widespread and systematized involvement. They may be present at birth or develop early during childhood. {ECO:0000269|PubMed:22499344}. Note=The disease is caused by mutations affecting the gene represented in this entry.
Sequence similarity: Belongs to the small GTPase superfamily. Ras family. {ECO:0000305}.
General information above from UniProt

NRAS was discovered by researchers at the Institute of Cancer Research, funded by the Cancer Research Campaign (now Cancer Research UK). NRAS gene is a member of the Ras gene family. It is mapped on chromosome 1, and it is activated in HL60, a promyelocytic leukemia line. The mammalian ras gene family consists of the harvey and kirsten ras genes (HRAS and KRAS), an inactive pseudogene of each (c-Hras2 and c-Kras1) and the N-ras gene. They differ significantly only in the C-terminal 40 amino acids. These ras genes have GTP/GDP binding and GTPase activity, and their normal function may be as G-like regulatory proteins involved in the normal control of cell growth. The NRAS gene specifies two main transcripts of 2Kb and 4.3Kb. The difference between the two transcripts is a simple extension through the termination site of the 2Kb transcript. The NRAS gene consists of seven exons (-I, I, II, III, IV, V, VI).

NRAS / N-Ras Alternative Name

NS6,CMNS,NCMS,ALPS4,N-ras,NRAS1, [homo-sapiens]
CMNS,NCMS, [Human]
neuroblastoma ras oncogene,Nras,AV095280,N-ras,GTPase NRas,transforming protein N-Ras, [mouse]
N-ras,AV095280, [mus-musculus]

NRAS / N-Ras Related Studies

  • Marshall CJ. et al., 1982, Nature. 299 (5879): 171-3.
  • Hall Alan. et al., 1983, Nature. 303 (5916): 396-400.
  • McCormick F. 1996, Mol Reprod Dev. 42 (4): 500-6.
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