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

Expression host: E. coli  
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NRAS / N-Ras Related Area

NRAS / N-Ras Summary & Protein Information

NRAS / N-Ras Background

Enzyme regulation: Alternate 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.
Subcellular location: Cell membrane; Lipid-anchor; Cytoplasmic side. Golgi apparatus membrane; Lipid-anchor. 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.
Acetylation at Lys-104 prevents interaction with guanine nucleotide exchange factors (GEFs) (By similarity).
Involvement in 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.
Noonan syndrome 6 (NS6) [MIM:613224]: A syndrome characterized by facial dysmorphic features such as hypertelorism, a downward eyeslant and low-set posteriorly rotated ears. Other features can include short stature, a short neck with webbing or redundancy of skin, cardiac anomalies, deafness, motor delay and variable intellectual deficits. Note=The disease is caused by mutations affecting the gene represented in this entry.
Autoimmune lymphoproliferative syndrome 4 (ALPS4) [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. Note=The disease is caused by mutations affecting the gene represented in this entry.
Sequence similarity: Belongs to the small GTPase superfamily. Ras family.
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]
neuroblastoma RAS viral (v-ras) oncogene homolog,NRAS,RP5-1000E10.2,ALPS4,N-ras,NRAS1,NS6,GTPase NRas,N-ras protein part 4,transforming protein N-Ras,v-ras neuroblastoma RAS viral oncogene homolog, [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.