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Gene Review

NRAS  -  neuroblastoma RAS viral (v-ras) oncogene...

Homo sapiens

Synonyms: ALPS4, CMNS, GTPase NRas, HRAS1, N-ras, ...
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Disease relevance of NRAS


Psychiatry related information on NRAS


High impact information on NRAS

  • We show that Nras is transiently localized in the Golgi prior to the plasma membrane (PM) [10].
  • Genomic DNA was extracted from 39 tumor specimens obtained by thoracotomy and was examined for activating point mutations in codons 12, 13, and 61 of the H-ras, K-ras, and N-ras genes [11].
  • We conclude that mutational K-ras activation may be an important early event in the pathogenesis of adenocarcinoma of the lung but that amplification of ras genes or mutational activation of H-ras or N-ras does not play a major part in non-small-cell lung cancer [11].
  • Activated N-ras controls the transformed phenotype of HT1080 human fibrosarcoma cells [12].
  • To investigate whether the activated N-ras oncogene of HT1080 human fibrosarcoma cells contributes to the expression of the transformed phenotype, we have isolated flat revertants [12].

Chemical compound and disease context of NRAS


Biological context of NRAS


Anatomical context of NRAS


Associations of NRAS with chemical compounds

  • In addition, angiotensin II may be produced in various tissues by enzymes of the renin-angiotensin system (RAS) or the nonrenin-angiotensin system (NRAS) [27].
  • Construction of chimeric molecules between the transforming and the normal N-ras genes and subsequent biological and sequence analysis of these constructs revealed that the transforming gene was altered by a point mutation changing amino acid 12 of the N-ras protein from glycine to aspartic acid [28].
  • From this we predicted a glutamine-to-lysine substitution in amino acid 61, a change confirmed by conventional sequencing of the first and second exons of N-ras from cell line Mel Swift [29].
  • Eighty percent of the mutations involved substitution of aspartic acid for glycine (G----A) in the 12th or 13th codons of N-ras or K-ras [30].
  • Such cells, designated UR61, undergo neuronal differentiation upon exposure to nanomolar concentrations of dexamethasone, as a consequence of expression of the activated N-ras gene (I. Guerrero, A. Pellicer, and D.E. Burstein, Biochem, Biophys. Res. Commun. 150:1185-1192, 1988) [31].

Regulatory relationships of NRAS

  • We found 16 cell lines (30%) with alterations in PTEN/MMAC1 and 11 cell lines (21%) with activating NRAS mutations; only 1 cell line had concurrent alterations in both genes [22].
  • CMs frequently harbor an activating mutation in either NRAS or the RAS-regulated kinase BRAF, suggesting that either of these oncogenes may increase signaling through the mitogen-activated protein (MAP) kinase pathway and promote melanoma development [32].
  • The HT1080 also contains an activated N-ras oncogene [33].

Other interactions of NRAS

  • RESULTS: We detected BRAF mutations in 2 of 19 cases and NRAS mutations in none of the cases [34].
  • Intact, human HRAS sequences were observed in 2 of the 11 tumor groups, whereas no hybridization was detected when human KRAS or NRAS probes were used [35].
  • The relative reciprocity of PTEN/MMAC1 abrogation and NRAS activation suggests that the two genetic changes, in a subset of cutaneous melanomas, are functionally overlapping [22].
  • Longitudinal studies revealed that the NRAS mutation was a late-appearing event, while the TP53 mutations were detectable at the presentation of MDS [21].
  • The order is cen-CD2-NGFB-NRAS [36].

Analytical, diagnostic and therapeutic context of NRAS


  1. Anti-oncogenic role of the endoplasmic reticulum differentially activated by mutations in the MAPK pathway. Denoyelle, C., Abou-Rjaily, G., Bezrookove, V., Verhaegen, M., Johnson, T.M., Fullen, D.R., Pointer, J.N., Gruber, S.B., Su, L.D., Nikiforov, M.A., Kaufman, R.J., Bastian, B.C., Soengas, M.S. Nat. Cell Biol. (2006) [Pubmed]
  2. Activated protooncogenes in human lung tumors from smokers. Reynolds, S.H., Anna, C.K., Brown, K.C., Wiest, J.S., Beattie, E.J., Pero, R.W., Iglehart, J.D., Anderson, M.W. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  3. Analysis of RAS oncogene mutations in human lymphoid malignancies. Neri, A., Knowles, D.M., Greco, A., McCormick, F., Dalla-Favera, R. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  4. Genetic analysis is consistent with the hypothesis that NF1 limits myeloid cell growth through p21ras. Kalra, R., Paderanga, D.C., Olson, K., Shannon, K.M. Blood (1994) [Pubmed]
  5. Activated Ras enhances insulin-like growth factor I induction of vascular endothelial growth factor in prostate epithelial cells. Stearns, M., Tran, J., Francis, M.K., Zhang, H., Sell, C. Cancer Res. (2005) [Pubmed]
  6. NRAS mutation causes a human autoimmune lymphoproliferative syndrome. Oliveira, J.B., Bidère, N., Niemela, J.E., Zheng, L., Sakai, K., Nix, C.P., Danner, R.L., Barb, J., Munson, P.J., Puck, J.M., Dale, J., Straus, S.E., Fleisher, T.A., Lenardo, M.J. Proc. Natl. Acad. Sci. U.S.A. (2007) [Pubmed]
  7. Clinical correlates of NRAS and BRAF mutations in primary human melanoma. Ellerhorst, J.A., Greene, V.R., Ekmekcioglu, S., Warneke, C.L., Johnson, M.M., Cooke, C.P., Wang, L.E., Prieto, V.G., Gershenwald, J.E., Wei, Q., Grimm, E.A. Clin. Cancer Res. (2011) [Pubmed]
  8. Induction of p21ras in Alzheimer pathology. Gärtner, U., Holzer, M., Heumann, R., Arendt, T. Neuroreport (1995) [Pubmed]
  9. Preferential repair of the N-ras gene in K 562 cells after exposure to cisplatin. Dempke, W., Voigt, W., Grothey, A., Schmoll, H.J. Anticancer Drugs (1999) [Pubmed]
  10. Endomembrane trafficking of ras: the CAAX motif targets proteins to the ER and Golgi. Choy, E., Chiu, V.K., Silletti, J., Feoktistov, M., Morimoto, T., Michaelson, D., Ivanov, I.E., Philips, M.R. Cell (1999) [Pubmed]
  11. Mutational activation of the K-ras oncogene. A possible pathogenetic factor in adenocarcinoma of the lung. Rodenhuis, S., van de Wetering, M.L., Mooi, W.J., Evers, S.G., van Zandwijk, N., Bos, J.L. N. Engl. J. Med. (1987) [Pubmed]
  12. Activated N-ras controls the transformed phenotype of HT1080 human fibrosarcoma cells. Paterson, H., Reeves, B., Brown, R., Hall, A., Furth, M., Bos, J., Jones, P., Marshall, C. Cell (1987) [Pubmed]
  13. Distinct gene expression patterns associated with FLT3- and NRAS-activating mutations in acute myeloid leukemia with normal karyotype. Neben, K., Schnittger, S., Brors, B., Tews, B., Kokocinski, F., Haferlach, T., Müller, J., Hahn, M., Hiddemann, W., Eils, R., Lichter, P., Schoch, C. Oncogene (2005) [Pubmed]
  14. Suppression of oncogenic NRAS by RNA interference induces apoptosis of human melanoma cells. Eskandarpour, M., Kiaii, S., Zhu, C., Castro, J., Sakko, A.J., Hansson, J. Int. J. Cancer (2005) [Pubmed]
  15. Structure and activation of the human N-ras gene. Taparowsky, E., Shimizu, K., Goldfarb, M., Wigler, M. Cell (1983) [Pubmed]
  16. Transient response to imatinib in a chronic eosinophilic leukemia associated with ins(9;4)(q33;q12q25) and a CDK5RAP2-PDGFRA fusion gene. Walz, C., Curtis, C., Schnittger, S., Schultheis, B., Metzgeroth, G., Schoch, C., Lengfelder, E., Erben, P., Müller, M.C., Haferlach, T., Hochhaus, A., Hehlmann, R., Cross, N.C., Reiter, A. Genes Chromosomes Cancer (2006) [Pubmed]
  17. Transformation and stimulation of DNA synthesis in NIH-3T3 cells are a titratable function of normal p21N-ras expression. McKay, I.A., Marshall, C.J., Calés, C., Hall, A. EMBO J. (1986) [Pubmed]
  18. RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years. Bowen, D.T., Frew, M.E., Hills, R., Gale, R.E., Wheatley, K., Groves, M.J., Langabeer, S.E., Kottaridis, P.D., Moorman, A.V., Burnett, A.K., Linch, D.C. Blood (2005) [Pubmed]
  19. Coexpression of NRASQ61R and BRAFV600E in human melanoma cells activates senescence and increases susceptibility to cell-mediated cytotoxicity. Petti, C., Molla, A., Vegetti, C., Ferrone, S., Anichini, A., Sensi, M. Cancer Res. (2006) [Pubmed]
  20. RAS mutations and clonality analysis in children with juvenile myelomonocytic leukemia (JMML). Flotho, C., Valcamonica, S., Mach-Pascual, S., Schmahl, G., Corral, L., Ritterbach, J., Hasle, H., Aricò, M., Biondi, A., Niemeyer, C.M. Leukemia (1999) [Pubmed]
  21. Genetic aberrations in the development and subsequent progression of myelodysplastic syndrome. Misawa, S., Horiike, S., Kaneko, H., Kashima, K. Leukemia (1997) [Pubmed]
  22. Relative reciprocity of NRAS and PTEN/MMAC1 alterations in cutaneous melanoma cell lines. Tsao, H., Zhang, X., Fowlkes, K., Haluska, F.G. Cancer Res. (2000) [Pubmed]
  23. Detection of preferential NRAS mutations in human male germ cell tumors by the polymerase chain reaction. Ganguly, S., Murty, V.V., Samaniego, F., Reuter, V.E., Bosl, G.J., Chaganti, R.S. Genes Chromosomes Cancer (1990) [Pubmed]
  24. Detection of RAS mutations in archival testicular germ cell tumors by polymerase chain reaction and oligonucleotide hybridization. Moul, J.W., Theune, S.M., Chang, E.H. Genes Chromosomes Cancer (1992) [Pubmed]
  25. Molecular events in follicular thyroid tumors. Kroll, T.G. Cancer Treat. Res. (2004) [Pubmed]
  26. Recurrent KRAS Codon 146 Mutations in Human Colorectal Cancer. Edkins, S., O'meara, S., Parker, A., Stevens, C., Reis, M., Jones, S., Greenman, C., Davies, H., Dalgliesh, G., Forbes, S., Hunter, C., Smith, R., Stephens, P., Goldstraw, P., Nicholson, A., Chan, T.L., Velculescu, V.E., Yuen, S.T., Leung, S.Y., Stratton, M.R., Futreal, P.A. Cancer Biol. Ther. (2006) [Pubmed]
  27. Human adipose tissue expresses angiotensinogen and enzymes required for its conversion to angiotensin II. Karlsson, C., Lindell, K., Ottosson, M., Sjöström, L., Carlsson, B., Carlsson, L.M. J. Clin. Endocrinol. Metab. (1998) [Pubmed]
  28. Activation of an N-ras gene in acute myeloblastic leukemia through somatic mutation in the first exon. Gambke, C., Hall, A., Moroni, C. Proc. Natl. Acad. Sci. U.S.A. (1985) [Pubmed]
  29. Activation of N-ras in a human melanoma cell line. Padua, R.A., Barrass, N.C., Currie, G.A. Mol. Cell. Biol. (1985) [Pubmed]
  30. RAS mutations are rare events in Philadelphia chromosome-negative/bcr gene rearrangement-negative chronic myelogenous leukemia, but are prevalent in chronic myelomonocytic leukemia. Hirsch-Ginsberg, C., LeMaistre, A.C., Kantarjian, H., Talpaz, M., Cork, A., Freireich, E.J., Trujillo, J.M., Lee, M.S., Stass, S.A. Blood (1990) [Pubmed]
  31. Oncogene N-ras mediates selective inhibition of c-fos induction by nerve growth factor and basic fibroblast growth factor in a PC12 cell line. Thomson, T.M., Green, S.H., Trotta, R.J., Burstein, D.E., Pellicer, A. Mol. Cell. Biol. (1990) [Pubmed]
  32. Absence of BRAF and NRAS mutations in uveal melanoma. Cruz, F., Rubin, B.P., Wilson, D., Town, A., Schroeder, A., Haley, A., Bainbridge, T., Heinrich, M.C., Corless, C.L. Cancer Res. (2003) [Pubmed]
  33. Tumorigenicity of human HT1080 fibrosarcoma X normal fibroblast hybrids: chromosome dosage dependency. Benedict, W.F., Weissman, B.E., Mark, C., Stanbridge, E.J. Cancer Res. (1984) [Pubmed]
  34. BRAF mutations distinguish anorectal from cutaneous melanoma at the molecular level. Helmke, B.M., Mollenhauer, J., Herold-Mende, C., Benner, A., Thome, M., Gassler, N., Wahl, W., Lyer, S., Poustka, A., Otto, H.F., Deichmann, M. Gastroenterology (2004) [Pubmed]
  35. Characterization of mutagen-activated cellular oncogenes that confer anchorage independence to human fibroblasts and tumorigenicity to NIH 3T3 cells: sequence analysis of an enzymatically amplified mutant HRAS allele. Stevens, C.W., Manoharan, T.H., Fahl, W.E. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  36. Determination of the gene order of the three loci CD2, NGFB, and NRAS at human chromosome band 1p13 and refinement of their localisation at the subband level by fluorescence in situ hybridisation. Mitchell, E.L., Jones, D., White, G.R., Varley, J.M., Santibanez Koref, M.F. Cytogenet. Cell Genet. (1995) [Pubmed]
  37. CYP1A1*2B (Val) allele is overrepresented in a subgroup of acute myeloid leukemia patients with poor-risk karyotype associated with NRAS mutation, but not associated with FLT3 internal tandem duplication. Bowen, D.T., Frew, M.E., Rollinson, S., Roddam, P.L., Dring, A., Smith, M.T., Langabeer, S.E., Morgan, G.J. Blood (2003) [Pubmed]
  38. RAS gene activation in acute myelogenous leukemia: analysis by in vitro amplification and DNA base sequence determination. Mane, S.M., Meltzer, S.J., Gutheil, J.C., Kapil, V., Lee, E.J., Needleman, S.W. Genes Chromosomes Cancer (1990) [Pubmed]
  39. RAS mutations in myelodysplasia detected by amplification, oligonucleotide hybridization, and transformation. Padua, R.A., Carter, G., Hughes, D., Gow, J., Farr, C., Oscier, D., McCormick, F., Jacobs, A. Leukemia (1988) [Pubmed]
  40. Sorafenib in advanced melanoma: a Phase II randomised discontinuation trial analysis. Eisen, T., Ahmad, T., Flaherty, K.T., Gore, M., Kaye, S., Marais, R., Gibbens, I., Hackett, S., James, M., Schuchter, L.M., Nathanson, K.L., Xia, C., Simantov, R., Schwartz, B., Poulin-Costello, M., O'Dwyer, P.J., Ratain, M.J. Br. J. Cancer (2006) [Pubmed]
  41. BRAF and NRAS mutations in melanoma and melanocytic nevi. Poynter, J.N., Elder, J.T., Fullen, D.R., Nair, R.P., Soengas, M.S., Johnson, T.M., Redman, B., Thomas, N.E., Gruber, S.B. Melanoma Res. (2006) [Pubmed]
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