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Gene Review

Hras  -  Harvey rat sarcoma virus oncogene

Mus musculus

Synonyms: GTPase HRas, H-Ras-1, H-ras, Ha-ras, Harvey-ras, ...
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Disease relevance of Hras1


Psychiatry related information on Hras1

  • Thus, the aim of this study was to investigate in mice, the relationships between the ras-dependent protein kinase ERK and MDMA-induced reinforcement using the conditioned place preference (CPP) and locomotor activity measurements [6].
  • The latency period between the time of infection and appearance of the lesions suggested that secondary alterations in addition to activated ras were necessary for neoplasms to develop [7].
  • Transformation of established murine fibroblasts with an activated cellular Harvey-ras oncogene or the polyoma virus middle T gene increases cell permissiveness to parvovirus minute-virus-of-mice [8].

High impact information on Hras1


Chemical compound and disease context of Hras1


Biological context of Hras1


Anatomical context of Hras1

  • Soft agar colony formation by NIH 3T3 cells transformed by ras oncogenes is not affected by anti-p185 antibody treatment [23].
  • Ha-ras and c-myc oncogene expression interferes with morphological and functional differentiation of mammary epithelial cells in single and double transgenic mice [24].
  • CONCLUSIONS: These results suggest that the activation of the p21ras and Py-MT/pp60c-src oncogenic pathways are critical effectors at different stages of colorectal carcinogenesis and in Caco-2 cells interferes with the program of enterocyte differentiation [25].
  • Ki-ras activation was detected in one primary rat liver tumor, and Ha-ras activation was detected in the cell line transformed in vitro with activated aflatoxin B1 [26].
  • The postmicrosomal fraction of the extract from NIH 3T3 and BALB/c 3T3 cells stimulated the hydrolysis of GTP bound to H-ras gene product p21 by severalfold [27].

Associations of Hras1 with chemical compounds

  • Neither class of transformants expressing Ki-ras or Ha-ras displayed a significant basal activity of polyphosphoinositide-specific phospholipase C, measured either in serum-starved cells or during exponential growth in the presence of growth factors of the tyrosine kinase family (EGF, FGF, insulin) [4].
  • To confirm that these aberrations occurred within the first cell cycle after mutant Ha-ras induction, the cells were arrested in G1 phase by serum depletion and, subsequently, released by administration of isopropyl beta-D-thiogalactoside or serum [28].
  • The NIH 3T3 cells used in this study contained mutant p53 genes and carried a selectively inducible activated (EJ) Ha-ras transgene under the control of bacterial lactose regulatory elements [28].
  • In contrast, proto-oncogenic forms of N-ras or H-ras had no apparent effects on the ability of C2 cells to differentiate [29].
  • A similar reduction in pp130 phosphorylation and reversion of morphology by herbimycin A were observed in v-src- and c-Ha-ras-transformed cells [30].
  • Basal tone of the H-ras(-/-) IAS was significantly higher and resistant to relaxation by Y 27632, compared with the H-ras(+/+) IAS [31].

Physical interactions of Hras1

  • In comparison with introduction of v-myc alone or both H-ras and v-myc oncogene, introduction of H-ras alone resulted in a loss of [125I]EGF binding activity to the cell surface EGF receptor [32].
  • Utilising a dominant negative mutant of p21ras we demonstrate that both insulin-induced Stat3 DNA-binding and also transactivation do not require p21ras [33].
  • Because c-Jun is the most potent transactivator in the AP-1 complex and is elevated in Ha-ras-transformed cells, in which c-Fos is downregulated, we focused on it as a potential target. c-Jun could convert input from an oncogenic signalling cascade into changes in gene expression [34].
  • Cellular ras genes encode a family of membrane-associated proteins (p21ras) that bind guanine nucleotide and possess a low intrinsic GTPase activity [35].
  • Previous studies have shown that the aberrant p21ras proteins are potential tumor-specific antigens in that CD4+ class II major histocompatibility complex-restricted T cells specific for the mutated segment of various oncogenic p21ras proteins can be elicited by immunization in vivo with synthetic peptides corresponding to the mutated segment [36].

Regulatory relationships of Hras1


Other interactions of Hras1


Analytical, diagnostic and therapeutic context of Hras1

  • In immunoblotting experiments, the affinity purified mAb, ras(53-69)Leu61, reacts specifically with the purified, bacterially produced rasLeu61 protein and does not react with bacterially produced normal H-ras protein [44].
  • Oral administration b.i.d. of R115777 to nude mice bearing s.c. tumors at doses ranging from 6.25-100 mg/kg inhibited the growth of tumors bearing mutant H-ras, mutant K-ras, and wild-type ras genes [45].
  • In one case, restriction enzyme analysis demonstrated the presence of a mutation in codon 12 of the activated Ha-ras oncogene [46].
  • RT-PCR analysis also showed much lower levels of EGF receptor gene expression in H-ras transfectants compared to that of parental untransformed cells (Balb-Neo1), v-myc and H-ras/v-myc transfectants [32].
  • To clarify the role of the H-Ras in vivo, we generated H-ras null mutant mice by gene targeting [47].


  1. Frequent mutations of the Trp53, Hras1 and beta-catenin (Catnb) genes in 1,3-butadiene-induced mammary adenocarcinomas in B6C3F1 mice. Zhuang, S.M., Wiseman, R.W., Söderkvist, P. Oncogene (2002) [Pubmed]
  2. Mutually exclusive mutations of the Pten and ras pathways in skin tumor progression. Mao, J.H., To, M.D., Perez-Losada, J., Wu, D., Del Rosario, R., Balmain, A. Genes Dev. (2004) [Pubmed]
  3. Mutation of the endogenous p53 gene in cells transformed by HPV-16 E7 and EJ c-ras confers a growth advantage involving an autocrine mechanism. Peacock, J.W., Benchimol, S. EMBO J. (1994) [Pubmed]
  4. Deregulation of hamster fibroblast proliferation by mutated ras oncogenes is not mediated by constitutive activation of phosphoinositide-specific phospholipase C. Seuwen, K., Lagarde, A., Pouysségur, J. EMBO J. (1988) [Pubmed]
  5. Chromosome assignments of four mouse cellular homologs of sarcoma and leukemia virus oncogenes. Sakaguchi, A.Y., Lalley, P.A., Zabel, B.U., Ellis, R.W., Scolnick, E.M., Naylor, S.L. Proc. Natl. Acad. Sci. U.S.A. (1984) [Pubmed]
  6. Importance of ERK activation in behavioral and biochemical effects induced by MDMA in mice. Salzmann, J., Marie-Claire, C., Le Guen, S., Roques, B.P., Noble, F. Br. J. Pharmacol. (2003) [Pubmed]
  7. Retroviral transduction of the human c-Ha-ras-1 oncogene into midgestation mouse embryos promotes rapid epithelial hyperplasia. Compere, S.J., Baldacci, P.A., Sharpe, A.H., Jaenisch, R. Mol. Cell. Biol. (1989) [Pubmed]
  8. Transformation of established murine fibroblasts with an activated cellular Harvey-ras oncogene or the polyoma virus middle T gene increases cell permissiveness to parvovirus minute-virus-of-mice. Mousset, S., Cornelis, J., Spruyt, N., Rommelaere, J. Biochimie (1986) [Pubmed]
  9. Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF. Kamijo, T., Zindy, F., Roussel, M.F., Quelle, D.E., Downing, J.R., Ashmun, R.A., Grosveld, G., Sherr, C.J. Cell (1997) [Pubmed]
  10. Cellular commitment to oncogene-induced transformation or apoptosis is dependent on the transcription factor IRF-1. Tanaka, N., Ishihara, M., Kitagawa, M., Harada, H., Kimura, T., Matsuyama, T., Lamphier, M.S., Aizawa, S., Mak, T.W., Taniguchi, T. Cell (1994) [Pubmed]
  11. Protein kinase C zeta isoform is critical for mitogenic signal transduction. Berra, E., Diaz-Meco, M.T., Dominguez, I., Municio, M.M., Sanz, L., Lozano, J., Chapkin, R.S., Moscat, J. Cell (1993) [Pubmed]
  12. Abnormal regulation of mammalian p21ras contributes to malignant tumor growth in von Recklinghausen (type 1) neurofibromatosis. DeClue, J.E., Papageorge, A.G., Fletcher, J.A., Diehl, S.R., Ratner, N., Vass, W.C., Lowy, D.R. Cell (1992) [Pubmed]
  13. A farnesyltransferase inhibitor induces tumor regression in transgenic mice harboring multiple oncogenic mutations by mediating alterations in both cell cycle control and apoptosis. Barrington, R.E., Subler, M.A., Rands, E., Omer, C.A., Miller, P.J., Hundley, J.E., Koester, S.K., Troyer, D.A., Bearss, D.J., Conner, M.W., Gibbs, J.B., Hamilton, K., Koblan, K.S., Mosser, S.D., O'Neill, T.J., Schaber, M.D., Senderak, E.T., Windle, J.J., Oliff, A., Kohl, N.E. Mol. Cell. Biol. (1998) [Pubmed]
  14. Changes in methyl-sensitive restriction sites of liver DNA from hamsters chronically exposed to hydrazine sulfate. Zheng, H., Shank, R.C. Carcinogenesis (1996) [Pubmed]
  15. p53 and H-ras mutations and microsatellite instability in renal pelvic carcinomas of NON / Shi mice treated with N-butyl-N-(4-hydroxybutyl)-nitrosamine: different genetic alteration from urinary bladder carcinoma. Gen, H., Yamamoto, S., Morimura, K., Min, W., Mitsuhashi, M., Murai, T., Mori, S., Hosono, M., Oohara, T., Makino, S., Wanibuchi, H., Fukushima, S. Jpn. J. Cancer Res. (2001) [Pubmed]
  16. Use of ras-transformed human ovarian surface epithelial cells as a model for studying ovarian cancer. Rosen, D.G., Yang, G., Bast, R.C., Liu, J. Meth. Enzymol. (2005) [Pubmed]
  17. Frequent p53 and H-ras Mutations in Benzene- and Ethylene Oxide-Induced Mammary Gland Carcinomas from B6C3F1 Mice. Houle, C.D., Ton, T.V., Clayton, N., Huff, J., Hong, H.H., Sills, R.C. Toxicologic pathology (2006) [Pubmed]
  18. Isoform-Specific Ras Activation and Oncogene Dependence during MYC- and Wnt-Induced Mammary Tumorigenesis. Jang, J.W., Boxer, R.B., Chodosh, L.A. Mol. Cell. Biol. (2006) [Pubmed]
  19. A region within murine chromosome 7F4, syntenic to the human 11q13 amplicon, is frequently amplified in 4NQO-induced oral cavity tumors. Yuan, B., Oechsli, M.N., Hendler, F.J. Oncogene (1997) [Pubmed]
  20. A Harvey-ras responsive transcription element is also responsive to a tumour-promoter and to serum. Imler, J.L., Schatz, C., Wasylyk, C., Chatton, B., Wasylyk, B. Nature (1988) [Pubmed]
  21. The carboxy-terminal catalytic domain of the GTPase-activating protein inhibits nuclear signal transduction and morphological transformation mediated by the CSF-1 receptor. Bortner, D.M., Ulivi, M., Roussel, M.F., Ostrowski, M.C. Genes Dev. (1991) [Pubmed]
  22. Loss of transcription factor IRF-1 affects tumor susceptibility in mice carrying the Ha-ras transgene or nullizygosity for p53. Nozawa, H., Oda, E., Nakao, K., Ishihara, M., Ueda, S., Yokochi, T., Ogasawara, K., Nakatsuru, Y., Shimizu, S., Ohira, Y., Hioki, K., Aizawa, S., Ishikawa, T., Katsuki, M., Muto, T., Taniguchi, T., Tanaka, N. Genes Dev. (1999) [Pubmed]
  23. Down-modulation of an oncogene protein product and reversion of the transformed phenotype by monoclonal antibodies. Drebin, J.A., Link, V.C., Stern, D.F., Weinberg, R.A., Greene, M.I. Cell (1985) [Pubmed]
  24. Ha-ras and c-myc oncogene expression interferes with morphological and functional differentiation of mammary epithelial cells in single and double transgenic mice. Andres, A.C., van der Valk, M.A., Schönenberger, C.A., Flückiger, F., LeMeur, M., Gerlinger, P., Groner, B. Genes Dev. (1988) [Pubmed]
  25. Neoplastic progression of human and rat intestinal cell lines after transfer of the ras and polyoma middle T oncogenes. Chastre, E., Empereur, S., Di Gioia, Y., el Mahdani, N., Mareel, M., Vleminckx, K., Van Roy, F., Bex, V., Emami, S., Spandidos, D.A. Gastroenterology (1993) [Pubmed]
  26. Activation of ras oncogene in aflatoxin-induced rat liver carcinogenesis. Sinha, S., Webber, C., Marshall, C.J., Knowles, M.A., Proctor, A., Barrass, N.C., Neal, G.E. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  27. Characterization of a factor that stimulates hydrolysis of GTP bound to ras gene product p21 (GTPase-activating protein) and correlation of its activity to cell density. Hoshino, M., Kawakita, M., Hattori, S. Mol. Cell. Biol. (1988) [Pubmed]
  28. The human Ha-ras oncogene induces genomic instability in murine fibroblasts within one cell cycle. Denko, N.C., Giaccia, A.J., Stringer, J.R., Stambrook, P.J. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  29. The oncogenic forms of N-ras or H-ras prevent skeletal myoblast differentiation. Olson, E.N., Spizz, G., Tainsky, M.A. Mol. Cell. Biol. (1987) [Pubmed]
  30. Ornithine decarboxylase- and ras-induced cell transformations: reversal by protein tyrosine kinase inhibitors and role of pp130CAS. Auvinen, M., Paasinen-Sohns, A., Hirai, H., Andersson, L.C., Hölttä, E. Mol. Cell. Biol. (1995) [Pubmed]
  31. H-ras inhibits RhoA/ROCK leading to a decrease in the basal tone in the internal anal sphincter. de Godoy, M.A., Patel, C.A., Waldman, S.A., Katsuki, M., Regan, R.F., Rattan, S. Gastroenterology (2007) [Pubmed]
  32. Regulation of epidermal growth factor receptor by activated H-ras and V-myc oncogenes in mouse Balb/3T3 cells: possible roles of AP-1. Okimoto, T., Kohno, K., Kuwano, M., Gopas, J., Kung, H.F., Ono, M. Oncogene (1996) [Pubmed]
  33. Insulin activates Stat3 independently of p21ras-ERK and PI-3K signal transduction. Coffer, P.J., van Puijenbroek, A., Burgering, B.M., Klop-de Jonge, M., Koenderman, L., Bos, J.L., Kruijer, W. Oncogene (1997) [Pubmed]
  34. Oncogenic and transcriptional cooperation with Ha-Ras requires phosphorylation of c-Jun on serines 63 and 73. Smeal, T., Binetruy, B., Mercola, D.A., Birrer, M., Karin, M. Nature (1991) [Pubmed]
  35. Co-capping of ras proteins with surface immunoglobulins in B lymphocytes. Graziadei, L., Riabowol, K., Bar-Sagi, D. Nature (1990) [Pubmed]
  36. Induction of T cells specific for the mutated segment of oncogenic P21ras protein by immunization in vivo with the oncogenic protein. Peace, D.J., Smith, J.W., Disis, M.L., Chen, W., Cheever, M.A. J. Immunother. (1993) [Pubmed]
  37. Identification of a ras-activated enhancer in the mouse osteopontin promoter and its interaction with a putative ETS-related transcription factor whose activity correlates with the metastatic potential of the cell. Guo, X., Zhang, Y.P., Mitchell, D.A., Denhardt, D.T., Chambers, A.F. Mol. Cell. Biol. (1995) [Pubmed]
  38. Loss of oncogenic H-ras-induced cell cycle arrest and p38 mitogen-activated protein kinase activation by disruption of Gadd45a. Bulavin, D.V., Kovalsky, O., Hollander, M.C., Fornace, A.J. Mol. Cell. Biol. (2003) [Pubmed]
  39. Induction of apoptosis by tamoxifen-activation of a p53-estrogen receptor fusion protein expressed in E1A and T24 H-ras transformed p53-/- mouse embryo fibroblasts. Vater, C.A., Bartle, L.M., Dionne, C.A., Littlewood, T.D., Goldmacher, V.S. Oncogene (1996) [Pubmed]
  40. Involvement of H- and N-Ras isoforms in transforming growth factor-beta1-induced proliferation and in collagen and fibronectin synthesis. Martínez-Salgado, C., Fuentes-Calvo, I., García-Cenador, B., Santos, E., López-Novoa, J.M. Exp. Cell Res. (2006) [Pubmed]
  41. Three different activated ras genes in mouse tumours; evidence for oncogene activation during progression of a mouse lymphoma. Vousden, K.H., Marshall, C.J. EMBO J. (1984) [Pubmed]
  42. Activation of extracellular signal-regulated kinase, ERK2, by p21ras oncoprotein. Leevers, S.J., Marshall, C.J. EMBO J. (1992) [Pubmed]
  43. Epidermal growth factor receptor, but not c-erbB-2, activation prevents lactogenic hormone induction of the beta-casein gene in mouse mammary epithelial cells. Hynes, N.E., Taverna, D., Harwerth, I.M., Ciardiello, F., Salomon, D.S., Yamamoto, T., Groner, B. Mol. Cell. Biol. (1990) [Pubmed]
  44. Detection of transforming ras proteins containing leucine at position 61 by a new mouse monoclonal antibody, ras(53-69)Leu61. Bizub, D., Fischberg-Bender, E., Heimer, E.P., Felix, A., Skalka, A.M. Cancer Res. (1989) [Pubmed]
  45. Characterization of the antitumor effects of the selective farnesyl protein transferase inhibitor R115777 in vivo and in vitro. End, D.W., Smets, G., Todd, A.V., Applegate, T.L., Fuery, C.J., Angibaud, P., Venet, M., Sanz, G., Poignet, H., Skrzat, S., Devine, A., Wouters, W., Bowden, C. Cancer Res. (2001) [Pubmed]
  46. Detection of activated ras oncogenes in human thyroid carcinomas. Suárez, H.G., Du Villard, J.A., Caillou, B., Schlumberger, M., Tubiana, M., Parmentier, C., Monier, R. Oncogene (1988) [Pubmed]
  47. Targeted deletion of the H-ras gene decreases tumor formation in mouse skin carcinogenesis. Ise, K., Nakamura, K., Nakao, K., Shimizu, S., Harada, H., Ichise, T., Miyoshi, J., Gondo, Y., Ishikawa, T., Aiba, A., Katsuki, M. Oncogene (2000) [Pubmed]
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