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Gene Review

ras  -  resistance to audiogenic seizures

Mus musculus

Synonyms: asr
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Disease relevance of ras

  • In a more detailed analysis, the v-Ha-ras transfectants OV-ras4 and OV-ras7 were found to form colonies in various organs by metastasis from tumors after s.c. injection, as well as lung colonies after i.v. injection [1].
  • These findings suggest that Bin1 loss cooperates with ras activation to drive progression, establishing a role for Bin1 as a negative modifier of oncogenicity and progression in breast cancer [2].
  • Experiments were designed to examine the efficacy of IL-2 gene therapy in a surgical minimal residual tumour disease, using moderately immunogenic MK16/1/IIIABC murine cells transformed by activated ras and HPV 16 E6/E7 oncogenes (MK16 cells) [3].
  • The ras mutation, which is observed in 20-30% of human nonsmall cell lung cancers (NSCLCs), is one of common genetic alterations and has been proposed to be a prognostic factor in lung cancer [4].
  • Human rhabdomyosarcomas (RMSs) frequently demonstrate genetic alterations in ras and p53 [5].

High impact information on ras

  • A new study indicates that wildtype Kras2 has properties of a tumor suppressor gene and may have the capacity to reduce the transforming potential of oncogenically activated ras [6].
  • BACKGROUND: Point mutations in the ras proto-oncogene that activate its oncogenic potential occur in approximately 30% of human cancers [7].
  • BACKGROUND: Activated forms of the ras proto-oncogene have been found in approximately 30% of human malignancies, including pancreatic, colon, and lung adenocarcinomas [8].
  • We previously reported that mouse NIH 3T3 cells transformed by transfection of activated human c-Ha-ras become apparently normal upon treatment with the antibiotic azatyrosine [9].
  • To address the role of ras signaling in monocytic phagocytes in vivo, the expression of two dominant suppressors of in vitro ras signaling pathways, the carboxyl-terminal region of the GTPase-activating protein (GAP-C) and the DNA binding domain of the transcription factor ets-2, were targeted to this cell compartment [10].

Biological context of ras

  • Activations of oncogenes, ras, mos, abl, etc. and mutations in tumor suppressor genes such as p53 were also detected in specific tumors in cancer-prone descendants [11].
  • The results indicate that ras action is critical in monocytic cells after these cells have lost the capacity to traverse the cell cycle [10].
  • Analysis of the pattern of methylation of specific genes reveals that different types of genes are demethylated in the ras transfectants: skeletal muscle specific genes, a gene specifically expressed in the adrenal cortex (c21), ubiquitous genes, and exogenously introduced sequences [12].
  • The regions from -3700 to -220 and +500 to +4400 contributed equally to the ras-mediated inhibition of the parental plasmid [13].
  • We conclude that ras transformation suppresses the function of a cell-specific enhancer in the first intron of the alpha 1(I) collagen gene [13].

Anatomical context of ras

  • Alterations in differentiation and behavior of monocytic phagocytes in transgenic mice that express dominant suppressors of ras signaling [10].
  • We have previously shown that transformation of fibroblasts by ras results in transcriptional inhibition of the alpha 1(I) gene [13].
  • A radiation-induced murine ovarian granulosa cell tumor line: introduction of v-ras gene potentiates a high metastatic ability [1].
  • Lysyl oxidase (ras recision gene) expression in human amnion: ontogeny and cellular localization [14].
  • CD44s (standard isoform) levels and hyaluronan-binding activity were investigated in Balb/c 3T3 cells and their derivatives transformed with ras or sis oncogenes as a function of serum concentration in the medium [15].

Associations of ras with chemical compounds


Regulatory relationships of ras


Other interactions of ras

  • Thus, the lysyl oxidase propeptide, which is released during extracellular proteolytic processing of pro-lysyl oxidase, functions to inhibit ras-dependent cell transformation [20].
  • A 43-kDa nuclear IRF-1 protein was expressed biphasically during the cell cycle in primary mouse embryo fibroblasts, nontransformed NIH 3T3 cells, and ras revertants [21].
  • These data demonstrate that serum factors, specifically PDGF, mediate regulation of CD44 levels in BAlb/c 3T3 cells and that transformation of 3T3 cells by ras renders CD44 expression insensitive to the modulating effects of serum in vitro [15].
  • In PB-3c mastocytes, ionophore-induced IL-3 and GM-CSF expression is primarily the result of mRNA stabilization, and is enhanced by oncogenic ras [22].
  • The ras-related GTPase rac1 regulates a proliferative pathway selectively utilized by G-protein coupled receptors [23].

Analytical, diagnostic and therapeutic context of ras


  1. A radiation-induced murine ovarian granulosa cell tumor line: introduction of v-ras gene potentiates a high metastatic ability. Yanagihara, K., Nii, M., Tsumuraya, M., Numoto, M., Seito, T., Seyama, T. Jpn. J. Cancer Res. (1995) [Pubmed]
  2. Bin1 ablation in mammary gland delays tissue remodeling and drives cancer progression. Chang, M.Y., Boulden, J., Sutanto-Ward, E., Duhadaway, J.B., Soler, A.P., Muller, A.J., Prendergast, G.C. Cancer Res. (2007) [Pubmed]
  3. Interleukin 2 gene therapy of residual disease in mice carrying tumours induced by HPV 16. Bubeník, J., Símová, J., Hájková, R., Sobota, V., Jandlová, T., Smahel, M., Sobotková, E., Vonka, V. Int. J. Oncol. (1999) [Pubmed]
  4. Knockdown of Mutant K-ras Expression by Adenovirus-Mediated siRNA Inhibits the In Vitro and in Vivo Growth of Lung Cancer Cells. Zhang, Z., Jiang, G., Yang, F., Wang, J. Cancer Biol. Ther. (2006) [Pubmed]
  5. Cooperation of oncogenic K-ras and p53 deficiency in pleomorphic rhabdomyosarcoma development in adult mice. Tsumura, H., Yoshida, T., Saito, H., Imanaka-Yoshida, K., Suzuki, N. Oncogene (2006) [Pubmed]
  6. A new verdict for an old convict. Pfeifer, G.P. Nat. Genet. (2001) [Pubmed]
  7. Induction of T-cell immunity against Ras oncoproteins by soluble protein or Ras-expressing Escherichia coli. Fenton, R.G., Keller, C.J., Hanna, N., Taub, D.D. J. Natl. Cancer Inst. (1995) [Pubmed]
  8. Cytotoxic T-cell response and in vivo protection against tumor cells harboring activated ras proto-oncogenes. Fenton, R.G., Taub, D.D., Kwak, L.W., Smith, M.R., Longo, D.L. J. Natl. Cancer Inst. (1993) [Pubmed]
  9. Isolation of genes specifically expressed in flat revertant cells derived from activated ras-transformed NIH 3T3 cells by treatment with azatyrosine. Krzyzosiak, W.J., Shindo-Okada, N., Teshima, H., Nakajima, K., Nishimura, S. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
  10. Alterations in differentiation and behavior of monocytic phagocytes in transgenic mice that express dominant suppressors of ras signaling. Jin, D.I., Jameson, S.B., Reddy, M.A., Schenkman, D., Ostrowski, M.C. Mol. Cell. Biol. (1995) [Pubmed]
  11. Transgenerational effects of radiation and chemicals in mice and humans. Nomura, T. J. Radiat. Res. (2006) [Pubmed]
  12. Ras induces a general DNA demethylation activity in mouse embryonal P19 cells. Szyf, M., Theberge, J., Bozovic, V. J. Biol. Chem. (1995) [Pubmed]
  13. Transcriptional repression of the alpha 1(I) collagen gene by ras is mediated in part by an intronic AP1 site. Slack, J.L., Parker, M.I., Bornstein, P. J. Cell. Biochem. (1995) [Pubmed]
  14. Lysyl oxidase (ras recision gene) expression in human amnion: ontogeny and cellular localization. Casey, M.L., MacDonald, P.C. J. Clin. Endocrinol. Metab. (1997) [Pubmed]
  15. CD44 protein levels and its biological activity are regulated in Balb/c 3T3 fibroblasts by serum factors and by transformation with the ras but not with the sis oncogene. Kogerman, P., Sy, M.S., Culp, L.A. J. Cell. Physiol. (1996) [Pubmed]
  16. Retinoic acid prevents downregulation of ras recision gene/lysyl oxidase early in adipocyte differentiation. Dimaculangan, D.D., Chawla, A., Boak, A., Kagan, H.M., Lazar, M.A. Differentiation (1994) [Pubmed]
  17. Regulation of p21/ras protein expression by diallyl sulfide in DMBA induced neoplastic changes in mouse skin. Arora, A., Kalra, N., Shukla, Y. Cancer Lett. (2006) [Pubmed]
  18. Activation of the lutropin/choriogonadotropin receptor in MA-10 cells stimulates tyrosine kinase cascades that activate ras and the extracellular signal regulated kinases (ERK1/2). Shiraishi, K., Ascoli, M. Endocrinology (2006) [Pubmed]
  19. Comparative functional study of the lysyl oxidase promoter in fibroblasts, Ras-transformed fibroblasts, myofibroblasts and smooth muscle cells. Reynaud, C., Gleyzal, C., Jourdan-Le Saux, C., Sommer, P. Cell. Mol. Biol. (Noisy-le-grand) (1999) [Pubmed]
  20. The propeptide domain of lysyl oxidase induces phenotypic reversion of ras-transformed cells. Palamakumbura, A.H., Jeay, S., Guo, Y., Pischon, N., Sommer, P., Sonenshein, G.E., Trackman, P.C. J. Biol. Chem. (2004) [Pubmed]
  21. Deregulated expression of interferon regulatory factor-1 in oncogene-transformed mouse fibroblasts. Contente, S., Attard, F.A., Yeh, T.J., Buchhagen, D.L., Friedman, R.M. J. Interferon Cytokine Res. (2003) [Pubmed]
  22. Modulation of cytokine expression in PB-3c mastocytes by IBMX and PMA. Hahn, S., Moroni, C. Lymphokine Cytokine Res. (1994) [Pubmed]
  23. The ras-related GTPase rac1 regulates a proliferative pathway selectively utilized by G-protein coupled receptors. Burstein, E.S., Hesterberg, D.J., Gutkind, J.S., Brann, M.R., Currier, E.A., Messier, T.L. Oncogene (1998) [Pubmed]
  24. Persistence, immune specificity, and functional ability of murine mutant ras epitope-specific CD4(+) and CD8(+) T lymphocytes following in vivo adoptive transfer. Bristol, J.A., Schlom, J., Abrams, S.I. Cell. Immunol. (1999) [Pubmed]
  25. Gene expression profiling defined pathways correlated with fibroblast cell proliferation induced by Opisthorchis viverrini excretory/secretory product. Thuwajit, C., Thuwajit, P., Uchida, K., Daorueang, D., Kaewkes, S., Wongkham, S., Miwa, M. World J. Gastroenterol. (2006) [Pubmed]
  26. Can oncogene (RAS) activation predict susceptibility of human melanoma to activated lymphocytes and, therefore, the clinical response of such neoplasms to adoptive immunotherapy? Parmiani, G., Anichini, A., Carbone, G., Sensi, M. Melanoma Res. (1992) [Pubmed]
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