Requirement for c-ras proteins during viral oncogene transformation - PubMed (original) (raw)
Requirement for c-ras proteins during viral oncogene transformation
M R Smith et al. Nature. 1986 Apr.
Abstract
Many retroviral oncogenes have been classified into one of several categories based on structure, enzymology and cellular localization. These genes originated from host cells and are probably derived from genes normally involved in the control of cell proliferation. The cellular counterparts of three oncogenes have been identified as a growth factor or growth factor receptor; related oncogenes include receptor-like membrane proteins which often express tyrosine kinase activity. These growth factor-related oncogenes are structurally and biochemically distinct from the membrane-associated ras gene family, which bind and hydrolyse GTP. Oncogenes localized primarily in the cytoplasm which probably have serine kinase activity, have also been identified. Although the structure and biochemistry of many oncogenes have been extensively studied, relatively little is known about the functional relationships of oncogene proteins within the cell. An opportunity to study such interaction is provided by the identification of a monoclonal antibody that neutralizes cellular ras proteins when microinjected into cells. It has been shown previously that the injected antibody inhibits the initiation of S-phase in NIH 3T3 cells. In the present study we injected this monoclonal antibody into NIH 3T3 cells transformed by a variety of oncogenes. The results show that transformation by three growth factor receptor-like oncogenes depends on c-ras proteins, while transformation by two cytoplasmic oncogenes appears to be independent of c-ras protein.
Similar articles
- Critical role of cellular ras proteins in proliferative signal transduction.
Stacey DW, Tsai MH, Yu CL, Smith JK. Stacey DW, et al. Cold Spring Harb Symp Quant Biol. 1988;53 Pt 2:871-81. doi: 10.1101/sqb.1988.053.01.100. Cold Spring Harb Symp Quant Biol. 1988. PMID: 3076101 - Dominant inhibitory Ras mutants demonstrate the requirement for Ras activity in the action of tyrosine kinase oncogenes.
Stacey DW, Roudebush M, Day R, Mosser SD, Gibbs JB, Feig LA. Stacey DW, et al. Oncogene. 1991 Dec;6(12):2297-304. Oncogene. 1991. PMID: 1766676 - Comparative biochemical properties of p21 ras molecules coded for by viral and cellular ras genes.
Papageorge A, Lowy D, Scolnick EM. Papageorge A, et al. J Virol. 1982 Nov;44(2):509-19. doi: 10.1128/JVI.44.2.509-519.1982. J Virol. 1982. PMID: 6292515 Free PMC article. - The insulin/Ras pathway of adipocytic differentiation of 3T3 L1 cells: dissociation between Raf-1 kinase and the MAPK/RSK cascade.
Porras A, Santos E. Porras A, et al. Int J Obes Relat Metab Disord. 1996 Mar;20 Suppl 3:S43-51. Int J Obes Relat Metab Disord. 1996. PMID: 8680477 Review. - Interactions between Ras and Raf: key regulatory proteins in cellular transformation.
Marshall M. Marshall M. Mol Reprod Dev. 1995 Dec;42(4):493-9. doi: 10.1002/mrd.1080420418. Mol Reprod Dev. 1995. PMID: 8607981 Review.
Cited by
- Clinical practice guidelines for molecular tumor markers, 2nd edition review part 1.
Kikuchi Y, Shimada H, Hatanaka Y, Kinoshita I, Ikarashi D, Nakatsura T, Kitano S, Naito Y, Tanaka T, Yamashita K, Oshima Y, Nanami T. Kikuchi Y, et al. Int J Clin Oncol. 2024 Jan;29(1):1-19. doi: 10.1007/s10147-023-02430-x. Epub 2023 Nov 29. Int J Clin Oncol. 2024. PMID: 38019341 - Ubiquitin-specific protease 28: the decipherment of its dual roles in cancer development.
Ren X, Jiang M, Ding P, Zhang X, Zhou X, Shen J, Liu D, Yan X, Ma Z. Ren X, et al. Exp Hematol Oncol. 2023 Mar 6;12(1):27. doi: 10.1186/s40164-023-00389-z. Exp Hematol Oncol. 2023. PMID: 36879346 Free PMC article. Review. - Drug resistance in targeted cancer therapies with RAF inhibitors.
Degirmenci U, Yap J, Sim YRM, Qin S, Hu J. Degirmenci U, et al. Cancer Drug Resist. 2021 Jun 17;4(3):665-683. doi: 10.20517/cdr.2021.36. eCollection 2021. Cancer Drug Resist. 2021. PMID: 35582307 Free PMC article. Review. - Targeting Aberrant RAS/RAF/MEK/ERK Signaling for Cancer Therapy.
Degirmenci U, Wang M, Hu J. Degirmenci U, et al. Cells. 2020 Jan 13;9(1):198. doi: 10.3390/cells9010198. Cells. 2020. PMID: 31941155 Free PMC article. Review. - c-Raf in KRas Mutant Cancers: A Moving Target.
McCormick F. McCormick F. Cancer Cell. 2018 Feb 12;33(2):158-159. doi: 10.1016/j.ccell.2018.01.017. Cancer Cell. 2018. PMID: 29438690 Free PMC article.
References
- Bishop JM, Varmus HE. RNA Tumor Viruses: Molecular Biology of Tumor Viruses. 1984. pp. 999–1108.
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources