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Resistance to Oncogenic Transformation in Revertant R1 of Human ras-Transformed NIH 3T3 cells
| Title: | Resistance to Oncogenic Transformation in Revertant R1 of Human ras-Transformed NIH 3T3 cells |
| Authors: | Kuzumaki, Noboru1 Browse this author | | Ogiso, Yoshifumi Browse this author | | Oda, Atsushi Browse this author | | Fujita, Hisakazu Browse this author | | Suzuki, Hiroaki Browse this author | | Sato, Chiharu Browse this author | | Mullauer, Leonhard Browse this author |
| Authors(alt): | 葛巻, 暹1 |
| Issue Date: | 1989 |
| Publisher: | American Society for Microbiology |
| Journal Title: | Molecular and Cellular Biology |
| Volume: | 9 |
| Issue: | 5 |
| Start Page: | 2258 |
| End Page: | 2263 |
| Abstract: | A flat revertant, R1, was isolated from human activated c-Ha-ras-1 (hu-ac-Ha-ras) gene-transformed NIH 3T3 cells (EJ-NIH 3T3) treated with mutagens. R1 contained unchanged transfected hu-ac-Ha-ras DNA and expressed high levels of hu-ac-Ha-ras-specific mRNA and p21 protein. Transfection experiments revealed that NIH 3T3 cells could be transformed by DNA from R1 cells but R1 cells could not be retransformed by Kirsten sarcoma virus, DNA from EJ-NIH 3T3 cells, hu-ac-Ha-ras, v-src, v-mos, simian virus 40 large T antigen, or polyomavirus middle T antigen. Somatic cell hybridization studies showed that R1 was not retransformed by fusion with NIH 3T3 cells and suppressed anchorage independence of EJ-NIH 3T3 and hu-ac-Ha-ras gene-transformed rat W31 cells in soft agar. These results suggest that the reversion and resistance to several oncogenes in R1 is due not to cellular defects in the production of the transformed phenotype but rather to enhancement of cellular mechanisms that suppress oncogenic transformation. |
| Rights: | Copyright (c) 1989 American Society for Microbiology |
| Type: | article (author version) |
| URI: | http://hdl.handle.net/2115/753 |
| Appears in Collections: | 遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 葛巻 暹
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