Morphology of Ras- Transformed Cells Becomes Apparently Normal Again with Tyrosine Kinase Inhibitors without a Decrease in the Ras- GTP Complex^1
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- KWON Ho Jeong
- Department of Biotechnology The University of Tokyo
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- YOSHIDA Minoru
- Department of Biotechnology The University of Tokyo
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- MUROYA Kenkoh
- Division of Biochemistry and Cellular Biology, National Institute of Neuroscience, National Center of Neurology and Psychiatry
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- HATTORI Seisuke
- Division of Biochemistry and Cellular Biology, National Institute of Neuroscience, National Center of Neurology and Psychiatry
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- NISHIDA Eisuke
- Department of Genetics and Molecular Biology, Institute for Virus Research, Kyoto University
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- FUKUI Yasuhisa
- Department of Applied Biological Chemistry The University of Tokyo
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- BEPPU Teruhiko
- Department of Biotechnology The University of Tokyo
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- HORINOUCHI Sueharu
- Department of Biotechnology The University of Tokyo
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抄録
Radicicol, an inhibitor of protein-tyrosine kinase, was found to cause morphological reversion of v-Ha-ras-transformed NIH3T3 fibroblasts and T24 human urinary bladder carcinoma cells that contain an activated ras mutation. The network of actin stress fibers was restored during the treatment with radicicol. A similar morphological change was observed with another protein-tyrosine kinase inhibitor, herbimycin A. Radicicol did not cause any changes in the proportion of the active GTP binding form of p21ras or, its subcellular localization. These results rule out the possibility that the morphological reversion by radicicol is due to direct or indirect inhibition of the p21ras function. Cycloheximide and actinomycin D inhibited the morphological change by radicicol, suggesting that the induced transcription of a gene (s) followed by de novo protein synthesis is required for suppression of the transformed phenotype in ras-transformed cells by tyrosine kinase inhibitors.
収録刊行物
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- The journal of biochemistry
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The journal of biochemistry 118 (1), 221-228, 1995-07-01
社団法人 日本生化学会
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詳細情報 詳細情報について
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- CRID
- 1573950399121867776
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- NII論文ID
- 10005183336
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- NII書誌ID
- AA00694073
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- ISSN
- 0021924X
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- 本文言語コード
- en
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- データソース種別
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- CiNii Articles