Lymphoid Cells Transformed by Abelson Virus Require the v-abl Protein- Tyrosine Kinase Only During Early G<sub>1</sub>
Cells infected with temperature-sensitive transformation mutants of the Abelson murine leukemia virus express low levels of kinase activity at the nonpermissive temperature, causing transformed pre-B cells to die under these conditions. Examination of cell cycle profiles of such populations prior to...
| Veröffentlicht in: | Proceedings of the National Academy of Sciences of the United States of America. - National Academy of Sciences of the United States of America. - 89(1992), 15, Seite 6683-6687 |
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| Format: | Online-Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
1992
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| Zugriff auf das übergeordnete Werk: | Proceedings of the National Academy of Sciences of the United States of America |
| Schlagworte: | Genetics Apoptosis Transformation v-abl Oncogene Cell Cycle Biological sciences Physical sciences Health sciences |
| Zusammenfassung: | Cells infected with temperature-sensitive transformation mutants of the Abelson murine leukemia virus express low levels of kinase activity at the nonpermissive temperature, causing transformed pre-B cells to die under these conditions. Examination of cell cycle profiles of such populations prior to cell death reveals that the cells accumulate in the G<sub>1</sub> phase of the cell cycle. Following G<sub>1</sub> arrest, the cells die via apoptosis, an active process of cell elimination. Cell synchronization and temperature-shift experiments show that G<sub>1</sub> arrest reflects the requirement for a functional v-abl protein during early G<sub>1</sub> and that the molecule is not required at other phases of the cell cycle. These data indicate that the substrate(s) critical to v-abl-mediated transformation is involved in regulating G<sub>1</sub> transit and that these interactions are dominant over all other changes required for the multistep process that results in the fully malignant phenotype associated with v-abl expression in lymphoid cells. |
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| ISSN: | 10916490 |