Caspase-dependent apoptosis by ectopic expression of E2F-4
| Autor: | Nicholas H. Heintz, Sharon Illenye, Young-Chae Chang, Yun-Sik Lee, Kiyoshi Sawai, Hiroo Nakajima, Ikuya Fujiwara, Nobuko Honjo, Junji Magae, Kaname Saida, Tazuko Makiyama, Youji Mitsui, Naruhiko Mizuta |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
DNA Replication
Transcriptional Activation Cancer Research Recombinant Fusion Proteins E2F6 Transcription Factor Apoptosis Cell Cycle Proteins CHO Cells E2F4 Transcription Factor Biology Transfection Caspase-Dependent Apoptosis Cricetulus Cricetinae Genetics Animals Promoter Regions Genetic E2F Molecular Biology Transcription factor Chinese hamster ovary cell Cell Cycle E2F1 Transcription Factor Tetracycline Cell cycle Molecular biology E2F Transcription Factors Cell biology DNA-Binding Proteins stomatognathic diseases Gene Expression Regulation Caspases Ectopic expression biological phenomena cell phenomena and immunity Carrier Proteins Retinoblastoma-Binding Protein 1 Transcription Factors |
| Zdroj: | Oncogene. 19:4713-4720 |
| ISSN: | 1476-5594 0950-9232 |
| Popis: | E2F is a family of transcription factors which regulates cell cycle and apoptosis of mammalian cells. E2F-1-3 localize in the nucleus, and preferentially bind pRb, while E2F-4 and 5 have no nuclear localization signal and preferentially bind p107/p130. E2F-6 suppresses the transcriptional activity of other E2F proteins. DP-1 and 2 are heterodimeric partners of each E2F protein. Using tetracycline-responsive promoters, here we compared the effects of ectopic expression of E2F-1, DP-1 and E2F-4 on cell cycle progression and apoptosis in Chinese hamster cell lines. We found that E2F-4, as well as DP-1 and E2F-1, induced growth arrest and caspase-dependent apoptosis. E2F-4 did not have a marked effect on cell cycle progression, while E2F-1 induced DNA synthesis of resting cells and DP-1 arrested cells in G1. Ectopic expression of E2F-4 did not activate E2F-dependent transcription. Our results suggest that expression of E2F-4 at elevated levels induces growth arrest and apoptosis of mammalian cells through a mechanism distinct from E2F-1 and DP-1. |
| Databáze: | OpenAIRE |
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