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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Zhu, Zhiyi Lopez, Charles D. Chen, Dexi Yu, Zhiyong |
| Description | Author Affiliation: Chen D ( Department of Medicine, Division of Hematology and Medical Oncology, Oregon Health and Science University, 3181 S.W. Sam Jackson Park Road, Portland, OR 97239, USA.) |
| Abstract | The E2F1 transcription factor activates S-phase-promoting genes, mediates apoptosis, and stimulates DNA repair through incompletely understood mechanisms. XRCC1 (x-ray repair cross-complementing group 1) protein is important for efficient single strand break/base excision repair. Although both damage and proliferative signals increase XRCC1 levels, the mechanisms regulating XRCC1 transcription remain unclear. To study these upstream mechanisms, the XRCC1 promoter was cloned into a luciferase reporter. Ectopic expression of wild-type E2F1, but not an inactive mutant E2F1(132E), activated the XRCC1 promoter-luciferase reporter, and deletion of predicted E2F1 binding sites in the promoter attenuated E2F1-induced activation. Endogenous XRCC1 expression increased in cells conditionally expressing wild-type, but not mutant E2F1, and methyl methanesulfonate-induced DNA damage stimulated XRCC1 expression in E2F1(+/+) but not E2F1(-/-) mouse embryo fibroblasts (MEFs). Additionally, E2F1(-/-) MEFs displayed attenuated DNA repair after methyl methanesulfonate-induced damage compared with E2F1(+/+) MEFs. Moreover, Chinese hamster ovary cells with mutant XRCC1 (EM9) were more sensitive to E2F1-induced apoptosis compared with Chinese hamster ovary cells with wild-type XRCC1 (AA8). These results provide new mechanistic insight into the role of the E2F pathway in maintaining genomic stability. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 22 |
| Volume Number | 283 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2008-05-30 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | DNA Repair Physiology DNA-Binding Proteins Metabolism E2F1 Transcription Factor Fibroblasts Response Elements S Phase Animals Apoptosis Drug Effects Genetics CHO Cells Cell Line Cricetinae Cricetulus Embryo, Mammalian Cytology Genomic Instability Mesylates Pharmacology Mice Sequence Deletion Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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