Defying death after DNA damage
DNA damage frequently triggers death by apoptosis. The irreversible decision to die can be facilitated or forestalled through integration of a wide variety of stimuli from within and around the cell. Here we address some fundamental questions that arise from this model. Why should DNA damage initiat...
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| Veröffentlicht in: | Nature (London) 2000-10, Vol.407 (6805), p.777-783 |
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| creator | Rich, Tina Allen, Rachel L. Wyllie, Andrew H. |
| description | DNA damage frequently triggers death by apoptosis. The irreversible decision to die can be facilitated or forestalled through integration of a wide variety of stimuli from within and around the cell. Here we address some fundamental questions that arise from this model. Why should DNA damage initiate apoptosis in the first place? In damaged cells, what are the alternatives to death and why should they be selected in some circumstances but not others? What signals register DNA damage and how do they impinge on the effector pathways of apoptosis? Is there a suborganellar apoptosome complex effecting the integration of death signals within the nucleus, just as there is in the cytoplasm? And what are the consequences of failure to initiate apoptosis in response to DNA damage? |
| doi_str_mv | 10.1038/35037717 |
| format | Article |
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The irreversible decision to die can be facilitated or forestalled through integration of a wide variety of stimuli from within and around the cell. Here we address some fundamental questions that arise from this model. Why should DNA damage initiate apoptosis in the first place? In damaged cells, what are the alternatives to death and why should they be selected in some circumstances but not others? What signals register DNA damage and how do they impinge on the effector pathways of apoptosis? Is there a suborganellar apoptosome complex effecting the integration of death signals within the nucleus, just as there is in the cytoplasm? And what are the consequences of failure to initiate apoptosis in response to DNA damage?</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>DOI: 10.1038/35037717</identifier><identifier>PMID: 11048728</identifier><identifier>CODEN: NATUAS</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Apoptosis ; Ataxia Telangiectasia Mutated Proteins ; Carrier Proteins ; Cell Cycle Proteins ; Cells ; Cellular biology ; Deoxyribonucleic acid ; DNA ; DNA Damage ; DNA-Binding Proteins ; E2F Transcription Factors ; Forecasting ; Humanities and Social Sciences ; Humans ; Mortality ; multidisciplinary ; Protein-Serine-Threonine Kinases - physiology ; Proto-Oncogene Proteins c-abl - physiology ; Retinoblastoma-Binding Protein 1 ; review-article ; Science ; Science (multidisciplinary) ; Transcription Factor DP1 ; Transcription Factors - physiology ; Tumor Suppressor Protein p53 - physiology ; Tumor Suppressor Proteins</subject><ispartof>Nature (London), 2000-10, Vol.407 (6805), p.777-783</ispartof><rights>Macmillan Magazines Ltd. 2000</rights><rights>COPYRIGHT 2000 Nature Publishing Group</rights><rights>Copyright Macmillan Journals Ltd. 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The irreversible decision to die can be facilitated or forestalled through integration of a wide variety of stimuli from within and around the cell. Here we address some fundamental questions that arise from this model. Why should DNA damage initiate apoptosis in the first place? In damaged cells, what are the alternatives to death and why should they be selected in some circumstances but not others? What signals register DNA damage and how do they impinge on the effector pathways of apoptosis? Is there a suborganellar apoptosome complex effecting the integration of death signals within the nucleus, just as there is in the cytoplasm? 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| subjects | Animals Apoptosis Ataxia Telangiectasia Mutated Proteins Carrier Proteins Cell Cycle Proteins Cells Cellular biology Deoxyribonucleic acid DNA DNA Damage DNA-Binding Proteins E2F Transcription Factors Forecasting Humanities and Social Sciences Humans Mortality multidisciplinary Protein-Serine-Threonine Kinases - physiology Proto-Oncogene Proteins c-abl - physiology Retinoblastoma-Binding Protein 1 review-article Science Science (multidisciplinary) Transcription Factor DP1 Transcription Factors - physiology Tumor Suppressor Protein p53 - physiology Tumor Suppressor Proteins |
| title | Defying death after DNA damage |
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