H2AX Phosphorylation: Its Role in DNA Damage Response and Cancer Therapy
Double-strand breaks (DSBs) are the most deleterious DNA lesions, which, if left unrepaired, may have severe consequences for cell survival, as they lead to chromosome aberrations, genomic instability, or cell death. Various physical, chemical, and biological factors are involved in DSB induction....
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| Format: | Article |
| Language: | English |
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Wiley
2010-01-01
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| Series: | Journal of Nucleic Acids |
| Online Access: | http://dx.doi.org/10.4061/2010/920161 |
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| _version_ | 1832565395944374272 |
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| author | Monika Podhorecka Andrzej Skladanowski Przemyslaw Bozko |
| author_facet | Monika Podhorecka Andrzej Skladanowski Przemyslaw Bozko |
| author_sort | Monika Podhorecka |
| collection | DOAJ |
| description | Double-strand breaks (DSBs) are the most deleterious DNA lesions, which, if left unrepaired, may have severe consequences for cell survival, as they lead to chromosome aberrations, genomic instability, or cell death. Various physical, chemical, and biological factors are involved in DSB induction. Cells respond to DNA damage by activating the so-called DNA damage response (DDR), a complex molecular mechanism developed to detect and repair DNA damage. The formation of DSBs triggers activation of many factors, including phosphorylation of the histone variant H2AX, producing γH2AX. Phosphorylation of H2AX plays a key role in DDR and is required for the assembly of DNA repair proteins at the sites containing damaged chromatin as well as for activation of checkpoints proteins which arrest the cell cycle progression. In general, analysis of γH2AX expression can be used to detect the genotoxic effect of different toxic substances. When applied to clinical samples from cancer patients, evaluation of γH2AX levels may allow not only to monitor the efficiency of anticancer treatment but also to predict of tumor cell sensitivity to DNA damaging anticancer agents and toxicity of anticancer treatment toward normal cells. |
| format | Article |
| id | doaj-art-8a38a3f830eb48ccaa450481dd63e123 |
| institution | Kabale University |
| issn | 2090-021X |
| language | English |
| publishDate | 2010-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Nucleic Acids |
| spelling | doaj-art-8a38a3f830eb48ccaa450481dd63e1232025-02-03T01:07:50ZengWileyJournal of Nucleic Acids2090-021X2010-01-01201010.4061/2010/920161920161H2AX Phosphorylation: Its Role in DNA Damage Response and Cancer TherapyMonika Podhorecka0Andrzej Skladanowski1Przemyslaw Bozko2Department of Haematooncology and Bone Marrow Transplantation, Medical University of Lublin, 20081 Lublin, PolandLaboratory of Molecular and Cellular Pharmacology, Department of Pharmaceutical Technology and Biochemistry, Gdansk University of Technology, 80233 Gdansk, PolandInstitute of Experimental Internal Medicine, Medical Faculty, Otto von Guericke University, 39120 Magdeburg, GermanyDouble-strand breaks (DSBs) are the most deleterious DNA lesions, which, if left unrepaired, may have severe consequences for cell survival, as they lead to chromosome aberrations, genomic instability, or cell death. Various physical, chemical, and biological factors are involved in DSB induction. Cells respond to DNA damage by activating the so-called DNA damage response (DDR), a complex molecular mechanism developed to detect and repair DNA damage. The formation of DSBs triggers activation of many factors, including phosphorylation of the histone variant H2AX, producing γH2AX. Phosphorylation of H2AX plays a key role in DDR and is required for the assembly of DNA repair proteins at the sites containing damaged chromatin as well as for activation of checkpoints proteins which arrest the cell cycle progression. In general, analysis of γH2AX expression can be used to detect the genotoxic effect of different toxic substances. When applied to clinical samples from cancer patients, evaluation of γH2AX levels may allow not only to monitor the efficiency of anticancer treatment but also to predict of tumor cell sensitivity to DNA damaging anticancer agents and toxicity of anticancer treatment toward normal cells.http://dx.doi.org/10.4061/2010/920161 |
| spellingShingle | Monika Podhorecka Andrzej Skladanowski Przemyslaw Bozko H2AX Phosphorylation: Its Role in DNA Damage Response and Cancer Therapy Journal of Nucleic Acids |
| title | H2AX Phosphorylation: Its Role in DNA Damage Response and Cancer Therapy |
| title_full | H2AX Phosphorylation: Its Role in DNA Damage Response and Cancer Therapy |
| title_fullStr | H2AX Phosphorylation: Its Role in DNA Damage Response and Cancer Therapy |
| title_full_unstemmed | H2AX Phosphorylation: Its Role in DNA Damage Response and Cancer Therapy |
| title_short | H2AX Phosphorylation: Its Role in DNA Damage Response and Cancer Therapy |
| title_sort | h2ax phosphorylation its role in dna damage response and cancer therapy |
| url | http://dx.doi.org/10.4061/2010/920161 |
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