Chapter 8 Signalling DNA Damage
During our lifetime, the genome is constantly being exposed to different types of damage caused either by exogenous sources (radiations and/or genotoxic compound) but also as byproducts of endogenous processes (reactive oxigen species during respiration, stalled forks during replication, eroded telo...
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InTechOpen
2021
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| Acceso en línea: | 612634 |
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| author | Lopez-Contreras, Andres Joaquin Fernandez-Capetillo, Oscar Joaquin, Andres Fernandez-Capetillo, Oscar |
| author_browse | Fernandez-Capetillo, Oscar Joaquin, Andres Lopez-Contreras, Andres Joaquin |
| author_facet | Lopez-Contreras, Andres Joaquin Fernandez-Capetillo, Oscar Joaquin, Andres Fernandez-Capetillo, Oscar |
| author_sort | Lopez-Contreras, Andres Joaquin |
| collection | Directory of Open Access Books |
| description | During our lifetime, the genome is constantly being exposed to different types of damage caused either by exogenous sources (radiations and/or genotoxic compound) but also as byproducts of endogenous processes (reactive oxigen species during respiration, stalled forks during replication, eroded telomeres, etc). From a structural point of view, there are many types of DNA damage including single or double strand breaks, base modifications and losses or base-pair mismatches. The amount of lesions that we face is enormous with estimates suggesting that each of our 1013 cells has to deal with around 10.000 lesions per day [1]. While the majority of these events are properly resolved by specialized mechanisms, a deficient response to DNA damage, and particularly to DSB, harbors a serious threat to human health [2].
DSB can be formed [1] following an exposure to ionizing radiation (X- or γ-rays) or clastogenic drugs; [2] endogenously, during DNA replication, or [3], as a consequence of reactive oxygen species (ROS) generated during oxidative metabolism. In addition, programmed DSB are used as repair intermediates during V(D)J and Class-Switch recombination (CSR) in lymphocytes [3], or during meiotic recombination [4]. Because of this, immunodeficiency and/or sterility problems are frequently associated with DDR-related pathologies. |
| format | Online |
| id | doab-20.500.12854ir-33854 |
| institution | Directory of Open Access Books |
| language | eng |
| publishDate | 2021 |
| publishDateRange | 2021 |
| publishDateSort | 2021 |
| publisher | InTechOpen |
| publisherStr | InTechOpen |
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| spelling | doab-20.500.12854ir-338542025-05-08T11:27:18Z Chapter 8 Signalling DNA Damage Lopez-Contreras, Andres Joaquin Fernandez-Capetillo, Oscar Joaquin, Andres Fernandez-Capetillo, Oscar dna damage dna damage Apoptosis Ataxia telangiectasia and Rad3 related ATM serine/threonine kinase DNA repair DNA-PKcs Phosphorylation Protein Ubiquitin During our lifetime, the genome is constantly being exposed to different types of damage caused either by exogenous sources (radiations and/or genotoxic compound) but also as byproducts of endogenous processes (reactive oxigen species during respiration, stalled forks during replication, eroded telomeres, etc). From a structural point of view, there are many types of DNA damage including single or double strand breaks, base modifications and losses or base-pair mismatches. The amount of lesions that we face is enormous with estimates suggesting that each of our 1013 cells has to deal with around 10.000 lesions per day [1]. While the majority of these events are properly resolved by specialized mechanisms, a deficient response to DNA damage, and particularly to DSB, harbors a serious threat to human health [2]. DSB can be formed [1] following an exposure to ionizing radiation (X- or γ-rays) or clastogenic drugs; [2] endogenously, during DNA replication, or [3], as a consequence of reactive oxygen species (ROS) generated during oxidative metabolism. In addition, programmed DSB are used as repair intermediates during V(D)J and Class-Switch recombination (CSR) in lymphocytes [3], or during meiotic recombination [4]. Because of this, immunodeficiency and/or sterility problems are frequently associated with DDR-related pathologies. 2021-02-10T12:58:18Z 2019-10-04 14:39:07 2020-04-01T14:06:36Z 2016-08-01 23:55 2019-10-04 14:39:07 2020-04-01T14:06:36Z 2016-12-31 23:55:55 2019-10-04 14:39:07 2020-04-01T14:06:36Z 2012 chapter 612634 OCN: 1030821210 http://library.oapen.org/handle/20.500.12657/32323 https://directory.doabooks.org/handle/20.500.12854/33854 eng open access image/jpeg image/jpeg image/jpeg image/jpeg image/jpeg n/a n/a n/a n/a n/a https://library.oapen.org/bitstream/20.500.12657/32323/1/612634.pdf https://library.oapen.org/bitstream/20.500.12657/32323/1/612634.pdf https://library.oapen.org/bitstream/20.500.12657/32323/1/612634.pdf https://library.oapen.org/bitstream/20.500.12657/32323/1/612634.pdf https://library.oapen.org/bitstream/20.500.12657/32323/1/612634.pdf InTechOpen 10.5772/50863 10.5772/50863 035ecc65-6737-43cf-a13a-6bdf67ce01f4 Protein Phosphorylation in Human Health FP7 Ideas: European Research Council 7292b17b-f01a-4016-94d3-d7fb5ef9fb79 European Research Council (ERC) EU collection 210520 FP7 open access |
| spellingShingle | dna damage dna damage Apoptosis Ataxia telangiectasia and Rad3 related ATM serine/threonine kinase DNA repair DNA-PKcs Phosphorylation Protein Ubiquitin Lopez-Contreras, Andres Joaquin Fernandez-Capetillo, Oscar Joaquin, Andres Fernandez-Capetillo, Oscar Chapter 8 Signalling DNA Damage |
| title | Chapter 8 Signalling DNA Damage |
| title_full | Chapter 8 Signalling DNA Damage |
| title_fullStr | Chapter 8 Signalling DNA Damage |
| title_full_unstemmed | Chapter 8 Signalling DNA Damage |
| title_short | Chapter 8 Signalling DNA Damage |
| title_sort | chapter 8 signalling dna damage |
| topic | dna damage dna damage Apoptosis Ataxia telangiectasia and Rad3 related ATM serine/threonine kinase DNA repair DNA-PKcs Phosphorylation Protein Ubiquitin |
| topic_facet | dna damage dna damage Apoptosis Ataxia telangiectasia and Rad3 related ATM serine/threonine kinase DNA repair DNA-PKcs Phosphorylation Protein Ubiquitin |
| url | 612634 |
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