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oapen-20.500.12657-323232021-11-12T16:25:00Z 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 bic Book Industry Communication::P Mathematics & science::PD Science: general issues 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. 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 2020-04-01T14:06:36Z 2012 chapter 612634 OCN: 1030821210 http://library.oapen.org/handle/20.500.12657/32323 eng application/pdf n/a 612634.pdf InTechOpen Protein Phosphorylation in Human Health 10.5772/50863 10.5772/50863 09f6769d-48ed-467d-b150-4cf2680656a1 3fcc457e-7b5b-42bf-8b8b-00f21d1da8d3 7292b17b-f01a-4016-94d3-d7fb5ef9fb79 European Research Council (ERC) 1 210520 FP7 FP7 Ideas: European Research Council FP7-IDEAS-ERC - Specific Programme: "Ideas" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013) open access
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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.
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