TY  - CHAP
AU  - Lopez-Contreras, Andres Joaquin
AU  - Fernandez-Capetillo, Oscar
AU  - Joaquin, Andres
AU  - Fernandez-Capetillo, Oscar
AB  - 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.
DO  - 10.5772/50863
ID  - OAPEN ID: 612634
ID  - OAPEN ID: OCN: 1030821210
KW  - dna damage
KW  - dna damage
KW  - Apoptosis
KW  - Ataxia telangiectasia and Rad3 related
KW  - ATM serine/threonine kinase
KW  - DNA repair
KW  - DNA-PKcs
KW  - Phosphorylation
KW  - Protein
KW  - Ubiquitin
L1  - https://library.oapen.org/bitstream/id/c9788738-0c61-476c-9b21-8707a8368d92/612634.pdf
LA  - English
LK  - http://library.oapen.org/handle/20.500.12657/32323
PB  - InTechOpen
PY  - 2012
TI  - Chapter 8 Signalling DNA Damagenull
ER  - 
