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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Lopez-Contreras, Andres Joaquin [verfasserIn] |
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E-Book |
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| Sprache: |
Englisch |
| Erschienen: |
Erscheinungsort nicht ermittelbar: InTechOpen ; 2012 |
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| Rechteinformationen: |
Open Access Creative Commons ; https://creativecommons.org/licenses/by/3.0 |
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1 Online-Ressource |
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(DE-627)1836416644 (DE-599)KEP062142011 (OCoLC)1286417023 (OAPEN)32323 (EBP)062142011 DE-627 eng DE-627 rda eng PD bicssc Lopez-Contreras, Andres Joaquin verfasserin aut Chapter 8 Signalling DNA Damage [Erscheinungsort nicht ermittelbar] InTechOpen 2012 1 Online-Ressource Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Open Access Unrestricted online access star 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 Creative Commons https://creativecommons.org/licenses/by/3.0 cc English Science: general issues Fernandez-Capetillo, Oscar oth Joaquin, Andres oth Fernandez-Capetillo, Oscar oth https://library.oapen.org/bitstream/id/c9788738-0c61-476c-9b21-8707a8368d92/612634.pdf X:OAPEN Verlag OAPEN Library: download the publication kostenfrei http://library.oapen.org/handle/20.500.12657/32323 X:OAPEN Verlag OAPEN Library: description of the publication kostenfrei ZDB-94-OAL GBV_ILN_22 ISIL_DE-18 SYSFLAG_1 GBV_KXP GBV_ILN_23 ISIL_DE-830 GBV_ILN_30 ISIL_DE-104 GBV_ILN_31 ISIL_DE-27 GBV_ILN_34 ISIL_DE-18-302 GBV_ILN_39 ISIL_DE-547 GBV_ILN_40 ISIL_DE-7 GBV_ILN_63 ISIL_DE-Wim2 GBV_ILN_65 ISIL_DE-3 GBV_ILN_70 ISIL_DE-89 GBV_ILN_72 ISIL_DE-35 GBV_ILN_95 ISIL_DE-542 GBV_ILN_110 ISIL_DE-Luen4 GBV_ILN_136 ISIL_DE-Wis1 GBV_ILN_147 ISIL_DE-Fl3 GBV_ILN_161 ISIL_DE-960 GBV_ILN_187 ISIL_DE-Ki95 GBV_ILN_213 ISIL_DE-551 GBV_ILN_230 ISIL_DE-552 GBV_ILN_283 ISIL_DE-Ha163 GBV_ILN_293 ISIL_DE-960-3 GBV_ILN_370 ISIL_DE-1373 GBV_ILN_603 ISIL_DE-B1556 GBV_ILN_808 GBV_ILN_2403 ISIL_DE-LFER BO 22 01 0018 4280075441 OLR-ZDB-94-OAL OAPEN Library zu 01-03-23 23 01 0830 428062724X OLR-OAPEN f z 01-03-23 30 01 0104 4280987378 GBV-OAPEN z 01-03-23 31 01 0027 4280270163 z 01-03-23 34 01 3551 4278825714 OLR-OAPEN zi002 01-03-23 39 01 0547 428117799X GBV-OAPEN ke 01-03-23 40 01 0007 4279894213 OLR-OAPEN xsn 01-03-23 63 01 3401 4281558152 E-Books LF GBV-OAPEN z 01-03-23 65 01 0003 4281795278 OLR-OAPEN z 01-03-23 70 01 0089 4280448353 OLR-OAPEN-OA OAPEN Online Library Open Access eBook z 01-03-23 72 01 0035 4278644469 OLR-OAPEN-OA OAPEN Online Library Open Access eBook z 01-03-23 95 01 3095 4343173747 OLR-OAL Vervielfältigungen (z.B. Kopien, Downloads) sind nur von einzelnen Kapiteln oder Seiten und nur zum eigenen wissenschaftlichen Gebrauch erlaubt. Die Weitergabe an Dritte sowie systematisches Downloaden sind untersagt. z 24-06-23 110 01 3110 4281362770 OLR-GBV-OAPEN Open Access z 01-03-23 136 01 3526 4279535280 OLR-OAPEN z 01-03-23 147 01 3528 4282006226 OLR-OAPEN frei verfügbar für Europa-Universität Flensburg, Hochschule Flensburg und Zentrale Hochschulbibliothek Vervielfältigungen (z.B. Kopien, Downloads) sind nur von einzelnen Kapiteln oder Seiten und nur zum eigenen wissenschaftlichen Gebrauch erlaubt. Die Weitergabe an Dritte sowie systematisches Downloaden sind untersagt. z 01-03-23 161 01 0960 4278081871 OLR-OAPEN OAPEN Online Library Open Access eBook z 28-02-23 187 01 3520 4278466889 JSTOR Open Access eBook z 28-02-23 213 01 0551 427918089X OLR-OAPEN OAPEN Online Library Open Access eBook z 01-03-23 230 01 0552 4279358079 OLR-OAPEN OAPEN Online Library Open Access eBook z 01-03-23 283 01 3283 4279716986 OLR-OAL z 01-03-23 293 01 3293 4278261101 OLR-OAPEN OAPEN Online Library Open Access eBook z 28-02-23 370 01 4370 4279003467 OLR-FREE Kostenloser Zugriff z 01-03-23 603 01 4603 4277904041 OLR-OAPEN Bitte beachten Sie die Nutzungsbedingungen und Copyright-Bestimmungen des Verlages/Herausgebers. z 28-02-23 808 01 4808 4280806179 OLR-OAPEN OAPEN Library zg 01-03-23 2403 01 DE-LFER 4307489918 00 --%%-- --%%-- n --%%-- l01 11-04-23 22 01 0018 Volltextzugang http://library.oapen.org/handle/20.500.12657/32323 23 01 0830 http://library.oapen.org/handle/20.500.12657/32323 30 01 0104 Open Access http://library.oapen.org/handle/20.500.12657/32323 31 01 0027 eBook GBV-OAPEN http://library.oapen.org/handle/20.500.12657/32323 34 01 3551 OpenAccess http://library.oapen.org/handle/20.500.12657/32323 40 01 0007 Volltext, Open Access http://library.oapen.org/handle/20.500.12657/32323 63 01 3401 E-Book http://library.oapen.org/handle/20.500.12657/32323 65 01 0003 Open Access http://library.oapen.org/handle/20.500.12657/32323 65 01 0003 Dieser Titel ist Teil einer Datenbank http://www.bibliothek.uni-regensburg.de/dbinfo/detail.php?titel_id=10728&bib_id=ulb_hal 70 01 0089 http://library.oapen.org/handle/20.500.12657/32323 LF 72 01 0035 http://library.oapen.org/handle/20.500.12657/32323 95 01 3095 http://library.oapen.org/handle/20.500.12657/32323 110 01 3110 Open Access http://library.oapen.org/handle/20.500.12657/32323 136 01 3526 Open Access http://library.oapen.org/handle/20.500.12657/32323 147 01 3528 http://library.oapen.org/handle/20.500.12657/32323 161 01 0960 http://library.oapen.org/handle/20.500.12657/32323 LF 187 01 3520 http://library.oapen.org/handle/20.500.12657/32323 213 01 0551 http://library.oapen.org/handle/20.500.12657/32323 230 01 0552 http://library.oapen.org/handle/20.500.12657/32323 283 01 3283 http://library.oapen.org/handle/20.500.12657/32323 293 01 3293 http://library.oapen.org/handle/20.500.12657/32323 LF 370 01 4370 http://library.oapen.org/handle/20.500.12657/32323 603 01 4603 http://library.oapen.org/handle/20.500.12657/32323 808 01 4808 Volltextzugang http://library.oapen.org/handle/20.500.12657/32323 2403 01 DE-LFER https://library.oapen.org/bitstream/id/c9788738-0c61-476c-9b21-8707a8368d92/612634.pdf 31 01 0027 00 eBook GBV-OAPEN 22 01 0018 OLR-ZDB-94-OAL 23 01 0830 OLR-OAPEN 30 01 0104 GBV-OAPEN 34 01 3551 OLR-OAPEN 39 01 0547 GBV-OAPEN 39 01 0547 LF 40 01 0007 OLR-OAPEN 63 01 3401 E-Books LF GBV-OAPEN 65 01 0003 OLR-OAPEN 70 01 0089 OLR-OAPEN-OA 72 01 0035 OLR-OAPEN-OA 95 01 3095 OLR-OAL 110 01 3110 OLR-GBV-OAPEN 136 01 3526 OLR-OAPEN 147 01 3528 OLR-OAPEN 161 01 0960 OLR-OAPEN 213 01 0551 OLR-OAPEN 230 01 0552 OLR-OAPEN 283 01 3283 OLR-OAL 293 01 3293 OLR-OAPEN 370 01 4370 OLR-FREE 370 01 4370 olr-ebook GBV-OAPEN 603 01 4603 OLR-OAPEN 808 01 4808 OLR-OAPEN |
| spelling |
(DE-627)1836416644 (DE-599)KEP062142011 (OCoLC)1286417023 (OAPEN)32323 (EBP)062142011 DE-627 eng DE-627 rda eng PD bicssc Lopez-Contreras, Andres Joaquin verfasserin aut Chapter 8 Signalling DNA Damage [Erscheinungsort nicht ermittelbar] InTechOpen 2012 1 Online-Ressource Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Open Access Unrestricted online access star 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 Creative Commons https://creativecommons.org/licenses/by/3.0 cc English Science: general issues Fernandez-Capetillo, Oscar oth Joaquin, Andres oth Fernandez-Capetillo, Oscar oth https://library.oapen.org/bitstream/id/c9788738-0c61-476c-9b21-8707a8368d92/612634.pdf X:OAPEN Verlag OAPEN Library: download the publication kostenfrei http://library.oapen.org/handle/20.500.12657/32323 X:OAPEN Verlag OAPEN Library: description of the publication kostenfrei ZDB-94-OAL GBV_ILN_22 ISIL_DE-18 SYSFLAG_1 GBV_KXP GBV_ILN_23 ISIL_DE-830 GBV_ILN_30 ISIL_DE-104 GBV_ILN_31 ISIL_DE-27 GBV_ILN_34 ISIL_DE-18-302 GBV_ILN_39 ISIL_DE-547 GBV_ILN_40 ISIL_DE-7 GBV_ILN_63 ISIL_DE-Wim2 GBV_ILN_65 ISIL_DE-3 GBV_ILN_70 ISIL_DE-89 GBV_ILN_72 ISIL_DE-35 GBV_ILN_95 ISIL_DE-542 GBV_ILN_110 ISIL_DE-Luen4 GBV_ILN_136 ISIL_DE-Wis1 GBV_ILN_147 ISIL_DE-Fl3 GBV_ILN_161 ISIL_DE-960 GBV_ILN_187 ISIL_DE-Ki95 GBV_ILN_213 ISIL_DE-551 GBV_ILN_230 ISIL_DE-552 GBV_ILN_283 ISIL_DE-Ha163 GBV_ILN_293 ISIL_DE-960-3 GBV_ILN_370 ISIL_DE-1373 GBV_ILN_603 ISIL_DE-B1556 GBV_ILN_808 GBV_ILN_2403 ISIL_DE-LFER BO 22 01 0018 4280075441 OLR-ZDB-94-OAL OAPEN Library zu 01-03-23 23 01 0830 428062724X OLR-OAPEN f z 01-03-23 30 01 0104 4280987378 GBV-OAPEN z 01-03-23 31 01 0027 4280270163 z 01-03-23 34 01 3551 4278825714 OLR-OAPEN zi002 01-03-23 39 01 0547 428117799X GBV-OAPEN ke 01-03-23 40 01 0007 4279894213 OLR-OAPEN xsn 01-03-23 63 01 3401 4281558152 E-Books LF GBV-OAPEN z 01-03-23 65 01 0003 4281795278 OLR-OAPEN z 01-03-23 70 01 0089 4280448353 OLR-OAPEN-OA OAPEN Online Library Open Access eBook z 01-03-23 72 01 0035 4278644469 OLR-OAPEN-OA OAPEN Online Library Open Access eBook z 01-03-23 95 01 3095 4343173747 OLR-OAL Vervielfältigungen (z.B. Kopien, Downloads) sind nur von einzelnen Kapiteln oder Seiten und nur zum eigenen wissenschaftlichen Gebrauch erlaubt. Die Weitergabe an Dritte sowie systematisches Downloaden sind untersagt. z 24-06-23 110 01 3110 4281362770 OLR-GBV-OAPEN Open Access z 01-03-23 136 01 3526 4279535280 OLR-OAPEN z 01-03-23 147 01 3528 4282006226 OLR-OAPEN frei verfügbar für Europa-Universität Flensburg, Hochschule Flensburg und Zentrale Hochschulbibliothek Vervielfältigungen (z.B. Kopien, Downloads) sind nur von einzelnen Kapiteln oder Seiten und nur zum eigenen wissenschaftlichen Gebrauch erlaubt. Die Weitergabe an Dritte sowie systematisches Downloaden sind untersagt. z 01-03-23 161 01 0960 4278081871 OLR-OAPEN OAPEN Online Library Open Access eBook z 28-02-23 187 01 3520 4278466889 JSTOR Open Access eBook z 28-02-23 213 01 0551 427918089X OLR-OAPEN OAPEN Online Library Open Access eBook z 01-03-23 230 01 0552 4279358079 OLR-OAPEN OAPEN Online Library Open Access eBook z 01-03-23 283 01 3283 4279716986 OLR-OAL z 01-03-23 293 01 3293 4278261101 OLR-OAPEN OAPEN Online Library Open Access eBook z 28-02-23 370 01 4370 4279003467 OLR-FREE Kostenloser Zugriff z 01-03-23 603 01 4603 4277904041 OLR-OAPEN Bitte beachten Sie die Nutzungsbedingungen und Copyright-Bestimmungen des Verlages/Herausgebers. z 28-02-23 808 01 4808 4280806179 OLR-OAPEN OAPEN Library zg 01-03-23 2403 01 DE-LFER 4307489918 00 --%%-- --%%-- n --%%-- l01 11-04-23 22 01 0018 Volltextzugang http://library.oapen.org/handle/20.500.12657/32323 23 01 0830 http://library.oapen.org/handle/20.500.12657/32323 30 01 0104 Open Access http://library.oapen.org/handle/20.500.12657/32323 31 01 0027 eBook GBV-OAPEN http://library.oapen.org/handle/20.500.12657/32323 34 01 3551 OpenAccess http://library.oapen.org/handle/20.500.12657/32323 40 01 0007 Volltext, Open Access http://library.oapen.org/handle/20.500.12657/32323 63 01 3401 E-Book http://library.oapen.org/handle/20.500.12657/32323 65 01 0003 Open Access http://library.oapen.org/handle/20.500.12657/32323 65 01 0003 Dieser Titel ist Teil einer Datenbank http://www.bibliothek.uni-regensburg.de/dbinfo/detail.php?titel_id=10728&bib_id=ulb_hal 70 01 0089 http://library.oapen.org/handle/20.500.12657/32323 LF 72 01 0035 http://library.oapen.org/handle/20.500.12657/32323 95 01 3095 http://library.oapen.org/handle/20.500.12657/32323 110 01 3110 Open Access http://library.oapen.org/handle/20.500.12657/32323 136 01 3526 Open Access http://library.oapen.org/handle/20.500.12657/32323 147 01 3528 http://library.oapen.org/handle/20.500.12657/32323 161 01 0960 http://library.oapen.org/handle/20.500.12657/32323 LF 187 01 3520 http://library.oapen.org/handle/20.500.12657/32323 213 01 0551 http://library.oapen.org/handle/20.500.12657/32323 230 01 0552 http://library.oapen.org/handle/20.500.12657/32323 283 01 3283 http://library.oapen.org/handle/20.500.12657/32323 293 01 3293 http://library.oapen.org/handle/20.500.12657/32323 LF 370 01 4370 http://library.oapen.org/handle/20.500.12657/32323 603 01 4603 http://library.oapen.org/handle/20.500.12657/32323 808 01 4808 Volltextzugang http://library.oapen.org/handle/20.500.12657/32323 2403 01 DE-LFER https://library.oapen.org/bitstream/id/c9788738-0c61-476c-9b21-8707a8368d92/612634.pdf 31 01 0027 00 eBook GBV-OAPEN 22 01 0018 OLR-ZDB-94-OAL 23 01 0830 OLR-OAPEN 30 01 0104 GBV-OAPEN 34 01 3551 OLR-OAPEN 39 01 0547 GBV-OAPEN 39 01 0547 LF 40 01 0007 OLR-OAPEN 63 01 3401 E-Books LF GBV-OAPEN 65 01 0003 OLR-OAPEN 70 01 0089 OLR-OAPEN-OA 72 01 0035 OLR-OAPEN-OA 95 01 3095 OLR-OAL 110 01 3110 OLR-GBV-OAPEN 136 01 3526 OLR-OAPEN 147 01 3528 OLR-OAPEN 161 01 0960 OLR-OAPEN 213 01 0551 OLR-OAPEN 230 01 0552 OLR-OAPEN 283 01 3283 OLR-OAL 293 01 3293 OLR-OAPEN 370 01 4370 OLR-FREE 370 01 4370 olr-ebook GBV-OAPEN 603 01 4603 OLR-OAPEN 808 01 4808 OLR-OAPEN |
| allfields_unstemmed |
(DE-627)1836416644 (DE-599)KEP062142011 (OCoLC)1286417023 (OAPEN)32323 (EBP)062142011 DE-627 eng DE-627 rda eng PD bicssc Lopez-Contreras, Andres Joaquin verfasserin aut Chapter 8 Signalling DNA Damage [Erscheinungsort nicht ermittelbar] InTechOpen 2012 1 Online-Ressource Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Open Access Unrestricted online access star 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 Creative Commons https://creativecommons.org/licenses/by/3.0 cc English Science: general issues Fernandez-Capetillo, Oscar oth Joaquin, Andres oth Fernandez-Capetillo, Oscar oth https://library.oapen.org/bitstream/id/c9788738-0c61-476c-9b21-8707a8368d92/612634.pdf X:OAPEN Verlag OAPEN Library: download the publication kostenfrei http://library.oapen.org/handle/20.500.12657/32323 X:OAPEN Verlag OAPEN Library: description of the publication kostenfrei ZDB-94-OAL GBV_ILN_22 ISIL_DE-18 SYSFLAG_1 GBV_KXP GBV_ILN_23 ISIL_DE-830 GBV_ILN_30 ISIL_DE-104 GBV_ILN_31 ISIL_DE-27 GBV_ILN_34 ISIL_DE-18-302 GBV_ILN_39 ISIL_DE-547 GBV_ILN_40 ISIL_DE-7 GBV_ILN_63 ISIL_DE-Wim2 GBV_ILN_65 ISIL_DE-3 GBV_ILN_70 ISIL_DE-89 GBV_ILN_72 ISIL_DE-35 GBV_ILN_95 ISIL_DE-542 GBV_ILN_110 ISIL_DE-Luen4 GBV_ILN_136 ISIL_DE-Wis1 GBV_ILN_147 ISIL_DE-Fl3 GBV_ILN_161 ISIL_DE-960 GBV_ILN_187 ISIL_DE-Ki95 GBV_ILN_213 ISIL_DE-551 GBV_ILN_230 ISIL_DE-552 GBV_ILN_283 ISIL_DE-Ha163 GBV_ILN_293 ISIL_DE-960-3 GBV_ILN_370 ISIL_DE-1373 GBV_ILN_603 ISIL_DE-B1556 GBV_ILN_808 GBV_ILN_2403 ISIL_DE-LFER BO 22 01 0018 4280075441 OLR-ZDB-94-OAL OAPEN Library zu 01-03-23 23 01 0830 428062724X OLR-OAPEN f z 01-03-23 30 01 0104 4280987378 GBV-OAPEN z 01-03-23 31 01 0027 4280270163 z 01-03-23 34 01 3551 4278825714 OLR-OAPEN zi002 01-03-23 39 01 0547 428117799X GBV-OAPEN ke 01-03-23 40 01 0007 4279894213 OLR-OAPEN xsn 01-03-23 63 01 3401 4281558152 E-Books LF GBV-OAPEN z 01-03-23 65 01 0003 4281795278 OLR-OAPEN z 01-03-23 70 01 0089 4280448353 OLR-OAPEN-OA OAPEN Online Library Open Access eBook z 01-03-23 72 01 0035 4278644469 OLR-OAPEN-OA OAPEN Online Library Open Access eBook z 01-03-23 95 01 3095 4343173747 OLR-OAL Vervielfältigungen (z.B. Kopien, Downloads) sind nur von einzelnen Kapiteln oder Seiten und nur zum eigenen wissenschaftlichen Gebrauch erlaubt. Die Weitergabe an Dritte sowie systematisches Downloaden sind untersagt. z 24-06-23 110 01 3110 4281362770 OLR-GBV-OAPEN Open Access z 01-03-23 136 01 3526 4279535280 OLR-OAPEN z 01-03-23 147 01 3528 4282006226 OLR-OAPEN frei verfügbar für Europa-Universität Flensburg, Hochschule Flensburg und Zentrale Hochschulbibliothek Vervielfältigungen (z.B. Kopien, Downloads) sind nur von einzelnen Kapiteln oder Seiten und nur zum eigenen wissenschaftlichen Gebrauch erlaubt. Die Weitergabe an Dritte sowie systematisches Downloaden sind untersagt. z 01-03-23 161 01 0960 4278081871 OLR-OAPEN OAPEN Online Library Open Access eBook z 28-02-23 187 01 3520 4278466889 JSTOR Open Access eBook z 28-02-23 213 01 0551 427918089X OLR-OAPEN OAPEN Online Library Open Access eBook z 01-03-23 230 01 0552 4279358079 OLR-OAPEN OAPEN Online Library Open Access eBook z 01-03-23 283 01 3283 4279716986 OLR-OAL z 01-03-23 293 01 3293 4278261101 OLR-OAPEN OAPEN Online Library Open Access eBook z 28-02-23 370 01 4370 4279003467 OLR-FREE Kostenloser Zugriff z 01-03-23 603 01 4603 4277904041 OLR-OAPEN Bitte beachten Sie die Nutzungsbedingungen und Copyright-Bestimmungen des Verlages/Herausgebers. z 28-02-23 808 01 4808 4280806179 OLR-OAPEN OAPEN Library zg 01-03-23 2403 01 DE-LFER 4307489918 00 --%%-- --%%-- n --%%-- l01 11-04-23 22 01 0018 Volltextzugang http://library.oapen.org/handle/20.500.12657/32323 23 01 0830 http://library.oapen.org/handle/20.500.12657/32323 30 01 0104 Open Access http://library.oapen.org/handle/20.500.12657/32323 31 01 0027 eBook GBV-OAPEN http://library.oapen.org/handle/20.500.12657/32323 34 01 3551 OpenAccess http://library.oapen.org/handle/20.500.12657/32323 40 01 0007 Volltext, Open Access http://library.oapen.org/handle/20.500.12657/32323 63 01 3401 E-Book http://library.oapen.org/handle/20.500.12657/32323 65 01 0003 Open Access http://library.oapen.org/handle/20.500.12657/32323 65 01 0003 Dieser Titel ist Teil einer Datenbank http://www.bibliothek.uni-regensburg.de/dbinfo/detail.php?titel_id=10728&bib_id=ulb_hal 70 01 0089 http://library.oapen.org/handle/20.500.12657/32323 LF 72 01 0035 http://library.oapen.org/handle/20.500.12657/32323 95 01 3095 http://library.oapen.org/handle/20.500.12657/32323 110 01 3110 Open Access http://library.oapen.org/handle/20.500.12657/32323 136 01 3526 Open Access http://library.oapen.org/handle/20.500.12657/32323 147 01 3528 http://library.oapen.org/handle/20.500.12657/32323 161 01 0960 http://library.oapen.org/handle/20.500.12657/32323 LF 187 01 3520 http://library.oapen.org/handle/20.500.12657/32323 213 01 0551 http://library.oapen.org/handle/20.500.12657/32323 230 01 0552 http://library.oapen.org/handle/20.500.12657/32323 283 01 3283 http://library.oapen.org/handle/20.500.12657/32323 293 01 3293 http://library.oapen.org/handle/20.500.12657/32323 LF 370 01 4370 http://library.oapen.org/handle/20.500.12657/32323 603 01 4603 http://library.oapen.org/handle/20.500.12657/32323 808 01 4808 Volltextzugang http://library.oapen.org/handle/20.500.12657/32323 2403 01 DE-LFER https://library.oapen.org/bitstream/id/c9788738-0c61-476c-9b21-8707a8368d92/612634.pdf 31 01 0027 00 eBook GBV-OAPEN 22 01 0018 OLR-ZDB-94-OAL 23 01 0830 OLR-OAPEN 30 01 0104 GBV-OAPEN 34 01 3551 OLR-OAPEN 39 01 0547 GBV-OAPEN 39 01 0547 LF 40 01 0007 OLR-OAPEN 63 01 3401 E-Books LF GBV-OAPEN 65 01 0003 OLR-OAPEN 70 01 0089 OLR-OAPEN-OA 72 01 0035 OLR-OAPEN-OA 95 01 3095 OLR-OAL 110 01 3110 OLR-GBV-OAPEN 136 01 3526 OLR-OAPEN 147 01 3528 OLR-OAPEN 161 01 0960 OLR-OAPEN 213 01 0551 OLR-OAPEN 230 01 0552 OLR-OAPEN 283 01 3283 OLR-OAL 293 01 3293 OLR-OAPEN 370 01 4370 OLR-FREE 370 01 4370 olr-ebook GBV-OAPEN 603 01 4603 OLR-OAPEN 808 01 4808 OLR-OAPEN |
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(DE-627)1836416644 (DE-599)KEP062142011 (OCoLC)1286417023 (OAPEN)32323 (EBP)062142011 DE-627 eng DE-627 rda eng PD bicssc Lopez-Contreras, Andres Joaquin verfasserin aut Chapter 8 Signalling DNA Damage [Erscheinungsort nicht ermittelbar] InTechOpen 2012 1 Online-Ressource Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Open Access Unrestricted online access star 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. 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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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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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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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| score |
7.169321 |