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A platform for research: civil engineering, architecture and urbanism
Functions of the MRE11-RAD50-NBS1 complex in DNA double strand break repair ; Funktionen des MRE11-RAD50-NBS1 Komplexes in der DNA-Doppelstrangbruchreparatur
In a living organism maintenance of genomic stability and integrity is of extreme importance. Thus, any chemical change in the cellular deoxyribonucleic acid (DNA) molecule is considered as damage. Among various forms of DNA damage the DNA double stand break (DSB) is the most deleterious DNA lesion, since if misrepaired or left unrepaired it can cause loss or rearrangement of genetic material. This can lead to permanent cell cycle arrest, apoptosis, mutations, genomic instability and with that to a variety of diseases ranging from genetic disorders, chronic diseases, cancer and accelerated ageing (Ward 1988; Olive 1998; Khanna and Jackson 2001; van Gent, Hoeijmakers et al. 2001; d'Adda di Fagagna, Reaper et al. 2003). To deal with these assaults, cells have evolved sophisticated mechanisms to efficiently detect, signal and repair DNA damage and thus to maintain genomic integrity (Shiloh and Lehmann 2004). Eukaryotic cells have at least two pathways to repair DSBs: (1) non-homologous end-joining (NHEJ) and (2) homologous recombination repair (HRR) (Kanaar, Hoeijmakers et al. 1998; Pardo, Gómez-González et al. 2009). In addition, an extensive signaling network, comprising several different proteins, recognizes DSBs and coordinates repair pathways with cellular checkpoint responses, commonly summarized under the term – DNA damage response (DDR). In summary, our results confirmed that following IR, MRN forms, in fixed and live cells, nuclear foci, which comprised the entire MRE11-RAD50-NBS1 protein complex, and which localized at the sites of DSBs. However, the results obtained also provided new insights. To date, we are the first to show a bimodal cell cycle-independent MRN IRIF response with different MRE11 foci patterns, using different radiation modalities. We documented small MRE11 IRIF mainly forming at early time points and which later developed to larger MRE11 foci. Notably, after high LET irradiation the initial MRE11 IRIF response mostly included large MRE11 foci. These observations indicated that the ...
Functions of the MRE11-RAD50-NBS1 complex in DNA double strand break repair ; Funktionen des MRE11-RAD50-NBS1 Komplexes in der DNA-Doppelstrangbruchreparatur
In a living organism maintenance of genomic stability and integrity is of extreme importance. Thus, any chemical change in the cellular deoxyribonucleic acid (DNA) molecule is considered as damage. Among various forms of DNA damage the DNA double stand break (DSB) is the most deleterious DNA lesion, since if misrepaired or left unrepaired it can cause loss or rearrangement of genetic material. This can lead to permanent cell cycle arrest, apoptosis, mutations, genomic instability and with that to a variety of diseases ranging from genetic disorders, chronic diseases, cancer and accelerated ageing (Ward 1988; Olive 1998; Khanna and Jackson 2001; van Gent, Hoeijmakers et al. 2001; d'Adda di Fagagna, Reaper et al. 2003). To deal with these assaults, cells have evolved sophisticated mechanisms to efficiently detect, signal and repair DNA damage and thus to maintain genomic integrity (Shiloh and Lehmann 2004). Eukaryotic cells have at least two pathways to repair DSBs: (1) non-homologous end-joining (NHEJ) and (2) homologous recombination repair (HRR) (Kanaar, Hoeijmakers et al. 1998; Pardo, Gómez-González et al. 2009). In addition, an extensive signaling network, comprising several different proteins, recognizes DSBs and coordinates repair pathways with cellular checkpoint responses, commonly summarized under the term – DNA damage response (DDR). In summary, our results confirmed that following IR, MRN forms, in fixed and live cells, nuclear foci, which comprised the entire MRE11-RAD50-NBS1 protein complex, and which localized at the sites of DSBs. However, the results obtained also provided new insights. To date, we are the first to show a bimodal cell cycle-independent MRN IRIF response with different MRE11 foci patterns, using different radiation modalities. We documented small MRE11 IRIF mainly forming at early time points and which later developed to larger MRE11 foci. Notably, after high LET irradiation the initial MRE11 IRIF response mostly included large MRE11 foci. These observations indicated that the ...
Functions of the MRE11-RAD50-NBS1 complex in DNA double strand break repair ; Funktionen des MRE11-RAD50-NBS1 Komplexes in der DNA-Doppelstrangbruchreparatur
Konkow, Swetlana (author)
2012-09-14
Theses
Electronic Resource
English
Tandem purification of Mre11/Rad50-dimers using the baculovirus expression system
| UB Braunschweig | 2012
| British Library Online Contents | 2006