TY - JOUR
T1 - ATM-dependent cellular response to DNA double strand breaks plays a pivotal role in the maintenance of the integrity of the genome
AU - Suzuki, K.
AU - Yamauchi, M.
AU - Yamashita, S.
N1 - Funding Information:
This work was supported in part by the Nagasaki University Global Century Center of Excellence (COE) Program, and Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan.
PY - 2011/2
Y1 - 2011/2
N2 - ATM-dependent cellular response to DNA double strand breaks plays a pivotal role in the maintenance of the integrity of the genome. Upon irradiation, activated ataxia-telangiectasia mutated (ATM) proteins phosphorylate various downstream mediators and effectors, such as histone H2AX, MDC1, 53BP1 and NBS1. These proteins create discrete foci within the nuclei, which are detectable under fluorescence microscopes. Interestingly, the size of the foci is also increasing as increasing the time after irradiation. Particularly, the residual foci form large foci, the sizes of which reach approximately 2 μm in diameter. We confirmed that such 'foci growth' is a mechanism, by which DNA damage signal is amplified. Especially, a proper DNA damage response of cells to lower doses of ionising radiation required amplification of the ATM-dependent damage signal by recruiting the DNA damage checkpoint factors to the site of chromatin.
AB - ATM-dependent cellular response to DNA double strand breaks plays a pivotal role in the maintenance of the integrity of the genome. Upon irradiation, activated ataxia-telangiectasia mutated (ATM) proteins phosphorylate various downstream mediators and effectors, such as histone H2AX, MDC1, 53BP1 and NBS1. These proteins create discrete foci within the nuclei, which are detectable under fluorescence microscopes. Interestingly, the size of the foci is also increasing as increasing the time after irradiation. Particularly, the residual foci form large foci, the sizes of which reach approximately 2 μm in diameter. We confirmed that such 'foci growth' is a mechanism, by which DNA damage signal is amplified. Especially, a proper DNA damage response of cells to lower doses of ionising radiation required amplification of the ATM-dependent damage signal by recruiting the DNA damage checkpoint factors to the site of chromatin.
UR - http://www.scopus.com/inward/record.url?scp=79952342142&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79952342142&partnerID=8YFLogxK
U2 - 10.1093/rpd/ncq533
DO - 10.1093/rpd/ncq533
M3 - Article
C2 - 21224259
AN - SCOPUS:79952342142
VL - 143
SP - 279
EP - 283
JO - Radiation Protection Dosimetry
JF - Radiation Protection Dosimetry
SN - 0144-8420
IS - 2-4
M1 - ncq533
ER -
