TY - JOUR
T1 - The ATM-mediated DNA-damage response
T2 - taking shape
AU - Shiloh, Yosef
N1 - Funding Information:
Present and previous work in the author's laboratory has been supported by The A-T Medical Research Foundation, The A-T Children's Project, The Israel Science Foundation, The National Institutes of Health (R01 NS31763), Israel Ministry of Science and Technology, The A-T Medical Research Trust, The Joint German-Israeli Project on Cancer Research, The A-T Ease Foundation and the Israeli Association for Fighting A-T.
PY - 2006/7
Y1 - 2006/7
N2 - Cellular responses to DNA damage are crucial for maintaining homeostasis and preventing the development of cancer. Our understanding of the DNA-damage response has evolved: whereas previously the focus was on DNA repair, we now appreciate that the response to DNA lesions involves a complex, highly branched signaling network. Defects in this response lead to severely debilitating, cancer-predisposing 'genomic instability syndromes'. Double strand breaks (DSBs) in DNA are potent triggers of the DNA-damage response, which is why they are used to study this pathway. The chief transducer of the DSB signal is the nuclear protein kinase ataxia-telangiectasia mutated (ATM). Genetic, biochemical and structural studies have recently provided insights into the ATM-mediated DSB response, reshaping our view of this signaling pathway while raising new questions.
AB - Cellular responses to DNA damage are crucial for maintaining homeostasis and preventing the development of cancer. Our understanding of the DNA-damage response has evolved: whereas previously the focus was on DNA repair, we now appreciate that the response to DNA lesions involves a complex, highly branched signaling network. Defects in this response lead to severely debilitating, cancer-predisposing 'genomic instability syndromes'. Double strand breaks (DSBs) in DNA are potent triggers of the DNA-damage response, which is why they are used to study this pathway. The chief transducer of the DSB signal is the nuclear protein kinase ataxia-telangiectasia mutated (ATM). Genetic, biochemical and structural studies have recently provided insights into the ATM-mediated DSB response, reshaping our view of this signaling pathway while raising new questions.
UR - http://www.scopus.com/inward/record.url?scp=33745823159&partnerID=8YFLogxK
U2 - 10.1016/j.tibs.2006.05.004
DO - 10.1016/j.tibs.2006.05.004
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AN - SCOPUS:33745823159
VL - 31
SP - 402
EP - 410
JO - Trends in Biochemical Sciences
JF - Trends in Biochemical Sciences
SN - 0376-5067
IS - 7
ER -