ATR signaling cooperates with ATM in the mechanism of low dose hypersensitivity induced by carbon ion beam
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- 作者：Lian Xuea ; b ; Yoshiya Furusawac ; Dong Yud ; yudong@suda.edu.com" class="auth_mail" title="E-mail the corresponding author
- 关键词：IR ; ionizing radiation ; LET ; linear energy transfer ; HRS ; hyper-radiosensitivity ; IRR ; induced radioresistance ; DSB ; DNA double strand break ; ATM ; ataxia telangiectasia mutated homolog ; ATR ; ataxia telangiectasia and Rad3 related ; DNA-PKcs ; DNA-dependent protein kinase catalytic subunit ; CHK1 ; checkpoint kinase 1 ; ssDNA ; single strand DNA ; RPA ; replication protein A ; NHEJ ; non-homologous end-joining ; HR ; homologous recombination
- 刊名：DNA Repair
- 出版年：2015
- 出版时间：October 2015
- 年：2015
- 卷：34
- 期：Complete
- 页码：1-8
- 全文大小：1236 K
文摘
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The early G2/M checkpoint is an important factor for the low dose HRS response to heavy ions.
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The early G2/M checkpoint can be observed in ATM deficient cells under low doses of heavy ion beams.
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The ATR pathway plays a pivotal role in the early G2/M checkpoint of ATM-deficient cells following heavy ion radiation.
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The ATR pathway was activated in a dose- and LET-dependent manner.
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The ATR pathway cooperates with ATM in low dose hypersensitivity induced by carbon ion beam.