Spontaneous tumor development in bone marrow-rescued DNA-PKcs3A/3A mice due to dysfunction of telomere leading strand deprotection-Reference-Cited by-同舟云学术

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Spontaneous tumor development in bone marrow-rescued DNA-PKcs3A/3A mice due to dysfunction of telomere leading strand deprotection

Published:2015-11-30 Issue:30 Volume:35 Page:3909-3918
ISSN:0950-9232
Container-title:Oncogene
language:en
Short-container-title:Oncogene

Author:

Zhang S,Matsunaga S,Lin Y-F,Sishc B,Shang Z,Sui J,Shih H-Y,Zhao Y,Foreman O,Story M D,Chen D J,Chen B P C

Publisher

Springer Science and Business Media LLC

Subject

Cancer Research,Genetics,Molecular Biology

Link

http://www.nature.com/articles/onc2015459.pdf

Reference49 articles.

1. Davis AJ, Chen DJ . DNA double strand break repair via non-homologous end-joining. Transl Cancer Res 2013; 2: 130–143.

2. Chen BP, Uematsu N, Kobayashi J, Lerenthal Y, Krempler A, Yajima H et al. Ataxia telangiectasia mutated (ATM) is essential for DNA-PKcs phosphorylations at the Thr-2609 cluster upon DNA double strand break. J Biol Chem 2007; 282: 6582–6587.

3. Ding Q, Reddy YV, Wang W, Woods T, Douglas P, Ramsden DA et al. Autophosphorylation of the catalytic subunit of the DNA-dependent protein kinase is required for efficient end processing during DNA double-strand break repair. Mol Cell Biol 2003; 23: 5836–5848.

4. Reddy YV, Ding Q, Lees-Miller SP, Meek K, Ramsden DA . Non-homologous end joining requires that the DNA-PK complex undergo an autophosphorylation-dependent rearrangement at DNA ends. J Biol Chem 2004; 279: 39408–39413.

5. Chan DW, Chen BP, Prithivirajsingh S, Kurimasa A, Story MD, Qin J et al. Autophosphorylation of the DNA-dependent protein kinase catalytic subunit is required for rejoining of DNA double-strand breaks. Genes Dev 2002; 16: 2333–2338.

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