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Sci Rep. 2014 Jun 27;4:5421. doi: 10.1038/srep05421.

Ataxia telangiectasia derived iPS cells show preserved x-ray sensitivity and decreased chromosomal instability.

Author information

1
1] Department of Reproductive Biology, National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan [2] School of BioMedical Science, Tokyo Medical and Dental University, Tokyo, 113-0034, Japan.
2
1] Department of Reproductive Biology, National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan [2] Department of Research Team for Geriatric Medicine, Tokyo Metropolitan Institute of Gerontology, Tokyo, 173-0015, Japan.
3
Department of Systems BioMedicine, National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
4
Department of Research Team for Geriatric Pathology, Tokyo Metropolitan Institute of Gerontology, Tokyo, 173-0015, Japan.
5
Department of Maternal-Fetal Biology, National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
6
Department of Reproductive Biology, National Research Institute for Child Health and Development, Tokyo, 157-8535, Japan.
7
Department of BioSciences, Kitasato University School of Science, Kanagawa, 252-0373, Japan.
8
1] Department of Chemical and Materials Engineering, National Central University, Taoyuan, 32001, Taiwan [2] College of Science, King Saud University, Riyadh, 11451, Saudi Arabia.

Abstract

Ataxia telangiectasia is a neurodegenerative inherited disease with chromosomal instability and hypersensitivity to ionizing radiation. iPS cells lacking ATM (AT-iPS cells) exhibited hypersensitivity to X-ray irradiation, one of the characteristics of the disease. While parental ataxia telangiectasia cells exhibited significant chromosomal abnormalities, AT-iPS cells did not show any chromosomal instability in vitro for at least 80 passages (560 days). Whole exome analysis also showed a comparable nucleotide substitution rate in AT-iPS cells. Taken together, these data show that ATM is involved in protection from irradiation-induced cell death.

PMID:
24970375
PMCID:
PMC4073166
DOI:
10.1038/srep05421
[Indexed for MEDLINE]
Free PMC Article
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