Ataxia-telangiectasia mutated (ATM) deficiency decreases reprogramming efficiency and leads to genomic instability in iPS cells

Biochemical and Biophysical Research Communications

Volumn 407, Issue 2, 2011, Pages 321-326

  Kinoshita, Taisuke ^a   Nagamatsu, Go ^a,b   Kosaka, Takeo ^c   Takubo, Keiyo ^a   Hotta, Akitsu ^b,d   Ellis, James ^e   Suda, Toshio ^a  

^a KEIO UNIVERSITY SCHOOL OF MEDICINE   (Japan)

^b JAPAN SCIENCE AND TECHNOLOGY AGENCY   (Japan)

^c KEIO UNIVERSITY   (Japan)

^d KYOTO UNIVERSITY   (Japan)

^e UNIVERSITY OF TORONTO   (Canada)

Author keywords

ATM; DNA damage; Pluripotency; Reprogramming

Indexed keywords

ATM PROTEIN; PROTEIN P53;

ANIMAL CELL; ARTICLE; CELL DIFFERENTIATION; CELL DIVISION; CELL PROLIFERATION; DNA DAMAGE; DOUBLE STRANDED DNA BREAK; FIBROBLAST; GENE INACTIVATION; GENE STRUCTURE; GENOMIC INSTABILITY; KARYOTYPE; MOUSE; NONHUMAN; PLURIPOTENT STEM CELL; PRIORITY JOURNAL; SOMATIC CELL;

ANIMALS; CELL CYCLE PROTEINS; CELLS, CULTURED; DNA-BINDING PROTEINS; GENOMIC INSTABILITY; HUMANS; INDUCED PLURIPOTENT STEM CELLS; KARYOTYPING; MICE; MICE, KNOCKOUT; NUCLEAR REPROGRAMMING; PROTEIN-SERINE-THREONINE KINASES; TUMOR SUPPRESSOR PROTEINS;

ATAXIA TELANGIECTASIA; IPS;

EID: 79953685437     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2011.03.013     Document Type: Article

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