| Rad54 is dispensable for the ALT pathway. | |
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MedLine Citation:
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PMID: 17054727 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Some immortal cells use the alternative lengthening of telomeres (ALT) pathway to maintain their telomeres instead of telomerase. Previous studies revealed that homologous recombination (HR) contributes to the ALT pathway. To further elucidate molecular mechanisms, we inactivated Rad54 involved in HR, in mouse ALT embryonic stem (ES) cells. Although Rad54-deficient ALT ES cells showed radiosensitivity in line with expectation, cell growth and telomeres were maintained for more than 200 cell divisions. Furthermore, although MMC-stimulated sister chromatid exchange (SCE) was suppressed in the Rad54-deficient ALT ES cells, ALT-associated telomere SCE was not affected. This is the first genetic evidence that mouse Rad54 is dispensable for the ALT pathway. |
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Authors:
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Koichi Akiyama; Kosuke Yusa; Hideharu Hashimoto; Anuradha Poonepalli; Manoor Prakash Hande; Naoki Kakazu; Junji Takeda; Makoto Tachibana; Yoichi Shinkai |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Genes to cells : devoted to molecular & cellular mechanisms Volume: 11 ISSN: 1356-9597 ISO Abbreviation: Genes Cells Publication Date: 2006 Nov |
Date Detail:
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Created Date: 2006-10-23 Completed Date: 2007-02-12 Revised Date: 2010-09-28 |
Medline Journal Info:
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Nlm Unique ID: 9607379 Medline TA: Genes Cells Country: England |
Other Details:
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Languages: eng Pagination: 1305-15 Citation Subset: IM |
Affiliation:
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Department of Life Science, Graduate School of Biostudies, Kyoto University, Kyoto, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Line Embryonic Stem Cells / metabolism Mice Mice, Knockout Nuclear Proteins / deficiency, genetics, metabolism* Recombination, Genetic Signal Transduction Sister Chromatid Exchange Telomere / metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Nuclear Proteins; EC 3.6.4.-/Rad54l protein, mouse |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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