Formaldehyde catabolism is essential in cells deficient for the Fanconi anemia DNA-repair pathway

被引：152

作者：

Rosado, Ivan V. ^{[1
]}

Langevin, Frederic ^{[1
]}

Crossan, Gerry P. ^{[1
]}

Takata, Minoru ^{[2
]}

Patel, Ketan J. ^{[1
,3
]}

机构：

[1] MRC, Mol Biol Lab, Cambridge CB2 2QH, England

[2] Kyoto Univ, Ctr Radiat Biol, Dept Late Effect Studies, Lab DNA Damage Signaling, Kyoto 606, Japan

[3] Univ Cambridge, Addenbrookes Hosp, Dept Med, Cambridge CB2 2QQ, England

来源：

NATURE STRUCTURAL & MOLECULAR BIOLOGY | 2011年 / 18卷 / 12期

关键词：

OXIDATIVE DEMETHYLATION; ESCHERICHIA-COLI; DAMAGE; SLX4; REPLICATION;

D O I：

10.1038/nsmb.2173

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Metabolism is predicted to generate formaldehyde, a toxic, simple, reactive aldehyde that can damage DNA. Here we report a synthetic lethal interaction in avian cells between ADH5, encoding the main formaldehyde-detoxifying enzyme, and the Fanconi anemia (FA) DNA-repair pathway. These results define a fundamental role for the combined action of formaldehyde catabolism and DNA cross-link repair in vertebrate cell survival.

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收藏

页码：1432 / 1434

页数：3

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