Conserved DNA methylation in Gadd45a-/- mice

被引：59

作者：

Engel, Nora ^{[1
]}

Tront, Jennifer S. ^{[1
]}

Erinle, Toyin ^{[1
]}

Nguyen, Nghi ^{[1
]}

Latham, Keith E. ^{[1
]}

Sapienza, Carmen ^{[1
]}

Hoffman, Barbara ^{[1
]}

Liebermann, Dan A. ^{[1
]}

机构：

[1] Temple Univ, Sch Med, Fels Inst Canc Res & Mol Biol, Philadelphia, PA 19122 USA

来源：

EPIGENETICS | 2009年 / 4卷 / 02期

关键词：

DNA methylation; DNA demethylation; Gadd45a; DNA repair; mouse; PATERNAL GENOME; DEMETHYLATION; ACTIVATION; STABILITY; PROMOTER;

D O I：

10.4161/epi.4.2.7858

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：

Gadd45a (growth arrest and DNA- damage- inducible protein 45 alpha) plays a pivotal role in cellular stress responses and is implicated in DNA repair, cell cycle arrest and apoptosis. 1 Recently, it was proposed that GADD45A is a key regulator of active DNA demethylation by way of its role in DNA repair.(2) Barreto et al. reported that Gadd45a overexpression activated transcription from methylation-silenced reporter plasmids and promoted global DNA demethylation. siRNA-mediated knockdown of Gadd45a levels resulted in increased levels of DNA methylation at specific endogenous loci. Based on these exciting results, Gadd45a(-/-) mice might be predicted to have a hypermethylation phenotype. We report here that neither global nor locus-specific methylation is increased in Gadd45a(-/-) mice.

引用

页码：98 / 99

页数：2

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