| First Author | Engel N | Year | 2009 |
| Journal | Epigenetics | Volume | 4 |
| Issue | 2 | Pages | 98-9 |
| PubMed ID | 19229137 | Mgi Jnum | J:232394 |
| Mgi Id | MGI:5776690 | Doi | 10.4161/epi.4.2.7858 |
| Citation | Engel N, et al. (2009) Conserved DNA methylation in Gadd45a(-/-) mice. Epigenetics 4(2):98-9 |
| abstractText | 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. |
