Tet1 Is Dispensable for Maintaining Pluripotency and Its Loss Is Compatible with Embryonic and Postnatal Development
Top Cited Papers
Open Access
- 5 August 2011
- journal article
- research article
- Published by Elsevier
- Vol. 9 (2) , 166-175
- https://doi.org/10.1016/j.stem.2011.07.010
Abstract
No abstract availableKeywords
Funding Information
- National Institutes of Health (5-R37-CA084198, 5-RO1-CA087869, 5-RO1-HDO45022)
- Boehringer Ingelheim Fonds
This publication has 21 references indexed in Scilit:
- Hydroxylation of 5-Methylcytosine by TET1 Promotes Active DNA Demethylation in the Adult BrainCell, 2011
- TET1 and hydroxymethylcytosine in transcription and DNA methylation fidelityNature, 2011
- Dual functions of Tet1 in transcriptional regulation in mouse embryonic stem cellsNature, 2011
- Reprogramming of the paternal genome upon fertilization involves genome-wide oxidation of 5-methylcytosineProceedings of the National Academy of Sciences, 2011
- Tet1 and Tet2 Regulate 5-Hydroxymethylcytosine Production and Cell Lineage Specification in Mouse Embryonic Stem CellsCell Stem Cell, 2011
- Role of Tet proteins in 5mC to 5hmC conversion, ES-cell self-renewal and inner cell mass specificationNature, 2010
- Active DNA demethylation: many roads lead to RomeNature Reviews Molecular Cell Biology, 2010
- Conversion of 5-Methylcytosine to 5-Hydroxymethylcytosine in Mammalian DNA by MLL Partner TET1Science, 2009
- The Nuclear DNA Base 5-Hydroxymethylcytosine Is Present in Purkinje Neurons and the BrainScience, 2009
- The Colorful History of Active DNA DemethylationCell, 2008