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Nuclear receptor SHP inhibition of Dnmt1 expression via ERRγ.

We describe a transcriptional mechanism regulating the expression of Dnmt1 by nuclear receptors. We show that ERRγ functions as a transcriptional activator of mouse and human Dnmt1 expression by direct binding to its response elements (ERE1/ERE2) in the dnmt1/DNMT1 promoters. The induction of Dnmt1 by ERRγ is repressed by SHP through SHP inhibition of ERRγ transactivity, diminishing ERRγ recruitment to the Dnmt1 promoter, and altering the conformation of local chromatin from an active mode by ERRγ to an inactive mode. Our study provides the first evidence for nuclear receptor mediated regulation of Dnmt1 expression through ERRγ and SHP crosstalk.

Pubmed ID: 21459093

Authors

  • Zhang Y
  • Wang L

Journal

FEBS letters

Publication Data

May 6, 2011

Associated Grants

  • Agency: NIDDK NIH HHS, Id: DK080440
  • Agency: NIDDK NIH HHS, Id: R01 DK080440
  • Agency: NIDDK NIH HHS, Id: R01 DK080440-02
  • Agency: NIDDK NIH HHS, Id: R01 DK080440-03
  • Agency: NCI NIH HHS, Id: T32CA092347

Mesh Terms

  • Acetylation
  • Animals
  • Cell Line
  • Cell Line, Tumor
  • DNA (Cytosine-5-)-Methyltransferase
  • Gene Expression Regulation, Enzymologic
  • HeLa Cells
  • Histones
  • Humans
  • Immunoblotting
  • Immunoprecipitation
  • Methylation
  • Mice
  • Mice, Knockout
  • Promoter Regions, Genetic
  • Protein Binding
  • RNA Interference
  • Receptor Cross-Talk
  • Receptors, Cytoplasmic and Nuclear
  • Receptors, Estrogen
  • Transcriptional Activation