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The histone demethylase UTX enables RB-dependent cell fate control.

Genes & development | Feb 15, 2010

http://www.ncbi.nlm.nih.gov/pubmed/20123895

Trimethylation of histone H3 on Lys 27 (H3K27me3) is key for cell fate regulation. The H3K27me3 demethylase UTX functions in development and tumor suppression with undefined mechanisms. Here, genome-wide chromatin occupancy analysis of UTX and associated histone modifications reveals distinct classes of UTX target genes, including genes encoding Retinoblastoma (RB)-binding proteins. UTX removes H3K27me3 and maintains expression of several RB-binding proteins, enabling cell cycle arrest. Genetic interactions in mammalian cells and Caenorhabditis elegans show that UTX regulates cell fates via RB-dependent pathways. Thus, UTX defines an evolutionarily conserved mechanism to enable coordinate transcription of a RB network in cell fate control.

Pubmed ID: 20123895 RIS Download

Mesh terms: Animals | Caenorhabditis elegans | Cell Differentiation | Cell Line, Tumor | Cell Proliferation | Cells, Cultured | Chromatin | Gene Expression Regulation | Genome | Humans | Jumonji Domain-Containing Histone Demethylases | Methylation | Mice | Neoplasms | Retinoblastoma Binding Proteins

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Associated grants

  • Agency: Medical Research Council, Id: G0600127
  • Agency: NCI NIH HHS, Id: R01-CA118487
  • Agency: NCI NIH HHS, Id: R01-CA118750
  • Agency: Howard Hughes Medical Institute, Id:

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