UTX and JMJD3 are histone H3K27 demethylases involved in HOX gene regulation and development

By K. Agger, P. Cloos, J. Christensen, Diego Pasini, Simon Rose, Juri Rappsilber, Irina Issaeva, E. Canaani, A. Salcini, K. Helin. Nature, 2007

1,354 citations recorded by the source corpus.

Subfields: Aging, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e774212f39d0d1be8a62cfcdda4b73842de35754

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Aging

1. Gregory J. Hannon

In Molecular Biology

1. D. Reinberg
2. A. Shilatifard
3. C. D. Allis
4. P. Voigt
5. Wee-Wei Tee
6. Dirk Schübeler
7. Edwin R. Smith
8. P. Chi

Citations in the corpus

• Mutations of polycomb‐associated gene ASXL1 in myelodysplastic syndromes and chronic myelomonocytic leukaemia (2009, background): “Second, deletions of TET2, TET3, ASXL1, ASXL2, DNMT3A, DNMT3B and UTX (Fig 2) suggest that regulators of gene expression via DNA methylation and histone modifications could be altered in the MDSs. UTX codes for a H3K27 demethylase (Agger et al, 2007).”
• Covalent histone modifications: miswritten, misinterpreted, and miserased in human cancers (2010, background): “For instance, UTX is a stable component of the MLL2- and MLL3-containing complexes, which erase H3K27me3 and also write H3K4me3 at target chromati”
• Ezh2 Orchestrates Gene Expression for the Stepwise Differentiation of Tissue-Specific Stem Cells (2009, background): “It is tempting to speculate that suprabasal Jmjd3 might ensure proper differentiation through efficient removal of the Ezh-mediated triMeK27-H3 (G and H) By contrast, PMA, which promotes AP1 activity, enhances precocious expression of EDC genes in Ezh2 cKO, but not WT basal cells (G).”
• Epithelialization in Wound Healing: A Comprehensive Review (2014, background): “Reduction of histone H3 lysine 27 trimethylation (H3K27me3) occurs at the healing edges of full-thickness wounds in mice.94 H3K27me3 is a silencing chromatin modification that can be set by the Polycomb Repressive Complex 2 (PCR2)95 or removed by the specific H3K27 demethylases Jmjd3 and Utx.96 Cons”
• Covalent modifications of histones during development and disease pathogenesis (2007, background): “The reciprocal relationship of H3K4 and H3K27 methylation exemplified by the TrxG and PcG antagonism is further strengthened by the existence of H3K27 demethylases, JMJD3 and the related UTX (refs”
• Lineage-specific polycomb targets and de novo DNA methylation define restriction and potential of neuronal progenitors. (2008, background): “However, while DNA methylation is considered a stable epigenetic silencer, Polycomb-mediated repression is reversible, as targets such as Hox genes are activated in a cell-type-specific manner (Agger et al., 2007; Bracken et al., 2006; Lan et al., 2007; Lee et al., 2007; Mikkelsen et al., 2007).”