期刊
EPIGENETICS
卷 9, 期 5, 页码 658-668出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/epi.28298
关键词
embryogenesis; reprogramming; MLL2; H3K27; UTX; cancer; RB; Kabuki; SWI/SNF; HOX
资金
- Fund for Scientific Research (FWO) Flanders [G.0198.08, G.0564.13N, G.0550.13N, G.0869.10N, G.A001.13N]
- Flemish Liga against Cancer (VLK)
- GOA-UGent [12051203]
- Cancer Plan from the Federal Public Service of Health
- Children Cancer Fund Ghent
- Belgian Program of Interuniversity Poles of Attraction IUAP
- Belgian Foundation Against Cancer [365O9110]
In 2007, the Ubiquitously Transcribed Tetratricopeptide Repeat on chromosome X (UTX) was identified as a histone demethylase that specifically targets di- and tri-methyl groups on lysine 27 of histone H3 (H3K27me2/3). Since then, UTX has been proven essential during normal development, as it is critically required for correct reprogramming, embryonic development and tissue-specific differentiation. UTX is a member of the MLL2 H3K4 methyltransferase complex and its catalytic activity has been linked to regulation of HOX and RB transcriptional networks. In addition, an H3K27me2/3 demethylase independent function for UTX was uncovered in promoting general chromatin remodeling in concert with the BRG1-containing SWI/SNF remodeling complex. Constitutional inactivation of UTX causes a specific hereditary disorder called the Kabuki syndrome, whereas somatic loss of UTX has been reported in a variety of human cancers. Here, we compile the breakthrough discoveries made from the first disclosure of UTX as a histone demethylase till the identification of disease-related UTX mutations and specific UTX inhibitors.
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