Control of Proinflammatory Gene Programs by Regulated Trimethylation and Demethylation of Histone H4K20
作者： Joshua D. Stender , Gabriel Pascual , Wen Liu , Minna U. Kaikkonen , Kevin Do
DOI: 10.1016/J.MOLCEL.2012.07.020
关键词:
摘要: Regulation of genes that initiate and amplify inflammatory programs gene expression is achieved by signal-dependent exchange coregulator complexes function to read, write, erase specific histone modifications linked transcriptional activation or repression. Here, we provide evidence for the role trimethylated H4 lysine 20 (H4K20me3) as a repression checkpoint restricts toll-like receptor 4 (TLR4) target in macrophages. H4K20me3 deposited at promoters subset these SMYD5 methyltransferase through its association with NCoR corepressor complexes. Signal-dependent erasure required effective NF-κB-dependent delivery demethylase PHF2. Liver X receptors antagonize TLR4-dependent maintaining NCoR/SMYD5-mediated These findings reveal H4K20 trimethylation/demethylation strategy integrates positive negative signaling inputs control immunity homeostasis.
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