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- W2154924534 abstract "Heart failure (HF) is driven by the interplay between regulatory transcription factors and dynamic alterations in chromatin structure. Pathologic gene transactivation in HF is associated with recruitment of histone acetyl-transferases and local chromatin hyperacetylation. We therefore assessed the role of acetyl-lysine reader proteins, or bromodomains, in HF. Using a chemical genetic approach, we establish a central role for BET family bromodomain proteins in gene control during HF pathogenesis. BET inhibition potently suppresses cardiomyocyte hypertrophy in vitro and pathologic cardiac remodeling in vivo. Integrative transcriptional and epigenomic analyses reveal that BET proteins function mechanistically as pause-release factors critical to expression of genes that are central to HF pathogenesis and relevant to the pathobiology of failing human hearts. This study implicates epigenetic readers as essential effectors of transcriptional pause release during HF pathogenesis and identifies BET coactivator proteins as therapeutic targets in the heart." @default.
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- W2154924534 date "2013-08-01" @default.
- W2154924534 modified "2023-10-14" @default.
- W2154924534 title "BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure" @default.
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- W2154924534 doi "https://doi.org/10.1016/j.cell.2013.07.013" @default.
- W2154924534 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4090947" @default.
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