BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure [ChIP-Seq]

ABSTRACT: Heart failure is driven by the interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. Coordinate activation of developmental, inflammatory, fibrotic and growth regulators underlies the hallmark phenotypes of pathologic cardiac hypertrophy and contractile failure. While transactivation in this context is known to be associated with recruitment of histone acetyl-transferase enzymes and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. We therefore undertook a first study of acetyl-lysine reader proteins, or bromodomains, in heart failure. Using a chemical genetic approach, we establish a central role for BET-family bromodomain proteins in gene control during the evolution of heart failure

ORGANISM(S): Mus musculus

SUBMITTER: James Bradner 

PROVIDER: E-GEOD-46668 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress