Class II histone deacetylases act as signal-responsive repressors of cardiac hypertrophy.

By Chun-li Zhang, T. McKinsey, Shurong Chang, C. Antos, Joseph A. Hill, E. Olson. Cell, 2002

1,016 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/08a179710bea91ee76535c0f65446649ca904cb9

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Citations in the corpus

Histone deacetylase 4 controls chondrocyte hypertrophy during skeletogenesis. (2004, background): “HDAC5 knockout mice disphy (Zhang et al., 2002; Chang et al., 2004).”
Histone Deacetylase Inhibitors: Overview and Perspectives (2007, background): “HDAC4 knockout mice have defects in chondrocyte differentiation (14); HDAC5 and HDAC9 knockouts have cardiac defects (15).”
Deacetylase inhibition promotes the generation and function of regulatory T cells (2007, background): “Likewise, activation-induced phosphorylation of HDAC9 leads to its nuclear export and depression of MEF2 in cardiac myocyte”
Mechanistic Pathways of Sex Differences in Cardiovascular Disease. (2017, background): “Histone acetyltransferases and deacetylases control cardiac hypertrophy, and a dysregulation of histone methylation profiles is found in HF (179, 392, 446).”
HDAC family: What are the cancer relevant targets? (2009, background): “By the age of 8 months mice develop spontaneous cardiac hypertrophy due to sensitisation to hypertrophic signals [33].”
Histone deacetylase 5 epigenetically controls behavioral adaptations to chronic emotional stimuli. (2007, neutral): “Such translocation of HDAC5 out of the nucleus is thought to block HDAC5 function, since only its nuclear form can deacetylate histones (Czubryt et al., 2003; Zhang et al., 2002).”
Histone Deacetylases 5 and 9 Govern Responsiveness of the Heart to a Subset of Stress Signals and Play Redundant Roles in Heart Development (2004, background): “The cardiac phenotype of HDAC5 mutant mice is remarkably similar to that of HDAC9 mutant mice (45), strongly suggesting that these two HDACs play comparable roles in the control of cardiac growth.”