Histone Deacetylases 5 and 9 Govern Responsiveness of the Heart to a Subset of Stress Signals and Play Redundant Roles in Heart Development

By Shurong Chang, T. McKinsey, Chun-li Zhang, J. Richardson, Joseph A. Hill, E. Olson. Molecular and Cellular Biology, 2004

627 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/101b5fd3c061d9b6ffbc549e9c413f769758724a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. E. Olson
2. E. Nestler
3. V. Krishnan
4. Deepak Srivastava
5. R. Bassel-Duby
6. J. Richardson
7. E. Seto
8. S. Russo

In Oncology

1. E. Olson
2. E. Seto
3. G. Karsenty

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).”
• Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets (2015, background): “In contrast to ‘pro-hypertrophic’ class I HDACs, class IIa HDACs have been identified as negative regulators of cardiac hypertrophy, as genetic deletion of HDAC5 or HDAC9 in mice exacerbated the hypertrophic response to pressure overload and to transgenic expression of activated calcineurin (Chang e”
• The many roles of histone deacetylases in development and physiology: implications for disease and therapy (2009, background): “HDAC5 and HDAC9 are highly enriched in muscles, the heart and brai”
• Molecular mechanisms of diabetic cardiomyopathy (2014, neutral): “Class II HDACs (HDAC5, HDAC9) are able to suppress cardiac hypertrophy, while class I HDACs promote cardiac hypertrophy [138, 139].”
• HDAC family: What are the cancer relevant targets? (2009, background): “Mice lacking Hdac5 develop profoundly enlarged hearts in response to pressure overload resulting from aortic constriction or constitutive activation of cardiac stress signals [31].”
• Histone deacetylase 5 epigenetically controls behavioral adaptations to chronic emotional stimuli. (2007, positive): “However, when knockout mice are exposed to chronic cardiac stress via thoracic aortic banding, their hearts hypertrophy to significantly greater sizes than wildtype control mice (Chang et al., 2004).”
• Making or breaking the heart: from lineage determination to morphogenesis. (2006, background): “A direct role for HDACs was also demonstrated by a failure of ventricular growth in mutant mice lacking HDAC5 and HDAC9 (Chang et al., 2004b).”
• Erasers of histone acetylation: the histone deacetylase enzymes. (2014, background): “ing redundant functions of HDAC5 and HDAC9 in the control of cardiac development (Chang et al. 2004).”
• Covalent modifications of histones during development and disease pathogenesis (2007, background): “Histone acetylation status is also crucial during embryogenesis, as inactivation of either HDAC5 or HDAC9 leads to cardiac hypertrophy and stres”
• Regulation of cardiac hypertrophy by intracellular signalling pathways (2006, background): “More provocatively, Hdac5 - and Hdac9 -gene-deleted mice each showed spontaneous cardiac hypertrophy with age and enhanced hypertrophy in response to pathological stimul”
• MEF2: a central regulator of diverse developmental programs (2007, neutral): “2) (Arnold et al., 2007; Chang et al., 2004; Chang et al., 2006; Lu et al., 2000; Verzi et al., 2007; Youn and Liu, 2000).”