Salt-inducible kinase 1 maintains HDAC7 stability to promote pathologic cardiac remodeling.

  title={Salt-inducible kinase 1 maintains HDAC7 stability to promote pathologic cardiac remodeling.},
  author={Austin Hsu and Qiming Duan and Sarah McMahon and Yu Huang and Sarah Wood and Nathanael S. Gray and Biao Wang and Benoit G. Bruneau and Saptarsi M Haldar},
  journal={The Journal of clinical investigation},
Salt inducible kinases (SIKs) are key regulators of cellular metabolism and growth, but their role in cardiomyocyte plasticity and heart failure pathogenesis remains unknown. Here, we showed that loss of SIK1 kinase activity protected against adverse cardiac remodeling and heart failure pathogenesis in rodent models and human iPSC-derived cardiomyocytes. We found that SIK1 phosphorylated and stabilized histone deacetylase 7 (HDAC7) protein during cardiac stress, an event that is required for… Expand
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Regulation of Cardiac Stress Signaling by Protein Kinase D1
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Histone Deacetylases 5 and 9 Govern Responsiveness of the Heart to a Subset of Stress Signals and Play Redundant Roles in Heart Development
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Protein Kinases C and D Mediate Agonist-Dependent Cardiac Hypertrophy through Nuclear Export of Histone Deacetylase 5
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A proteolytic fragment of histone deacetylase 4 protects the heart from failure by regulating the hexosamine biosynthetic pathway
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Class II Histone Deacetylases Act as Signal-Responsive Repressors of Cardiac Hypertrophy
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SIK1 is a class II HDAC kinase that promotes survival of skeletal myocytes
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Myc controls transcriptional regulation of cardiac metabolism and mitochondrial biogenesis in response to pathological stress in mice.
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