Histone Deacetylases 5 and 9 Govern Responsiveness of the Heart to a Subset of Stress Signals and Play Redundant Roles in Heart Development
Author:
Affiliation:
1. Departments of Molecular Biology
2. Myogen, Inc., Westminster, Colorado
3. Pathology
4. Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas
Abstract
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Link
https://journals.asm.org/doi/pdf/10.1128/MCB.24.19.8467-8476.2004
Reference50 articles.
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2. Chien, K. R. 1999. Stress pathways and heart failure. Cell 98 : 555-558.
3. Davis, F. J., M. Gupta, B. Camoretti-Mercado, R. J. Schwartz, and M. P. Gupta. 2003. Calcium/calmodulin-dependent protein kinase activates serum response factor transcription activity by its dissociation from histone deacetylase, HDAC4. Implications in cardiac muscle gene regulation during hypertrophy. J. Biol. Chem. 278 : 20047-20058.
4. De Windt, L. J., H. W. Lim, O. F. Bueno, Q. Liang, U. Delling, J. C. Braz, B. J. Glascock, T. F. Kimball, F. del Monte, R. J. Hajjar, and J. D. Molkentin. 2001. Targeted inhibition of calcineurin attenuates cardiac hypertrophy in vivo. Proc. Natl. Acad. Sci. USA 98 : 3322-3327.
5. Fentzke, R. C., C. E. Korcarz, R. M. Lang, H. Lin, and J. M. Leiden. 1998. Dilated cardiomyopathy in transgenic mice expressing a dominant-negative CREB transcription factor in the heart. J. Clin. Investig. 101 : 2415-2426.
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