The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Control of Cardiac Growth by Histone Acetylation/Deacetylation
Abstract
Histones control gene expression by modulating the structure of chromatin and the accessibility of regulatory DNA sequences to transcriptional activators and repressors. Posttranslational modifications of histones have been proposed to establish a “code” that determines patterns of cellular gene expression. Acetylation of histones by histone acetyltransferases stimulates gene expression by relaxing chromatin structure, allowing access of transcription factors to DNA, whereas deacetylation of histones by histone deacetylases promotes chromatin condensation and transcriptional repression. Recent studies demonstrate histone acetylation/deacetylation to be a nodal point for the control of cardiac growth and gene expression in response to acute and chronic stress stimuli. These findings suggest novel strategies for “transcriptional therapies” to control cardiac gene expression and function. Manipulation of histone modifying enzymes and the signaling pathways that impinge on them in the settings of pathological cardiac growth, remodeling, and heart failure represents an auspicious therapeutic approach.
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Drewes, G., Ebneth, A., Preuss, U., Mandelkow, E.-M., & Mandelkow, E. (1997) · Cell · doi:10.1016/s0092-8674(00)80208-1 · Cited by 878
Three proteins define a class of human histone deacetylases related to yeast Hda1p
Grozinger, C. M., Hassig, C. A., & Schreiber, S. L. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.9.4868 · Cited by 770
Fischle, W., Dequiedt, F., Hendzel, M. J., Guenther, M. G., Lazar, M. A., Voelter, W., & Verdin, E. (2002) · Molecular Cell · doi:10.1016/s1097-2765(01)00429-4 · Cited by 754
Czubryt, M. P., McAnally, J., Fishman, G. I., & Olson, E. N. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0337639100 · Cited by 418
Self-citationRegulation of MEF2 by Histone Deacetylase 4- and SIRT1 Deacetylase-Mediated Lysine Modifications
Zhao, X., Sternsdorf, T., Bolger, T. A., Evans, R. M., & Yao, T.-P. (2005) · Molecular and Cellular Biology · doi:10.1128/mcb.25.19.8456-8464.2005 · Cited by 264
MEF‐2 function is modified by a novel co‐repressor, MITR
Sparrow, D. B., Miska, E. A., Langley, E., Reynaud‐Deonauth, S., Kotecha, S., Towers, N., Spohr, G., Kouzarides, T., & Mohun, T. J. (1999) · The EMBO Journal · doi:10.1093/emboj/18.18.5085 · Cited by 196
James, J., Martin, L., Krenz, M., Quatman, C., Jones, F., Klevitsky, R., Gulick, J., & Robbins, J. (2005) · Circulation · doi:10.1161/01.cir.0000164233.09448.b1 · Cited by 77
Cited by
Calcium Cycling and Signaling in Cardiac Myocytes
Bers, D. M. (2008) · Annual Review of Physiology · doi:10.1146/annurev.physiol.70.113006.100455 · Cited by 1,302
Bernardo, B. C., Weeks, K. L., Pretorius, L., & McMullen, J. R. (2010) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2010.04.005 · Cited by 894
The world of protein acetylation
Drazic, A., Myklebust, L. M., Ree, R., & Arnesen, T. (2016) · Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics · doi:10.1016/j.bbapap.2016.06.007 · Cited by 804
Morimoto, T., Sunagawa, Y., Kawamura, T., Takaya, T., Wada, H., Nagasawa, A., Komeda, M., Fujita, M., Shimatsu, A., Kita, T., et al. (2008) · Journal of Clinical Investigation · doi:10.1172/jci33160 · Cited by 423
The role of sirtuins in cardiac disease
Matsushima, S., & Sadoshima, J. (2015) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00053.2015 · Cited by 375
Metadata
- Authors
- Backs, J., & Olson, E. N.
- Venue
- Circulation Research
- Published
- 2006-01-06
- Volume
- 98
- Issue
- 1
- Pages
- 15-24
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2156247910
- Cited by
- 440
- References
- 7
- FWCI
- 11.54
- Type
- journal article
- Language
- en
- Open access
- closed
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
