Cardiovascular Epigenetics : Phenotypes and Mechanisms The chromatin-binding protein Smyd 1 restricts adult mammalian heart growth

Sarah Franklin, Todd Kimball,* Tara L. Rasmussen,* Manuel Rosa-Garrido, Haodong Chen, Tam Tran, Mickey R. Miller, Ricardo Gray, Shanxi Jiang, Shuxun Ren, Yibin Wang, Haley O. Tucker, and Thomas M. Vondriska Departments of Anesthesiology & Perioperative Medicine, Medicine (Cardiology) and Physiology, David Geffen School of Medicine, University of California, Los Angeles, California; Department of Internal Medicine, Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah; and Department of Molecular Genetics and the Institute for Cellular and Molecular Biology, University of Texas at Austin, Texas

[1]  Haley O. Tucker,et al.  Mouse myofibers lacking the SMYD1 methyltransferase are susceptible to atrophy, internalization of nuclei and myofibrillar disarray , 2016, Disease Models & Mechanisms.

[2]  Haley O. Tucker,et al.  Defective myogenesis in the absence of the muscle-specific lysine methyltransferase SMYD1. , 2016, Developmental biology.

[3]  Axel Visel,et al.  Dynamic GATA4 enhancers shape the chromatin landscape central to heart development and disease , 2014, Nature Communications.

[4]  Talicia Tarver,et al.  HEART DISEASE AND STROKE STATISTICS–2014 UPDATE: A REPORT FROM THE AMERICAN HEART ASSOCIATION , 2014 .

[5]  S. Franklin,et al.  Systems proteomics of cardiac chromatin identifies nucleolin as a regulator of growth and cellular plasticity in cardiomyocytes. , 2013, American journal of physiology. Heart and circulatory physiology.

[6]  Yongwang Zhong,et al.  Smyd1b is required for skeletal and cardiac muscle function in zebrafish , 2013, Molecular biology of the cell.

[7]  Saptarsi M. Haldar,et al.  BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure , 2013, Cell.

[8]  J. Molkentin,et al.  Signaling effectors underlying pathologic growth and remodeling of the heart. , 2013, The Journal of clinical investigation.

[9]  S. Franklin,et al.  Quantitative analysis of chromatin proteomes in disease. , 2012, Journal of visualized experiments : JoVE.

[10]  Laurent A Bentolila,et al.  Features of endogenous cardiomyocyte chromatin revealed by super-resolution STED microscopy. , 2012, Journal of molecular and cellular cardiology.

[11]  Alexander R. Pico,et al.  Dynamic and Coordinated Epigenetic Regulation of Developmental Transitions in the Cardiac Lineage , 2012, Cell.

[12]  S. Franklin,et al.  Quantitative Analysis of the Chromatin Proteome in Disease Reveals Remodeling Principles and Identifies High Mobility Group Protein B2 as a Regulator of Hypertrophic Growth* , 2012, Molecular & Cellular Proteomics.

[13]  E. Ashley,et al.  Chromatin regulation by Brg1 underlies heart muscle development and disease , 2010, Nature.

[14]  J. Brunzelle,et al.  Crystal Structures of Histone and p53 Methyltransferase SmyD2 Reveal a Conformational Flexibility of the Autoinhibitory C-Terminal Domain , 2011, PloS one.

[15]  Aibin He,et al.  Co-occupancy by multiple cardiac transcription factors identifies transcriptional enhancers active in heart , 2011, Proceedings of the National Academy of Sciences.

[16]  P. Ping,et al.  Specialized compartments of cardiac nuclei exhibit distinct proteomic anatomy* , 2011, Molecular & Cellular Proteomics.

[17]  Y. Jang,et al.  Heat shock protein 90 regulates IκB kinase complex and NF-κB activation in angiotensin II-induced cardiac cell hypertrophy , 2010, Experimental & Molecular Medicine.

[18]  N. Abacı,et al.  The variations of BOP gene in hypertrophic cardiomyopathy. , 2010, Anadolu kardiyoloji dergisi : AKD = the Anatolian journal of cardiology.

[19]  Florian Diehl,et al.  Cardiac Deletion of Smyd2 Is Dispensable for Mouse Heart Development , 2010, PloS one.

[20]  R. Schwartz,et al.  SMYD1, the myogenic activator, is a direct target of serum response factor and myogenin , 2009, Nucleic acids research.

[21]  Y. Pinto,et al.  Avoidance of Transient Cardiomyopathy in Cardiomyocyte-Targeted Tamoxifen-Induced MerCreMer Gene Deletion Models , 2009, Circulation research.

[22]  Pornpimol Charoentong,et al.  ClueGO: a Cytoscape plug-in to decipher functionally grouped gene ontology and pathway annotation networks , 2009, Bioinform..

[23]  K. Webster,et al.  Quantitative Control of Adaptive Cardiac Hypertrophy by Acetyltransferase p300 , 2008, Circulation.

[24]  S. Vatner,et al.  A Redox-Dependent Pathway for Regulating Class II HDACs and Cardiac Hypertrophy , 2008, Cell.

[25]  P. Razeghi,et al.  Return to the fetal gene program protects the stressed heart: a strong hypothesis , 2007, Heart Failure Reviews.

[26]  I. Komuro,et al.  p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload , 2007, Nature.

[27]  S. Berger,et al.  Repression of p53 activity by Smyd2-mediated methylation , 2006, Nature.

[28]  Daniel Burkhoff,et al.  LVAD-induced reverse remodeling: basic and clinical implications for myocardial recovery. , 2006, Journal of cardiac failure.

[29]  Xungang Tan,et al.  SmyD1, a histone methyltransferase, is required for myofibril organization and muscle contraction in zebrafish embryos , 2006 .

[30]  Atsushi Takeda,et al.  Reverse remodeling following insertion of left ventricular assist devices (LVAD): a review of the morphological and molecular changes. , 2005, Cardiovascular research.

[31]  Scott J. Russo,et al.  Chromatin Remodeling Is a Key Mechanism Underlying Cocaine-Induced Plasticity in Striatum , 2005, Neuron.

[32]  A. Moorman,et al.  Expression and regulation of the atrial natriuretic factor encoding gene Nppa during development and disease. , 2005, Cardiovascular research.

[33]  K. Margulies,et al.  Mixed Messages: Transcription Patterns in Failing and Recovering Human Myocardium , 2005, Circulation research.

[34]  G. Dorn,et al.  Protein kinase cascades in the regulation of cardiac hypertrophy. , 2005, The Journal of clinical investigation.

[35]  P. Pandolfi,et al.  Role of the proto-oncogene Pokemon in cellular transformation and ARF repression , 2005, Nature.

[36]  P. Shannon,et al.  Cytoscape: a software environment for integrated models of biomolecular interaction networks. , 2003, Genome research.

[37]  J. Epstein,et al.  Cardiac hypertrophy and histone deacetylase-dependent transcriptional repression mediated by the atypical homeodomain protein Hop. , 2003, The Journal of clinical investigation.

[38]  T. Thum,et al.  Hallmarks of ion channel gene expression in end‐stage heart failure , 2003, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[39]  Michael D. Schneider,et al.  Sizing up the heart: development redux in disease. , 2003, Genes & development.

[40]  Chun Li Zhang,et al.  Class II Histone Deacetylases Act as Signal-Responsive Repressors of Cardiac Hypertrophy , 2002, Cell.

[41]  L. Field,et al.  Cardiomyocyte cell cycle regulation. , 2002, Circulation research.

[42]  D. Srivastava,et al.  Bop encodes a muscle-restricted protein containing MYND and SET domains and is essential for cardiac differentiation and morphogenesis , 2002, Nature Genetics.

[43]  M. Crackower,et al.  Temporally Regulated and Tissue-Specific Gene Manipulations in the Adult and Embryonic Heart Using a Tamoxifen-Inducible Cre Protein , 2001, Circulation research.

[44]  Deepak Srivastava,et al.  A genetic blueprint for cardiac development , 2000, Nature.

[45]  E. Olson,et al.  Cardiac plasticity. , 2008, The New England journal of medicine.

[46]  K. M. Mulder,et al.  Requirement of Smad3 and CREB-1 in mediating transforming growth factor-beta (TGF beta) induction of TGF beta 3 secretion. , 2006, The Journal of biological chemistry.

[47]  E. Olson,et al.  Control of cardiac hypertrophy and heart failure by histone acetylation/deacetylation. , 2006, Novartis Foundation symposium.

[48]  D. Durocher,et al.  Combinatorial interactions regulating cardiac transcription. , 1998, Developmental genetics.