PP2A negatively regulates the hypertrophic response by dephosphorylating HDAC2 S394 in the heart
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Seung Hoon Jeong | K. Kim | K. Nam | Young-Kook Kim | J. McMullen | Yong Sook Kim | U. Gergs | Y. Cho | J. Neumann | H. Kook | Somy Yoon | G. Eom | Gaeun Kang | D. Kwon | Hyun-Ki Min | Sera Shin | H. Joung | T. Kook | Mira Kim | Sumin Lee | Yunchul Park | Young-Ran Ahn | Jungchul Kim
[1] M. Fornage,et al. Heart Disease and Stroke Statistics—2017 Update: A Report From the American Heart Association , 2017, Circulation.
[2] Chao Fang,et al. Cardiomyocyte specific deletion of PP2A causes cardiac hypertrophy. , 2016, American journal of translational research.
[3] Somy Yoon,et al. HDAC and HDAC Inhibitor: From Cancer to Cardiovascular Diseases , 2016, Chonnam medical journal.
[4] Jonathan P. Davis,et al. Protein phosphatase 2A regulatory subunit B56α limits phosphatase activity in the heart , 2015, Science Signaling.
[5] W. Ho,et al. LB100, a small molecule inhibitor of PP2A with potent chemo- and radio-sensitizing potential , 2015, Cancer biology & therapy.
[6] H. Kook,et al. Role of histone deacetylase 2 and its posttranslational modifications in cardiac hypertrophy , 2015, BMB reports.
[7] Madhusoodanan Mottamal,et al. Histone Deacetylase Inhibitors in Clinical Studies as Templates for New Anticancer Agents , 2015, Molecules.
[8] Qingsong Liu,et al. HDAC2 Selectively Regulates FOXO3a-Mediated Gene Transcription during Oxidative Stress-Induced Neuronal Cell Death , 2015, The Journal of Neuroscience.
[9] E. Adashi,et al. Noncommunicable Diseases , 2015, Seminars in Reproductive Medicine.
[10] Qi Zhang,et al. Inhibition of protein phosphatase 2A sensitizes pancreatic cancer to chemotherapy by increasing drug perfusion via HIF-1α-VEGF mediated angiogenesis. , 2014, Cancer letters.
[11] K. Lemaire,et al. The Basic Biology of PP2A in Hematologic Cells and Malignancies , 2014, Front. Oncol..
[12] Haiyan Xu,et al. Mitogen-Activated Protein Kinase Phosphatase 3 (MKP-3)–Deficient Mice Are Resistant to Diet-Induced Obesity , 2014, Diabetes.
[13] J. Min,et al. Regulation of Acetylation of Histone Deacetylase 2 by p300/CBP-Associated Factor/Histone Deacetylase 5 in the Development of Cardiac Hypertrophy , 2014, Circulation research.
[14] Y. Xing,et al. PR65A Phosphorylation Regulates PP2A Complex Signaling , 2014, PloS one.
[15] S. Batra,et al. Phosphatase: PP2A structural importance, regulation and its aberrant expression in cancer. , 2013, Cancer letters.
[16] J. Davie,et al. Roles of histone deacetylases in epigenetic regulation: emerging paradigms from studies with inhibitors , 2012, Clinical Epigenetics.
[17] C. D. dos Remedios,et al. Protein phosphatase 2A affects myofilament contractility in non-failing but not in failing human myocardium , 2011, Journal of Muscle Research and Cell Motility.
[18] Hyung-Seok Kim,et al. Casein Kinase-2&agr;1 Induces Hypertrophic Response by Phosphorylation of Histone Deacetylase 2 S394 and its Activation in the Heart , 2011, Circulation.
[19] I. Rahman,et al. Protein kinase CK2-mediated phosphorylation of HDAC2 regulates co-repressor formation, deacetylase activity and acetylation of HDAC2 by cigarette smoke and aldehydes. , 2010, Archives of biochemistry and biophysics.
[20] O. Krämer. HDAC2: a critical factor in health and disease. , 2009, Trends in pharmacological sciences.
[21] W-S Xu,et al. Histone deacetylase inhibitors: Potential in cancer therapy , 2009, Journal of cellular biochemistry.
[22] I. Morita,et al. Protein kinase CK2 is a key activator of histone deacetylase in hypoxia‐associated tumors , 2008, International journal of cancer.
[23] X. Chen,et al. Krüppel-like Factor 4 Is Acetylated by p300 and Regulates Gene Transcription via Modulation of Histone Acetylation* , 2007, Journal of Biological Chemistry.
[24] J. Davie,et al. Differential Distribution of Unmodified and Phosphorylated Histone Deacetylase 2 in Chromatin* , 2007, Journal of Biological Chemistry.
[25] Xiaoxia Qi,et al. Histone deacetylases 1 and 2 redundantly regulate cardiac morphogenesis, growth, and contractility. , 2007, Genes & development.
[26] W. Wurst,et al. Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3β activity , 2007, Nature Medicine.
[27] Wenqing Xu,et al. Crystal structure of a protein phosphatase 2A heterotrimeric holoenzyme , 2007, Nature.
[28] Yigong Shi,et al. Structure of the Protein Phosphatase 2A Holoenzyme , 2006, Cell.
[29] Jason A. Lowry,et al. Analysis of the structure and function of the transcriptional coregulator HOP. , 2006, Biochemistry.
[30] D. Dobrev,et al. Role of calcineurin and protein phosphatase-2A in the regulation of phosphatase inhibitor-1 in cardiac myocytes. , 2006, Biochemical and biophysical research communications.
[31] M. Jeong,et al. Inhibition of Histone Deacetylation Blocks Cardiac Hypertrophy Induced by Angiotensin II Infusion and Aortic Banding , 2005, Circulation.
[32] Rick B. Vega,et al. Protein Kinases C and D Mediate Agonist-Dependent Cardiac Hypertrophy through Nuclear Export of Histone Deacetylase 5 , 2004, Molecular and Cellular Biology.
[33] Ulrich Gergs,et al. Overexpression of the Catalytic Subunit of Protein Phosphatase 2A Impairs Cardiac Function* , 2004, Journal of Biological Chemistry.
[34] 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.
[35] E. Seto,et al. Regulation of Histone Deacetylase 2 by Protein Kinase CK2* , 2002, The Journal of Biological Chemistry.
[36] K. Resing,et al. Phosphatase Inhibition Leads to Histone Deacetylases 1 and 2 Phosphorylation and Disruption of Corepressor Interactions* , 2002, The Journal of Biological Chemistry.
[37] K. Ahmed,et al. Joining the cell survival squad: an emerging role for protein kinase CK2. , 2002, Trends in cell biology.
[38] S. Schreiber,et al. Histone Deacetylase 1 Phosphorylation Promotes Enzymatic Activity and Complex Formation* , 2001, The Journal of Biological Chemistry.
[39] E. Olson,et al. Activation of the myocyte enhancer factor-2 transcription factor by calcium/calmodulin-dependent protein kinase-stimulated binding of 14-3-3 to histone deacetylase 5. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[40] R. Hajjar,et al. Role of the stress-activated protein kinases in endothelin-induced cardiomyocyte hypertrophy. , 1998, The Journal of clinical investigation.
[41] Wen‐Ming Yang,et al. Histone Deacetylases Associated with the mSin3 Corepressor Mediate Mad Transcriptional Repression , 1997, Cell.
[42] S. Schreiber,et al. Nuclear Receptor Repression Mediated by a Complex Containing SMRT, mSin3A, and Histone Deacetylase , 1997, Cell.
[43] A. Tajik,et al. The frequency of familial dilated cardiomyopathy in a series of patients with idiopathic dilated cardiomyopathy. , 1992, The New England journal of medicine.
[44] P. Simpson. Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha 1 adrenergic response. , 1983, The Journal of clinical investigation.
[45] K. Reddy,et al. Noncommunicable diseases. , 2013, The New England journal of medicine.
[46] E. Olson,et al. The many roles of histone deacetylases in development and physiology: implications for disease and therapy , 2009, Nature Reviews Genetics.
[47] E. Olson,et al. Cardiac plasticity. , 2008, The New England journal of medicine.
[48] J. Neumann. Altered phosphatase activity in heart failure, influence on Ca2+ movement , 2002, Basic Research in Cardiology.
[49] W. Schmitz,et al. Increased expression of cardiac phosphatases in patients with end-stage heart failure. , 1997, Journal of molecular and cellular cardiology.
[50] W. D. de Jong,et al. The mechanism of N-terminal acetylation of proteins. , 1985, CRC critical reviews in biochemistry.