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The Role of Cardiac Side Population Cells in Cardiac RegenerationThe transcription factor GATA-6 regulates pathological cardiac hypertrophyThe mitochondrial Na+/Ca2+ exchanger is essential for Ca2+ homeostasis and viability.c-kit+ cells minimally contribute cardiomyocytes to the heartParsing the roles of the transcription factors GATA-4 and GATA-6 in the adult cardiac hypertrophic response.Polymorphisms in the RAS and cardiac function.Serine 105 phosphorylation of transcription factor GATA4 is necessary for stress-induced cardiac hypertrophy in vivo.Placental growth factor regulates cardiac adaptation and hypertrophy through a paracrine mechanism.108th ENMC International Workshop, 3rd Workshop of the MYO-CLUSTER project: EUROMEN, 7th International Emery-Dreifuss Muscular Dystrophy (EDMD) Workshop, 13-15 September 2002, Naarden, The Netherlands.An emerging consensus on cardiac regeneration.Genetic Analysis of Connective Tissue Growth Factor as an Effector of Transforming Growth Factor β Signaling and Cardiac Remodeling.STIM1 elevation in the heart results in aberrant Ca²⁺ handling and cardiomyopathyDUSP8 Regulates Cardiac Ventricular Remodeling by Altering ERK1/2 Signaling.Differential expression of embryonic epicardial progenitor markers and localization of cardiac fibrosis in adult ischemic injury and hypertensive heart disease.Unraveling the complexities of cardiac remodeling and hypertrophy - high-content screening and computational modelingUnrestrained p38 MAPK activation in Dusp1/4 double-null mice induces cardiomyopathy.BEX1 is an RNA-dependent mediator of cardiomyopathy.Pathologic Stimulus Determines Lineage Commitment of Cardiac C-kit+ Cells.Often seen but rarely recognised: cardiac complications of lamin A/C mutations.Primary prevention of sudden death in patients with lamin A/C gene mutations.Cardiac c-Kit Biology Revealed by Inducible Transgenesis.Development of a Click-Chemistry Reagent Compatible with Mass Cytometry.Chromatin remodeling permits cardiac hypertrophy to develop.Most of the Dust Has Settled: cKit+ Progenitor Cells Are an Irrelevant Source of Cardiac Myocytes In Vivo.Severe Myocardial Fibrosis Caused by a Deletion of the 5’ End of the Lamin A/C Genevan Berlo et al. replyA conserved HH-Gli1-Mycn network regulates heart regeneration from newt to humanA Small Peptide Ac-SDKP Inhibits Radiation-Induced CardiomyopathyA-type lamins are essential for TGF-beta1 induced PP2A to dephosphorylate transcription factors
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hulumtues
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Jop H van Berlo
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Jop H van Berlo
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0000-0001-9229-4429