DUSP6 (MKP3) Null Mice Show Enhanced ERK1/2 Phosphorylation at Baseline and Increased Myocyte Proliferation in the Heart Affecting Disease Susceptibility
Open Access
- 1 November 2008
- journal article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 283 (45), 31246-31255
- https://doi.org/10.1074/jbc.m806085200
Abstract
No abstract availableKeywords
This publication has 51 references indexed in Scilit:
- Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failureJournal of Clinical Investigation, 2007
- Genetic inhibition of cardiac ERK1/2 promotes stress-induced apoptosis and heart failure but has no effect on hypertrophy in vivoProceedings of the National Academy of Sciences, 2007
- The ERK1/2 mitogen-activated protein kinase pathway as a master regulator of the G1- to S-phase transitionOncogene, 2007
- ERK2 but not ERK1 plays a key role in hepatocyte replicationHepatology, 2007
- Dusp6(Mkp3) is a negative feedback regulator of FGF-stimulated ERK signaling during mouse developmentDevelopment, 2007
- Age-Dependent Effect of Myostatin Blockade on Disease Severity in a Murine Model of Limb-Girdle Muscular DystrophyThe American Journal of Pathology, 2006
- Cardiac-Specific Deletion of Gata4 Reveals Its Requirement for Hypertrophy, Compensation, and Myocyte ViabilityCirculation Research, 2006
- Protein phosphatase 2A-mediated cross-talk between p38 MAPK and ERK in apoptosis of cardiac myocytesAmerican Journal of Physiology-Heart and Circulatory Physiology, 2004
- A Bipartite Mechanism for ERK2 Recognition by Its Cognate Regulators and SubstratesPublished by Elsevier ,2003
- Prognostic Implications of Echocardiographically Determined Left Ventricular Mass in the Framingham Heart StudyNew England Journal of Medicine, 1990