c-Jun N-Terminal Kinase Activation Mediates Downregulation of Connexin43 in Cardiomyocytes
- 4 October 2002
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 91 (7) , 640-647
- https://doi.org/10.1161/01.res.0000035854.11082.01
Abstract
Loss of gap junctions and impaired intercellular communication are characteristic features of pathological remodeling in heart failure as a result of stress or injury, yet the underlying regulatory...Keywords
This publication has 29 references indexed in Scilit:
- The role of myocardial gap junctions in electrical conduction and arrhythmogenesisCardiovascular Pathology, 2001
- Mechanical stress-induced cardiac hypertrophy: mechanisms and signal transduction pathwaysCardiovascular Research, 2000
- Advances in the molecular mechanisms of heart failureCurrent Opinion in Cardiology, 2000
- Heterotrimeric G proteins in heart diseaseCanadian Journal of Physiology and Pharmacology, 2000
- Wnt-1 regulation of connexin43 in cardiac myocytesJournal of Clinical Investigation, 2000
- DOWNREGULATION OF CONNEXIN 43 GENE EXPRESSION IN RAT HEART DURING INFLAMMATION. THE ROLE OF TUMOUR NECROSIS FACTORCytokine, 1999
- Chronic Pressure Overload Cardiac Hypertrophy and Failure in Guinea Pigs: III. Intercalated Disc RemodelingJournal of Molecular and Cellular Cardiology, 1999
- Heterogeneous Loss of Connexin43 Protein in Ischemic Dog HeartsJournal of Cardiovascular Electrophysiology, 1999
- Cellular mechanisms of cardiac hypertrophyJournal of Molecular Medicine, 1998
- Regulation of mitogen-activated protein kinase cascades in the heartAdvances in Enzyme Regulation, 1998