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Articles 1 - 3 of 3
Full-Text Articles in Medicine and Health Sciences
Research Priorities In Hypertrophic Cardiomyopathy: Report Of A Working Group Of The National Heart, Lung, And Blood Institute., Thomas Force, Robert O Bonow, Steven R Houser, R John Solaro, Ray E Hershberger, Bishow Adhikari, Mark E Anderson, Robin Boineau, Barry J Byrne, Thomas P Cappola, Raghu Kalluri, Martin M Lewinter, Martin S Maron, Jeffery D Molkentin, Steve R Ommen, Michael Regnier, W H Wilson Tang, Rong Tian, Marvin A Konstam, Barry J Maron, Christine E Seidman
Research Priorities In Hypertrophic Cardiomyopathy: Report Of A Working Group Of The National Heart, Lung, And Blood Institute., Thomas Force, Robert O Bonow, Steven R Houser, R John Solaro, Ray E Hershberger, Bishow Adhikari, Mark E Anderson, Robin Boineau, Barry J Byrne, Thomas P Cappola, Raghu Kalluri, Martin M Lewinter, Martin S Maron, Jeffery D Molkentin, Steve R Ommen, Michael Regnier, W H Wilson Tang, Rong Tian, Marvin A Konstam, Barry J Maron, Christine E Seidman
Center for Translational Medicine Faculty Papers
Hypertrophic cardiomyopathy (HCM) is a myocardial disorder characterized by left ventricular (LV) hypertrophy without dilatation and without apparent cause (ie, it occurs in the absence of severe hypertension, aortic stenosis, or other cardiac or systemic diseases that might cause LV hypertrophy). Numerous excellent reviews and consensus documents provide a wealth of additional background.1–8 HCM is the leading cause of sudden death in young people and leads to significant disability in survivors. It is caused by mutations in genes that encode components of the sarcomere. Cardiomyocyte and cardiac hypertrophy, myocyte disarray, interstitial and replacement fibrosis, and dysplastic intramyocardial arterioles characterize the …
Phospholemman: A Novel Cardiac Stress Protein., Joseph Y Cheung, Xue-Qian Zhang, Jianliang Song, Erhe Gao, Joseph E Rabinowitz, Tung O Chan, Jufang Wang
Phospholemman: A Novel Cardiac Stress Protein., Joseph Y Cheung, Xue-Qian Zhang, Jianliang Song, Erhe Gao, Joseph E Rabinowitz, Tung O Chan, Jufang Wang
Center for Translational Medicine Faculty Papers
Phospholemman (PLM), a member of the FXYD family of regulators of ion transport, is a major sarcolemmal substrate for protein kinases A and C in cardiac and skeletal muscle. In the heart, PLM co-localizes and co-immunoprecipitates with Na(+)-K(+)-ATPase, Na(+)/Ca(2+) exchanger, and L-type Ca(2+) channel. Functionally, when phosphorylated at serine(68), PLM stimulates Na(+)-K(+)-ATPase but inhibits Na(+)/Ca(2+) exchanger in cardiac myocytes. In heterologous expression systems, PLM modulates the gating of cardiac L-type Ca(2+) channel. Therefore, PLM occupies a key modulatory role in intracellular Na(+) and Ca(2+) homeostasis and is intimately involved in regulation of excitation-contraction (EC) coupling. Genetic ablation of PLM results …
Gsk-3alpha Directly Regulates Beta-Adrenergic Signaling And The Response Of The Heart To Hemodynamic Stress In Mice., Jibin Zhou, Hind Lal, Xiongwen Chen, Xiying Shang, Jianliang Song, Yingxin Li, Risto Kerkela, Bradley W Doble, Katrina Macaulay, Morgan Decaul, Walter J Koch, John Farber, James Woodgett, Erhe Gao, Thomas Force
Gsk-3alpha Directly Regulates Beta-Adrenergic Signaling And The Response Of The Heart To Hemodynamic Stress In Mice., Jibin Zhou, Hind Lal, Xiongwen Chen, Xiying Shang, Jianliang Song, Yingxin Li, Risto Kerkela, Bradley W Doble, Katrina Macaulay, Morgan Decaul, Walter J Koch, John Farber, James Woodgett, Erhe Gao, Thomas Force
Center for Translational Medicine Faculty Papers
The glycogen synthase kinase-3 (GSK-3) family of serine/threonine kinases consists of 2 highly related isoforms, alpha and beta. Although GSK-3beta has an important role in cardiac development, much remains unknown about the function of either GSK-3 isoform in the postnatal heart. Herein, we present what we believe to be the first studies defining the role of GSK-3alpha in the mouse heart using gene targeting. Gsk3a(-/-) mice over 2 months of age developed progressive cardiomyocyte and cardiac hypertrophy and contractile dysfunction. Following thoracic aortic constriction in young mice, we observed enhanced hypertrophy that rapidly transitioned to ventricular dilatation and contractile dysfunction. …