N
Nanette H. Bishopric
Researcher at University of Miami
Publications - 111
Citations - 7752
Nanette H. Bishopric is an academic researcher from University of Miami. The author has contributed to research in topics: Myocyte & Apoptosis. The author has an hindex of 44, co-authored 109 publications receiving 7371 citations. Previous affiliations of Nanette H. Bishopric include United States Department of Veterans Affairs & University of California, San Francisco.
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PI3K/mTOR inhibition can impair tumor invasion and metastasis in vivo despite a lack of antiproliferative action in vitro: implications for targeted therapy
Seth A. Wander,Dekuang Zhao,Alexandra H. Besser,Feng Hong,Jianqin Wei,Tan A. Ince,Clara Milikowski,Nanette H. Bishopric,Andy J. Minn,Chad J. Creighton,Joyce M. Slingerland +10 more
TL;DR: Novel PI3K/mTOR inhibitors may oppose tumor metastasis independent of their growth inhibitory effects, providing a rationale for clinical investigation of PI3k/m TOR inhibitors in settings to prevent micrometastasis.
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Coxsackie and Adenovirus Receptor Is a Modifier of Cardiac Conduction and Arrhythmia Vulnerability in the Setting of Myocardial Ischemia
Roos F. Marsman,Connie R. Bezzina,Fabian Freiberg,Arie O. Verkerk,Michiel E. Adriaens,Svitlana Podliesna,Chen Chen,Bettina Purfürst,Bastian Spallek,Tamara T. Koopmann,István Baczkó,Cristobal G. dos Remedios,Alfred L. George,Nanette H. Bishopric,Elisabeth M. Lodder,Jacques M.T. de Bakker,Robert Fischer,Ruben Coronel,Arthur A.M. Wilde,Michael Gotthardt,Carol Ann Remme +20 more
TL;DR: CAR is a novel modifier of ventricular conduction and arrhythmia vulnerability in the setting of myocardial ischemia and may constitute future targets for risk stratification of potentially lethal ventricular arrhythmias in patients with coronary artery disease.
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Molecular regulation of cardiac myocyte adaptations to chronic hypoxia.
TL;DR: It is proposed that cAMP may regulate some short and long-term adaptations of cardiac myocytes to chronic hypoxia and be associated with a pronounced decrease in the rate of calcium efflux during muscle relaxation.
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Analysis for Genetic Modifiers of Disease Severity in Patients with Long QT Syndrome Type 2
Iris C. R. M. Kolder,Michael W.T. Tanck,Pieter G. Postema,Julien Barc,Moritz F. Sinner,Sven Zumhagen,Anja Husemann,Birgit Stallmeyer,Tamara T. Koopmann,Nynke Hofman,A. Pfeufer,Peter Lichtner,Thomas Meitinger,Britt M. Beckmann,Robert J. Myerburg,Nanette H. Bishopric,Dan M. Roden,Stefan Kääb,Arthur A.M. Wilde,Jean-Jacques Schott,Eric Schulze-Bahr,Connie R. Bezzina +21 more
TL;DR: Unexpected large effects of NOS1AP SNPs on the QTc-interval and a trend for effects on risk of cardiac events are uncovered and for the first time, common genetic variation at KCNQ1 is linked with risk of long-QT syndrome.
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Adenovirus E1A inhibits cardiac myocyte-specific gene expression through its amino terminus.
TL;DR: It is concluded that cardiac-specific and general promoter inhibition by E1A occurs by distinct mechanisms and that heart-specific gene expression is modulated by cellular factors interacting with the E 1A p300/CBP-binding domain.