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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Journal ArticleDOI
Quantitative Control of Adaptive Cardiac Hypertrophy by Acetyltransferase p300
Jian Qin Wei,Lina A. Shehadeh,James Mitrani,Monica Pessanha,Tatiana I. Slepak,Keith A. Webster,Nanette H. Bishopric +6 more
TL;DR: Small increments in p300 are necessary and sufficient to drive myocardial hypertrophy, possibly through acetylation of MEF2 and upstream of signals promoting phosphorylation or nuclear export of histone deacetylases.
Journal ArticleDOI
Adrenergic regulation of the skeletal alpha-actin gene promoter during myocardial cell hypertrophy.
Nanette H. Bishopric,L Kedes +1 more
TL;DR: It is reported that NE positively regulates the human skeletal alpha-actin gene promoter in transiently transfected neonatal rat cardiac myocytes, and factors related to cell communication may influence the pathways mediating NE-regulated gene transcription during cardiac myocyte hypertrophy.
Journal ArticleDOI
Repression of miR-142 by p300 and MAPK is required for survival signalling via gp130 during adaptive hypertrophy
TL;DR: It is shown that both miRNA‐142‐3p and ‐5p are repressed by serum‐derived growth factors in cultured cardiac myocytes, in models of cardiac hypertrophy in vivo and in human cardiomyopathy.
Journal ArticleDOI
BNip3 and signal-specific programmed death in the heart.
TL;DR: In this article, a review of the specific role of BNip3 in cardiac myocyte apoptotic signaling during ischemia is presented. But this review is limited to the BH3-2 family of cell death-regulating factors.
Journal ArticleDOI
Mitochondrial signals initiate the activation of c-Jun N-terminal kinase (JNK) by hypoxia-reoxygenation
Christopher J. Dougherty,Lori A. Kubasiak,Donna P. Frazier,Huifang Li,Wen Cheng Xiong,Nanette H. Bishopric,Keith A. Webster +6 more
TL;DR: The signaling pathway is unique for the reoxygenation stimulus and provides a frame‐ work for other non‐receptor‐mediated pathways of MAPK activation in this model of ischemia‐reperfusion.