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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.

Papers
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Journal ArticleDOI

Expression of Lewy body protein septin 4 in postmortem brain of Parkinson's disease and control subjects.

TL;DR: Similar signal expression patterns and parallel accumulation of SEPT4 and α‐synuclein in well‐characterized postmortem PD brain are presented for the first time.
Journal ArticleDOI

Fusigenic Liposome-mediated DNA Transfer into Cardiac Myocytes

TL;DR: HVJ/liposome-mediated transfer is efficient for the transfection of both oligonucleotides and plasmids into cardiac myocytes both in vitro and in vivo, and may provide a new tool for the investigation of cardiac myocyte biology and disease.
Journal ArticleDOI

Reversal of pathological cardiac hypertrophy via the MEF2-coregulator interface.

TL;DR: It is concluded thatMEF2 acetylation is required for development and maintenance of pathological cardiac hypertrophy, and that blocking MEF2acetylation can permit recovery from hypertrotrophy without impairing physiologic adaptation.
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Acidosis Regulates the Stability, Hydrophobicity, and Activity of the BH3-Only Protein Bnip3

TL;DR: It is reported that acidic pH mediates increased half-lives of Bnip3 dimers and monomers as well as that of a faster-migrating fragment (>10-) and confers protection against degradation by protease and demonstrates a pH-sensitive shift in the stability and apparent hydrophobicity of BNip3 monomers that correlates closely with membrane binding and function.
Patent

Tissue specific hypoxia regulated therapeutic constructs

TL;DR: Methods and compositions relating to chimeric genes containing a tissue-specific promoter and a hypoxia response enhancer element, both of which are operably linked to a selected gene, such as a reporter gene, therapeutic gene (e.g., bcl-2, NOS, catalase and SOD), or deleterious gene are disclosed.