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Gerald W. Dorn

Researcher at Washington University in St. Louis

Publications -  191
Citations -  24128

Gerald W. Dorn is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Mitochondrion & mitochondrial fusion. The author has an hindex of 71, co-authored 173 publications receiving 20553 citations. Previous affiliations of Gerald W. Dorn include University of Cincinnati.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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PINK1- Phosphorylated Mitofusin 2 is a Parkin Receptor for Culling Damaged Mitochondria

TL;DR: It is shown that the mitochondrial outer membrane guanosine triphosphatase mitofusin (Mfn) 2 mediates Parkin recruitment to damaged mitochondria and is required for quality control of cardiac mitochondria.
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Cytoplasmic Signaling Pathways That Regulate Cardiac Hypertrophy

TL;DR: This review discusses the rapidly progressing field of cardiomyocyte signal transduction and the regulation of the hypertrophic response, which suggests an emerging paradigm whereby multiple pathways operate in concert to orchestrate a hypertrophicresponse.
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Enhanced Gαq signaling: A common pathway mediates cardiac hypertrophy and apoptotic heart failure

TL;DR: A mechanism in which moderate levels of Gq signaling stimulate cardiac hypertrophy whereas high level Gq activation results in cardiomyocyte apoptosis is suggested, which is a plausible mechanism for the progression of compensatedhypertrophy to decompensated heart failure.