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BethAnn McLaughlin

Researcher at Vanderbilt University

Publications -  58
Citations -  8284

BethAnn McLaughlin is an academic researcher from Vanderbilt University. The author has contributed to research in topics: Neuroprotection & Neurodegeneration. The author has an hindex of 28, co-authored 58 publications receiving 6318 citations. Previous affiliations of BethAnn McLaughlin include Allen Institute for Brain Science & Vanderbilt University Medical Center.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy 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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Induction of neuronal apoptosis by thiol oxidation: putative role of intracellular zinc release.

Elias Aizenman, +5 more
- 04 Jan 2002 - 
TL;DR: It is reported that brief exposure to DTDP triggers apoptotic cell death in cultured neurons, detected by the presence of both DNA laddering and asymmetric chromatin formation.
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Caspase 3 activation is essential for neuroprotection in preconditioning.

BethAnn McLaughlin, +6 more
- 21 Jan 2003 - 
TL;DR: A neuroprotective pathway where events normally associated with apoptotic cell death are critical for cell survival is outlined, and agents that blocked preconditioning also attenuated induction of HSP 70.
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Toxicity of dopamine to striatal neurons in vitro and potentiation of cell death by a mitochondrial inhibitor.

BethAnn McLaughlin, +3 more
- 13 Nov 2002 - 
TL;DR: The results suggest that dopamine causes primarily apoptotic death of striatal neurons in culture without damaging cells by an early adverse action on oxidative phosphorylation, however, when combined with minimal inhibition of mitochondrial function, dopamine neurotoxicity is markedly enhanced.