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Matthew J. LaVoie

Researcher at Brigham and Women's Hospital

Publications -  59
Citations -  13421

Matthew J. LaVoie is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Parkin & Presenilin. The author has an hindex of 39, co-authored 56 publications receiving 12171 citations. Previous affiliations of Matthew J. LaVoie include Harvard University & Icahn School of Medicine at Mount Sinai.

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Journal ArticleDOI

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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PINK1 and Parkin Target Miro for Phosphorylation and Degradation to Arrest Mitochondrial Motility

Xinnan Wang, +11 more
- 11 Nov 2011 - 
TL;DR: It is proposed that PINK1 phosphorylation of substrates triggers the subsequent action of Parkin and the proteasome, and the PINK/Parkin pathway may quarantine damaged mitochondria prior to their clearance.
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γ-Secretase is a membrane protein complex comprised of presenilin, nicastrin, aph-1, and pen-2

W. Taylor Kimberly, +5 more
- 27 May 2003 - 
TL;DR: It is shown that Aph-1 and Pen-2, two recently identified membrane proteins genetically linked to γ-secretase, associate directly with presenilin and nicastrin in the active protease complex and coassemble to form the active enzyme in mammalian cells.
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Dopamine covalently modifies and functionally inactivates parkin

Matthew J. LaVoie, +7 more
- 16 Oct 2005 - 
TL;DR: Dopamine covalently modifies parkin in living dopaminergic cells, a process that increases parkin insolubility and inactivates its E3 ubiquitin ligase function, suggesting a mechanism for the progressive loss of parkin function in dopamine neurons during aging and sporadic Parkinson disease.
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Dopamine Quinone Formation and Protein Modification Associated with the Striatal Neurotoxicity of Methamphetamine: Evidence against a Role for Extracellular Dopamine

Matthew J. LaVoie, +1 more
- 15 Feb 1999 - 
TL;DR: It is likely that dopamine oxidation contributes to methamphetamine-induced toxicity to dopamine terminals, adding support to the role of dopamine and the evidence of oxidative stress in this lesion model.