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Thomas M. Durcan

Researcher at Montreal Neurological Institute and Hospital

Publications -  108
Citations -  7351

Thomas M. Durcan is an academic researcher from Montreal Neurological Institute and Hospital. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 19, co-authored 73 publications receiving 6257 citations. Previous affiliations of Thomas M. Durcan include University of Notre Dame & McGill University.

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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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The three ‘P’s of mitophagy: PARKIN, PINK1, and post-translational modifications

TL;DR: It is evident that further insight into how PTMs regulate the PINK1-PARKIN pathway will be critical for the understanding of mitochondrial quality control.
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USP8 regulates mitophagy by removing K6‐linked ubiquitin conjugates from parkin

TL;DR: It is reported here that USP8/UBPY, a deubiquitinating enzyme not previously implicated in mitochondrial quality control, is critical for parkin‐mediated mitophagy and uncovers a novel role forUSP8‐mediated deUBiquitination of K6‐linked ubiquitin conjugates from parkin in mitochondrialquality control.
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Mfn2 ubiquitination by PINK1/parkin gates the p97-dependent release of ER from mitochondria to drive mitophagy

TL;DR: The mechanism by which Mfn2, a mitochondria-ER tether, gates the autophagic turnover of mitochondria by PINK1 and parkin is described, which suppresses mitophagy and describes a parkin-/PINK1-dependent mechanism that regulates the destruction of mitochondrial-ER contact sites.
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The machado-joseph disease-associated mutant form of ataxin-3 regulates parkin ubiquitination and stability

TL;DR: Parkin, an E3 ubiquitin-ligase responsible for a common familial form of Parkinson's disease, is identified as a novel ataxin-3 binding partner and promoted via the autophagy pathway, raising the intriguing possibility that increased turnover of parkin may contribute to the pathogenesis of MJD and help explain some of its parkinsonian features.