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David Sulzer

Researcher at Columbia University

Publications -  265
Citations -  44444

David Sulzer is an academic researcher from Columbia University. The author has contributed to research in topics: Dopamine & Dopaminergic. The author has an hindex of 88, co-authored 240 publications receiving 38879 citations. Previous affiliations of David Sulzer include Columbia University Medical Center & University of York.

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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.
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.
Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

Daniel J. Klionsky, +235 more
- 16 Feb 2008 - 
TL;DR: A set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes are presented.
Journal ArticleDOI

Impaired degradation of mutant α-synuclein by chaperone-mediated autophagy

TL;DR: It is found that wild-type α-synuclein was selectively translocated into lysosomes for degradation by the chaperone-mediated autophagy pathway, which may underlie the toxic gain-of-function by the A53T and A30P mutants.