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Caroline Mauvezin

Researcher at University of Barcelona

Publications -  26
Citations -  8004

Caroline Mauvezin is an academic researcher from University of Barcelona. The author has contributed to research in topics: Autophagy & Biology. The author has an hindex of 14, co-authored 21 publications receiving 6323 citations. Previous affiliations of Caroline Mauvezin include University of Minnesota & Carlos III Health Institute.

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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 (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.
Journal ArticleDOI

Bafilomycin A1 disrupts autophagic flux by inhibiting both V-ATPase-dependent acidification and Ca-P60A/SERCA-dependent autophagosome-lysosome fusion

Caroline Mauvezin, +1 more
- 08 Jul 2015 - 
TL;DR: Bafilomycin A1 disrupts autophagic flux by independently inhibiting V-ATPase-dependent acidification and Ca-P60A/SERCA-dependent autophagosome-lysosome fusion.
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Mfn2 modulates the UPR and mitochondrial function via repression of PERK.

Juan Pablo Muñoz, +21 more
- 28 Aug 2013 - 
TL;DR: The data indicate that Mfn2 is an upstream modulator of PERK, and Mfn1 loss‐of‐function reveals that PERK is a key regulator of mitochondrial morphology and function.
Journal ArticleDOI

Autophagosome-lysosome fusion is independent of V-ATPase-mediated acidification.

Caroline Mauvezin, +3 more
- 11 May 2015 - 
TL;DR: It is shown that loss of V-ATPase subunits in the Drosophila fat body causes an accumulation of non-functional lysosomes, leading to a block in autophagic flux, and that BafilomycinA1 inhibits fusion independent of its effect on lysOSomal pH.