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Paolo Paganetti

Researcher at University of Lugano

Publications -  111
Citations -  18108

Paolo Paganetti is an academic researcher from University of Lugano. The author has contributed to research in topics: Amyloid precursor protein & Huntingtin. The author has an hindex of 45, co-authored 104 publications receiving 16123 citations. Previous affiliations of Paolo Paganetti include University of Zurich & Howard Hughes Medical 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

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

Two amyloid precursor protein transgenic mouse models with Alzheimer disease-like pathology

Christine Sturchler-Pierrat, +15 more
- 25 Nov 1997 - 
TL;DR: These mice resemble major features of AD pathology and suggest a central role of A beta in the pathogenesis of the disease.
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Exogenous induction of cerebral beta-amyloidogenesis is governed by agent and host.

Melanie Meyer-Luehmann, +19 more
- 22 Sep 2006 - 
TL;DR: The phenotype of the exogenously induced amyloidosis depended on both the host and the source of the agent, suggesting the existence of polymorphic Aβ strains with varying biological activities reminiscent of prion strains.
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Role of EDEM in the release of misfolded glycoproteins from the calnexin cycle.

Maurizio Molinari, +4 more
- 28 Feb 2003 - 
TL;DR: The authors showed that EDEM overexpression resulted in faster release of folding-incompetent proteins from the calnexin cycle and earlier onset of degradation, whereas EDEM down-regulation prolonged folding attempts and delayed ERAD.