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Leonardo H. Travassos

Researcher at Federal University of Rio de Janeiro

Publications -  45
Citations -  15111

Leonardo H. Travassos is an academic researcher from Federal University of Rio de Janeiro. The author has contributed to research in topics: Autophagy & Innate immune system. The author has an hindex of 27, co-authored 39 publications receiving 12493 citations. Previous affiliations of Leonardo H. Travassos include University of Toronto & Rio de Janeiro State 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.
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 (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

Peptidoglycan molecular requirements allowing detection by Nod1 and Nod2.

TL;DR: It is shown here that Nod1 and Nod2 have evolved divergent strategies to achieve PG sensing, and how PG processing and modifications, either by host or bacterial enzymes, may affect innate immune responses.