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Evripidis Gavathiotis

Researcher at Albert Einstein College of Medicine

Publications -  98
Citations -  15472

Evripidis Gavathiotis is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Apoptosis & Autophagy. The author has an hindex of 37, co-authored 83 publications receiving 11243 citations. Previous affiliations of Evripidis Gavathiotis include Rockefeller University & University of Nottingham.

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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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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Lorenzo Galluzzi, +186 more
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
Journal Article

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Lorenzo Galluzzi, +168 more
- 01 Jan 2018 - 
TL;DR: An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed.
Journal ArticleDOI

BAX activation is initiated at a novel interaction site

TL;DR: It is demonstrated by NMR analysis that BIM SAHB binds BAX at an interaction site that is distinct from the canonical binding groove characterized for anti-apoptotic proteins, establishing a new target for therapeutic modulation of apoptosis.
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BH3-Triggered Structural Reorganization Drives the Activation of Proapoptotic BAX

TL;DR: This work delineates by NMR and biochemical methods the essential allosteric conformational changes that transform ligand-triggered BAX into a fully activated monomer capable of propagating its own activation.