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Helena L. A. Vieira

Researcher at Universidade Nova de Lisboa

Publications -  90
Citations -  11940

Helena L. A. Vieira is an academic researcher from Universidade Nova de Lisboa. The author has contributed to research in topics: Mitochondrion & Programmed cell death. The author has an hindex of 37, co-authored 84 publications receiving 10997 citations. Previous affiliations of Helena L. A. Vieira include Institut Gustave Roussy & University of Technology of Compiègne.

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Journal ArticleDOI

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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Bax and Adenine Nucleotide Translocator Cooperate in the Mitochondrial Control of Apoptosis

Isabel Marzo, +10 more
- 25 Sep 1998 - 
TL;DR: The proapoptotic molecule Bax and the constitutive mitochondrial protein ANT cooperate within the PTPC to increase mitochondrial membrane permeability and to trigger cell death.
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The HIV-1 Viral Protein R Induces Apoptosis via a Direct Effect on the Mitochondrial Permeability Transition Pore

Etienne Jacotot, +17 more
- 03 Jan 2000 - 
TL;DR: Coincubation of purified organelles revealed that nuclear apoptosis is only induced by Vpr when mitochondria are present yet can be abolished by PTPC inhibitors, suggesting that Vpr induces apoptosis via a direct effect on the mitochondrial PTPC.
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Mitochondrial membrane permeabilization is a critical step of lysosome-initiated apoptosis induced by hydroxychloroquine

Patricia Boya, +7 more
- 19 Jun 2003 - 
TL;DR: It is shown that hydroxychloroquine induces signs of lysosomal membrane permeabilization (LMP), and that Bax/Bak-dependent MMP is a critical step of LMP-induced cell death.
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Bcl-2 and Bax regulate the channel activity of the mitochondrial adenine nucleotide translocator.

Catherine Brenner, +10 more
- 20 Jan 2000 - 
TL;DR: Experimental data are compatible with a ménage à trois model of mitochondrial apoptosis regulation in which ANT, the likely pore forming protein within the PTPC, interacts with Bax or Bcl-2 which influence its pore formation potential in opposing manners.