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Marie-Josée Boucher

Researcher at Université de Sherbrooke

Publications -  25
Citations -  6825

Marie-Josée Boucher is an academic researcher from Université de Sherbrooke. The author has contributed to research in topics: MAPK/ERK pathway & Apoptosis. The author has an hindex of 18, co-authored 23 publications receiving 6299 citations. Previous affiliations of Marie-Josée Boucher include Faculté de médecine – Université de Sherbrooke & Umeå University.

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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.
Journal ArticleDOI

MEK/ERK signaling pathway regulates the expression of Bcl‐2, Bcl‐XL, and Mcl‐1 and promotes survival of human pancreatic cancer cells

Marie-Josée Boucher, +5 more
- 01 Dec 2000 - 
TL;DR: The data suggest that activation of the ERK pathway functions to protect pancreatic tumor cells from apoptosis as well as to regulate their progression in the cell cycle.
Journal ArticleDOI

Phosphatidylinositol 3-kinase controls human intestinal epithelial cell differentiation by promoting adherens junction assembly and p38 MAPK activation.

Patrick Laprise, +5 more
- 08 Mar 2002 - 
TL;DR: Results indicate that PI3K promotes assembly of adherens junctions, which, in turn, control p38 MAPK activation and enterocyte differentiation.
Journal ArticleDOI

Glycogen synthase kinase-3 (GSK3) inhibition induces prosurvival autophagic signals in human pancreatic cancer cells.

Benoit Marchand, +4 more
- 27 Feb 2015 - 
TL;DR: It is shown that GSK3 inhibition induces prosurvival signals through increased activity of the autophagy/lysosomal network, and a predominant nuclear localization of TFEB is unveiled in fully fed pancreatic cancer cells, whereas a reduction in T FEB expression significantly impairs their capacity for growth in an anchorage-independent manner.
Journal ArticleDOI

Phosphorylation Marks IPF1/PDX1 Protein for Degradation by Glycogen Synthase Kinase 3-dependent Mechanisms

Marie-Josée Boucher, +3 more
- 10 Mar 2006 - 
TL;DR: It is shown that a minor portion of IPF1/PDX1 is phosphorylated on serine 61 and/or serine 66 in pancreatic β-cells, and evidence that GSK3 activity participates in oxidative stress-induced effects onβ-cells is provided.