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Serge N. Manié

Researcher at Claude Bernard University Lyon 1

Publications -  9
Citations -  5462

Serge N. Manié is an academic researcher from Claude Bernard University Lyon 1. The author has contributed to research in topics: Cancer & Cancer research. The author has an hindex of 5, co-authored 5 publications receiving 4917 citations.

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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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The role of the unfolded protein response in cancer progression: From oncogenesis to chemoresistance.

TL;DR: The current knowledge of the UPR during oncogenesis, tumour growth, metastasis and chemoresistance is discussed, with a focus on the role of IRE1, PERK and ATF6.
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Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

Daniel J. Klionsky, +2522 more
- 01 Jan 2016 - 
TL;DR: Author(s): Klionsky, DJ; Abdelmohsen, K; Abe, A; Abedin, MJ; Abeliovich, H; A Frozena, AA; Adachi, H, Adeli, K, Adhihetty, PJ; Adler, SG; Agam, G; Agarwal, R; Aghi, MK; Agnello, M; Agostinis, P; Aguilar, PV; Aguirre-Ghis
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CDYL2 Epigenetically Regulates MIR124 to Control NF-κB/STAT3-Dependent Breast Cancer Cell Plasticity.

TL;DR: It is proposed that CDYL2 contributes to poor prognosis in breast cancer by recruiting G9a and EZH2 to epigenetically repress MIR124 genes, thereby promoting NF-κB and STAT3 signaling, as well as downstream cancer cell plasticity and malignant progression.
Journal ArticleDOI

mTOR inhibitors activate PERK signaling and favor viability of gastrointestinal neuroendocrine cell lines

TL;DR: In GI-NET cell lines, UPR signaling is functional and PERK arm is induced by mTOR inhibition, indicating that mTOR drives a PERK-dependent survival pathway, and the crosstalk between mTOR and UPR might contribute to the resistance to mTOR inhibitors and could be targeted by m TOR and PERk inhibitors in combination therapy.