Gemma Roest
Katholieke Universiteit Leuven
5 Papers
Gemma Roest is an academic researcher from Katholieke Universiteit Leuven. The author has contributed to research in topics: Autophagy & Endoplasmic reticulum. The author has an hindex of 5, co-authored 5 publications.
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Papers
Intracellular Ca(2+) signaling and Ca(2+) microdomains in the control of cell survival, apoptosis and autophagy.
TL;DR: The most recent insights in the emerging role of Ca(2+) signaling in cellular survival by controlling basal mitochondrial bioenergetics and by regulating apoptosis, a mitochondrial process, and autophagy, a lysosomal process, in response to cell damage and cell stress are discussed.
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The ER Stress Inducer l-Azetidine-2-Carboxylic Acid Elevates the Levels of Phospho-eIF2α and of LC3-II in a Ca2+-Dependent Manner
Gemma Roest,Evelien Hesemans,Kirsten Welkenhuyzen,Tomas Luyten,Nikolai Engedal,Geert Bultynck,Jan B. Parys +6 more
TL;DR: The proline analogue l-azetidine-2-carboxylic acid was used to induce ER stress, and its effect on autophagy and Ca2+ homeostasis and it was deduced that activation of the PERK branch is required for the AZC-induced lipidation of LC3.
IP3 Receptor Properties and Function at Membrane Contact Sites.
TL;DR: The most recent insights in the role of Ca2+ signaling in general and of the IP3R in particular are discussed, in the control of basal mitochondrial bioenergetics, apoptosis, and autophagy at the level of inter-organellar contact sites.
IP3 Receptor-Mediated Calcium Signaling and Its Role in Autophagy in Cancer.
TL;DR: The involvement of IP3Rs in the regulation of both autophagy and apoptosis, therefore, directly impact cancer cell biology and contribute to the molecular basis of tumor pathology.
Resveratrol-induced autophagy is dependent on IP3Rs and on cytosolic Ca2.
Tomas Luyten,Kirsten Welkenhuyzen,Gemma Roest,Elzbieta Kania,Liwei Wang,Mart Bittremieux,David I. Yule,Jan B. Parys,Geert Bultynck +8 more
TL;DR: Results reveal that IP3Rs and cytosolic Ca2+ signaling are fundamentally important for driving autophagic flux, not only in response to mTOR inhibition but also in responseto non-canonical autophagy inducers like resveratrol.