Journal
FEBS LETTERS
Volume 588, Issue 17, Pages 3062-3067Publisher
WILEY
DOI: 10.1016/j.febslet.2014.05.065
Keywords
Ischemia-reperfusion injury (IRI); Unfolded protein response (UPR); Endothelial cells (EC); Murine embryonic cells (MEC); Probabilistic polynomial dynamical systems (PDS); Gene regulatory networks (GRN)
Funding
- MESR
- Ecole de l'INSERM-Liliane Bet-tencourt
- EPSRC [EP/G055181/1]
- Wellcome Trust [084812/Z/08/Z, 093764/Z/10/Z]
- Engineering and Physical Sciences Research Council [EP/G055181/1] Funding Source: researchfish
- EPSRC [EP/G055181/1] Funding Source: UKRI
- Wellcome Trust [093764/Z/10/Z, 084812/Z/08/Z] Funding Source: Wellcome Trust
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The unfolded protein response (UPR) - the endoplasmic reticulum stress response - is found in various pathologies including ischemia-reperfusion injury (IRI). However, its role during IRI is still unclear. Here, by combining two different bioinformatical methods - a method based on ordinary differential equations (Time Series Network Inference) and an algebraic method (probabilistic polynomial dynamical systems) - we identified the IRE1 alpha-XBP1 and the ATF6 pathways as the main UPR effectors involved in cell's adaptation to IRI. We validated these findings experimentally by assessing the impact of their knock-out and knock-down on cell survival during IRI. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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