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Editorial

“Ca2+ signaling and cell death”: The ECS 2013 workshop in Leuven and a tribute to Humbert De Smedt.

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Krebs,  J.
Department of NMR Based Structural Biology, MPI for biophysical chemistry, Max Planck Society;

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Bultynck, G., & Krebs, J. (2014). “Ca2+ signaling and cell death”: The ECS 2013 workshop in Leuven and a tribute to Humbert De Smedt. Biochimica et Biophysica Acta-Molecular Cell Research, 1843(10), 2139-2142. doi:10.1016/j.bbamcr.2014.05.015.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0023-CE62-1
Abstract
In recent years it has become increasingly clear that changes in intracellular Ca2+ homeostasis and dynamics are intimately associated with cell death and survival processes, including proliferation, apoptosis, autophagy, and unfolded protein response. As such, different Ca2+ transport systems, including channels, transporters and pumps, control these processes. Furthermore, dysregulation of intracellular Ca2+-signaling events and remodeling of Ca2+-transport systems and their regulation by associated proteins and other cellular factors seem to be a hall-mark of several diseases, including different cancer types and neurodegenerative diseases. Understanding the molecular mechanisms underlying these events may now permit novel and unprecedented therapeutic strategies to target these Ca2+-transport systems and complexes. In this workshop, attended by more than 100 scientists from 20 different countries, four scientific sessions were organized, dealing with various aspects of Ca2+-signaling in cell survival and cell death. The role of mitochondria, autophagy, ER stress and other factors and their influence on diseases have been discussed. Three contributions were awarded with the best oral communication and best poster prizes by junior scientists. The scientific career, achievements and mentorship of Humbert De Smedt were celebrated at the end of this workshop. We summarize the lectures of this workshop, for details see the contributions of this special issue and the references listed therein.