Title: IP3 receptor-binding partners in cell-death mechanisms
Authors: Kiviluoto, Santeri
Akl, Haidar
Vervliet, Tim
Bultynck, Geert
Parys, Jan
Missiaen, Ludwig
De Smedt, Humbert # ×
Issue Date: Mar-2012
Publisher: Wiley
Series Title: Wiley Interdisciplinary Reviews: Membrane Transport and Signaling vol:1 pages:201-210
Abstract: A multiprotein complex, which involves the inositol 1,4,5-trisphosphate receptor (IP3R) on the endoplasmic reticulum (ER) and the voltage-dependent anion channel (VDAC) on the outer mitochondrial membrane (OMM) along with multiple other IP3R-binding partners, is responsible for a privileged and tightly controlled transfer of Ca2+ from the ER to the mitochondria. To stimulate cell metabolism and survival, the mitochondrial Ca2+ level [Ca2+]mit has to be kept within a small physiological range. Decreased or increased Ca2+ fluxes result in an adaptive cellular response involving, respectively, autophagy to meet cellular
energy demands or mitophagy to remove damaged mitochondria. Failure of these autophagic responses eventually leads to initiation of cell death. Malfunction of the interaction between the IP3R and its binding partners may have pathological consequences. In cancer cells, such malfunctions lead to an inability to generate large proapoptotic mitochondrial Ca2+ signals. In familial Alzheimer’s disease (FAD) and Huntington’s disease (HD) on the other hand, exaggerated Ca2+ signals may result in neuronal damage and cell death.
ISSN: 2190-4618
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Molecular and Cellular Signaling
× corresponding author
# (joint) last author

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