| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10802319 | Biochimica et Biophysica Acta (BBA) - Molecular Cell Research | 2013 | 15 Pages |
Abstract
⺠Gap junctions (GJs) provide a direct pathway to expand cell death. ⺠IP3 transfer through GJs is crucial to provoke bystander apoptosis. ⺠Additional factors are necessary to convert IP3 into a toxic molecule. ⺠Various GJ-permeable factors could sensitize cells to IP3-induced apoptosis. ⺠Intercellular IP3/Ca2 + signaling can play a role in different pathologies.
Keywords
PTPPKGBI-1VDACCytCIP3RGRPRyRPLCGPCRMEFsIP3pKaANTMAMMCUIICRBcl-2cGMPmitochondrial Ca2 + uniporterOMMN-terminalIP4cAMPG-protein-coupled receptorinositol 1,3,4,5-tetrakisphosphateinositol 1,4,5-trisphosphateROS[Ca2 +]iAdenosine TriphosphateATPCyclic adenosine monophosphateIntercellular communicationPermeability transition poreimmadenine nucleotide translocatorC-terminaltumor necrosis factor-αinner mitochondrial membraneBBBDamscytochrome cendoplasmic reticulumouter mitochondrial membranegap junctionTNF-αphospholipase CSERCAB-cell lymphoma-2Blood-brain barrierCell deathmouse embryonic fibroblastscyclic guanosine monophosphateknockoutHemichannelMolecular weightPresenilinsglucose-regulated proteinprotein kinase Aprotein kinase Gvoltage-dependent anion channelCalciumconnexinReactive oxygen speciesInositol 1,4,5-trisphosphate receptorRyanodine receptor
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Authors
Elke Decrock, Marijke De Bock, Nan Wang, Ashish K. Gadicherla, Mélissa Bol, Tinneke Delvaeye, Peter Vandenabeele, Mathieu Vinken, Geert Bultynck, Dmitri V. Krysko, Luc Leybaert,