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Title[redir]:
Role of the c subunit of the FO AT ... | Article | H1 Connect
Description:
The term "mitochondrial permeability transition" (MPT) refers to an abrupt increase in the permeability of the inner mitochondrial membrane to low molecula

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Topics {✒️}

mitochondrial-dependent cell death permeability transition pore mitochondrial permeability transition fo atp synthase cell death intrinsic mitochondrial constituents mitochondrial foatp synthase mitochondrial megachannel resides release mtdna fragments adp/atp translocator endoplasmic reticulum stress relevant contribution mitochondrial dna cell cycle cell signaling mitochondrial structure atpase c-subunit cancer faculty opinions molecular composition finding dimers mitochondrial physiology mitochondrial membrane mitochondrial matrix pinton mitochondrial functions foatp synthase mitochondrial cristae regulates respiration h1 company latest recommendation 2016 latest recommendation crucial responses finding doctors search article brings intensive investigation remained obscure abrupt permeabilization massive influx extracellular release utmost importance ensuing collapse cells deleted remarkably resistant manipulations aimed vivo proof knockout models kokoszka je baines cp

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ScholarlyArticle:
      context:https://schema.org
      headline:Role of the c subunit of the FO ATP synthase in mitochondrial permeability transition.
      abstract:The term "mitochondrial permeability transition" (MPT) refers to an abrupt increase in the permeability of the inner mitochondrial membrane to low molecular weight solutes. Due to osmotic forces, MPT is paralleled by a massive influx of water into the mitochondrial matrix, eventually leading to the structural collapse of the organelle. Thus, MPT can initiate mitochondrial outer membrane permeabilization (MOMP), promoting the activation of the apoptotic caspase cascade as well as of caspase-independent cell death mechanisms. MPT appears to be mediated by the opening of the so-called "permeability transition pore complex" (PTPC), a poorly characterized and versatile supramolecular entity assembled at the junctions between the inner and outer mitochondrial membranes. In spite of considerable experimental efforts, the precise molecular composition of the PTPC remains obscure and only one of its constituents, cyclophilin D (CYPD), has been ascribed with a crucial role in the regulation of cell death. Conversely, the results of genetic experiments indicate that other major components of the PTPC, such as voltage-dependent anion channel (VDAC) and adenine nucleotide translocase (ANT), are dispensable for MPT-driven MOMP. Here, we demonstrate that the c subunit of the FO ATP synthase is required for MPT, mitochondrial fragmentation and cell death as induced by cytosolic calcium overload and oxidative stress in both glycolytic and respiratory cell models. Our results strongly suggest that, similar to CYPD, the c subunit of the FO ATP synthase constitutes a critical component of the PTPC.
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         id:https://connect.h1.co/article/717988210
WebPage:
      id:https://connect.h1.co/article/717988210

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