The voltage-dependent anion channel is the target for a new class of inhibitors of the mitochondrial permeability transition pore.
Cesura Andrea,Emmanuel Pinard,Robert Schubenel,Valerie Goetschy,Arno Friedlein,Hanno Langen,Peter Polčic,Michael Forte,Paolo Bernardi,John A. Kemp +9 more
TLDR
Results obtained provide direct evidence that VDAC1 is a component of this mitochondrial pore, and a new class of inhibitors of the PTP and on the identification of their molecular target are reported.About:
This article is published in Journal of Biological Chemistry.The article was published on 2003-12-12 and is currently open access. It has received 114 citations till now. The article focuses on the topics: VDAC1 & Affinity labeling.read more
Citations
More filters
Journal ArticleDOI
Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death.
Christopher P. Baines,Robert A. Kaiser,Tatiana Sheiko,William J. Craigen,Jeffery D. Molkentin +4 more
TL;DR: The results indicate that Vdacs are dispensable for both MPT and Bcl-2 family member-driven cell death, as shown in mice with Vdac-deficient mitochondria.
Journal ArticleDOI
What is the mitochondrial permeability transition pore
TL;DR: In this paper, it was shown that the mitochondrial permeability transition pore (MPTP) is a major cause of reperfusion injury and an effective target for cardioprotection.
Journal ArticleDOI
The mitochondrial permeability transition from in vitro artifact to disease target
Paolo Bernardi,Alexandra Krauskopf,Emy Basso,Valeria Petronilli,Elizabeth Blalchy‐Dyson,Fabio Di Lisa,Michael Forte +6 more
TL;DR: Evidence indicating that the permeability transition pore plays a role in pathophysiology, with specific emphasis on in vivo models of disease is discussed, including results based on genetic inactivation of putative permeability Transition pore components.
Journal ArticleDOI
Mitochondrial creatine kinase in human health and disease
TL;DR: Under situations of compromised cellular energy state, two characteristics of mitochondrial creatine kinase are particularly relevant: its exquisite susceptibility to oxidative modifications and the compensatory up-regulation of its gene expression, in some cases leading to accumulation of crystalline MtCK inclusion bodies in mitochondria that are the clinical hallmarks for mitochondrial cytopathies.
Journal ArticleDOI
The role of mitochondria in protection of the heart by preconditioning
TL;DR: It is proposed that IP-mediated inhibition of MPTP opening at reperfusion does not involve direct phosphorylation of mitochondrial proteins, but rather reflects diminished oxidative stress during prolonged ischaemia and reperfusions.
References
More filters
Journal ArticleDOI
The mitochondrial permeability transition pore and its role in cell death.
TL;DR: Current evidence that the pore complex is involved in outer-membrane rupture and release of these proteins during programmed cell death is reviewed, along with indications that transient pore opening may provoke 'accidental' apoptosis.
Journal ArticleDOI
Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC
TL;DR: The results indicate that the Bcl-2 family of proteins bind to the VDAC in order to regulate the mitochondrial membrane potential and the release of cytochrome c during apoptosis.
Journal ArticleDOI
Mitochondrial Transport of Cations: Channels, Exchangers, and Permeability Transition
TL;DR: The review should provide the basic elements needed to understand both earlier mitochondrial literature and current problems associated with mitochondrial transport of cations and hopefully will foster new interest in the molecular definition of mitochondrial cation channels and exchangers as well as their roles in cell physiology.
Journal ArticleDOI
Mitochondria - Releasing Power for Life and Unleashing the Machineries of Death
TL;DR: A review of promising mechanisms proposed for mitochondrial involvement in cell death are examined, including oxidative phosphorylation, generation of oxygen radicals, dynamic morphological rearrangements, calcium overload, and permeability transition.