The permeability transition pore complex: another view.

By A. Halestrap, Gavin Peter McStay, S. Clarke. Biochimie, 2002

737 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/d7f5fe9a98abdeea9c36134b8f3108b9e1a4e550

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Guido Kroemer
2. L. Galluzzi
3. C. Brenner
4. Christopher P. Baines
5. J. Molkentin
6. Tian Xia
7. A. Nel
8. M. Liong

In Physiology

1. L. Galluzzi
2. Guido Kroemer
3. T. Nakagawa
4. A. Halestrap
5. Christopher P. Baines
6. V. Schirrmacher

Citations in the corpus

• Cyclophilin D deficiency attenuates mitochondrial and neuronal perturbation and ameliorates learning and memory in Alzheimer's disease (2008, neutral): “Opening of the mPTP collapses the membrane potential and amplifies apoptotic mechanisms by releasing proteins with apoptogenic potential from the inner membrane spac”
• Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death (2005, background): “The mPT pore is thought to consist of the adenine nucleotide translocator, a voltage-dependent anion channel, and cyclophilin D (the Ppif gene product), a prolyl isomerase located within the mitochondrial matri”
• Mitochondrial DNA in inflammation and immunity (2020, neutral): “5 kDa, much smaller than a mtDNA nucleoid [80,81].”
• Ultrashort electrical pulses open a new gateway into biological cells (2004, background): “The choice of this organelle was guided by experimental reports of possible breakdown of the mitochondrial membrane and opening of a mitochondrial permeability transition pore [24]–[ 26 ].”
• Mitochondrial permeability transition pore opening during myocardial reperfusion--a target for cardioprotection. (2004, background): “For a detailed account of the molecular mechanism of the MPTP, including the experimental evidence on which this is based, the reader is directed to other recent reviews from this and other laboratories [1,3,5].”
• Cationic polystyrene nanosphere toxicity depends on cell-specific endocytic and mitochondrial injury pathways. (2008, background): “CsA interferes in the ability of the Ca(2) -dependent PTP regulator, cyclophilin D, to engage in pore opening.(19) PI uptake studies reveal that, while CsA was capable of a significant reduction of NH2-PS cytotoxicity in RAW 264.”
• Bioelectric Effects of Intense Nanosecond Pulses (2007, background): “It is known that biochemicallyinduced apoptosis involves the mitochondrial permeability transition pore complex (MPTP) [70] and/or mitochondrial membrane voltage-dependent anion channels [67,71].”
• Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death (2007, neutral): “On the basis of biochemical evidence the standard model for the MPT pore consists of VDAC in the outer mitochondrial membrane, ANT in the inner mitochondrial membrane and cyclophilin D in the matrix (2-4,25,26).”
• Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death (2005, background): “The mitochondrial permeability transition (mPT) is a regulated Ca 2p -dependent increase in the permeability of the mitochondrial membrane, which results in a loss in mitochondrial membrane potential (Δ Ψ ), mitochondrial swelling and rupture of the outer membran”
• Mitochondrial membrane permeabilization in cell death. (2007, result): “These data confirm previous observations that CsA injections can attenuate ischemia-associated cell death in vivo (212, 278).”
• The mitochondrial membrane potential (Δψm) in apoptosis; an update (2003, neutral): “[28] for recent review).”