The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore

By J. Kokoszka, K. Waymire, S. Levy, J. Sligh, J. Cai, Dean P. Jones, G. MacGregor, Douglas C. Wallace. Nature, 2004

1,115 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/9d0453d082460b387fb358a68d14c574366d068f

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Citations in the corpus

Mitochondria and Mitophagy: The Yin and Yang of Cell Death Control (2012, background): “Similarly, mitochondria lacking ANT1/2 still undergo permeability transition, albeit at higher Ca thresholds.(32)”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “However, mitochondria isolated from Slc25a4 −/−Slc25a5−/− mouse livers are desensitized to Ca2+-driven MPT to a similar extent than mitochondria exposed to CsA [390].”
Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. (2014, background): “However, ANT was proposed to be a pore modulator (494) rather than a component of the core of the pore (235).”
Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death (2005, background): “Disagreement persists as to the function of the mitochondrial permeability transition pore in mediating apoptotic and/or necrotic cell deat”
Molecular mechanisms of necroptosis: an ordered cellular explosion (2010, background): “As it stands, CYPD seems to be the leading player of the PTPC, as genetic ablation of peptidylprolyl isomerase F ( Ppif ; the CYPD-encoding gene), but not of the genes coding for all known VDAC and ANT isoform”
Calcium, ATP, and ROS: a mitochondrial love-hate triangle. (2004, background): “Recently, doubt has been cast on the role of ANT, because mitochondria isolated from double-knockout ANT1 / , ANT2 / mice appear capable of undergoing PT (101).”
Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death (2007, background): “Although recent genetic studies have confirmed a regulatory role for cyclophilin D in MPT (24,27-29), mice lacking Ant1/2 still exhibit a classical MPT response that was inhibited with cyclosporine A (30).”
Expanding insights of mitochondrial dysfunction in Parkinson's disease (2006, background): “However, ANT might still have a role in the regulation of mPTP opening, and any post-translational modifications of ANT, such as phosphorylation, might be important for this regulatio”
Mitochondria, oxidative metabolism and cell death in stroke. (2010, neutral): “However, some doubts have been raised about the role of the adenine nucleotide translocase becausemitochondria frommice lacking expression of the major isoforms of this protein can still develop a permeability transition [67,72].”
Mechanisms of cytochrome c release from mitochondria (2006, background): “required for the induction of MPT and consequent apoptosis.(52) Moreover, mitochondria from CypD-deficient mice are relatively resistant to the induction of MPT by agents such as Ca2þ and ROS, yet are normally permeabilized by BAX and Functions of Cyt c in cell life and death C Garrido et al”