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Loss of cyclophilin D reveals a cr ... | Article | H1 Connect
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Mitochondria play a critical role in mediating both apoptotic and necrotic cell death. The mitochondrial permeability transition (mPT) leads to mitochondri
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Keywords {π}
cyclophilin, mitochondrial, cell, death, permeability, transition, apoptosis, latest, recommendation, finding, paper, mpt, role, pmid, necrotic, nakagawa, pore, nature, show, ptp, good, mice, feb, faculty, mar, apr, authors, cypd, opening, mitochondria, lacking, key, bcl, family, members, cells, proteins, membrane, loss, critical, baines, required, mediating, caspasedependent, protected, swelling, regulating, papers, induced, oxygen,
Topics {βοΈ}
caspase-dependent cell death mitochondrial-dependent cell death ischaemia-induced cell death bcl-2 family members outer membrane component permeability transition pore mitochondrial permeability transition caspase-dependent apoptosis mitochondrial permeability pore apoptotic cell death fo atp synthase spontaneous cell death necrotic cell death endoplasmic reticulum stress deficiency attenuates mitochondrial adp/atp translocator long running controversy trophic factor withdrawal peptidyl prolyl isomerization groups generated cyclophilin reactive oxygen species important feature concerns mitochondrial apoptosis induced paper strongly argues injury-induced apoptosis mice lacking cyp cells lacking cyclophilin cell death faculty opinions latest recommendation apoptotic signals h1 company mitochondrial swelling mitochondrial protein mitochondrial potential key step dramatic dissociation key mediator finding evaluations finding dimers finding cysteine 203 finding bax oxygen radicals appealing feature knockout mice cyclophilin folks doctors search baines cp finally resolves null animals
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headline:Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death.
abstract:Mitochondria play a critical role in mediating both apoptotic and necrotic cell death. The mitochondrial permeability transition (mPT) leads to mitochondrial swelling, outer membrane rupture and the release of apoptotic mediators. 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 matrix. Here we generated mice lacking Ppif and mice overexpressing cyclophilin D in the heart. Ppif null mice are protected from ischaemia/reperfusion-induced cell death in vivo, whereas cyclophilin D-overexpressing mice show mitochondrial swelling and spontaneous cell death. Mitochondria isolated from the livers, hearts and brains of Ppif null mice are resistant to mitochondrial swelling and permeability transition in vitro. Moreover, primary hepatocytes and fibroblasts isolated from Ppif null mice are largely protected from Ca2+-overload and oxidative stress-induced cell death. However, Bcl-2 family member-induced cell death does not depend on cyclophilin D, and Ppif null fibroblasts are not protected from staurosporine or tumour-necrosis factor-alpha-induced death. Thus, cyclophilin D and the mitochondrial permeability transition are required for mediating Ca2+- and oxidative damage-induced cell death, but not Bcl-2 family member-regulated death.
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