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Title[redir]:
Cysteine 203 of cyclophilin D is c ... | Article | H1 Connect
Description:
The mitochondrial permeability transition pore (mPTP) opening plays a critical role in mediating cell death during ischemia/reperfusion (I/R) injury. Our p

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mitochondrial, permeability, latest, recommendation, transition, finding, cell, pore, cyclophilin, death, biology, chemical, critical, activation, jan, mptp, faculty, cysteine, interesting, opening, mice, feb, aug, eduardo, rial, nov, study, mitochondria, cypd, relevant, related, genetics, mar, jul, drug, target, complex, hypothesis, protects, cells, opinions, collections, reviews, connecting, world, doctors, search, page, archived, nguyen,

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redox stress-induced activation drug target properties mitochondrial permeability pore mitochondrial permeability transition mechanistic processes related permeability transition pore mediating cell death deficiency attenuates mitochondrial ischemia/reperfusion injury adp/atp translocator atpase c-subunit outer membrane component peptidyl prolyl isomerization chemical biology finding p53 opens cell death finding respiratory complex permeability transition protects cells affect mptp opening faculty opinions 2016 latest recommendation 13 latest recommendation h1 company finding bax archived cysteine 203 finding cyclophilin doctors search nguyen tt biological chemistry investigating mitochondria wild-type baines cp atan gross 11 neuronal perturbation ameliorates learning kokoszka je trigger necrosis vaseva av inorganic polyphosphate elustondo pa mitochondria devoid bak function dysfunction due voltage threshold resting levels lin dt 10 blog faq privacy policy mptp opening

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ScholarlyArticle:
      context:https://schema.org
      headline:Cysteine 203 of cyclophilin D is critical for cyclophilin D activation of the mitochondrial permeability transition pore.
      abstract:The mitochondrial permeability transition pore (mPTP) opening plays a critical role in mediating cell death during ischemia/reperfusion (I/R) injury. Our previous studies have shown that cysteine 203 of cyclophilin D (CypD), a critical mPTP mediator, undergoes protein S-nitrosylation (SNO). To investigate the role of cysteine 203 in mPTP activation, we mutated cysteine 203 of CypD to a serine residue (C203S) and determined its effect on mPTP opening. Treatment of WT mouse embryonic fibroblasts (MEFs) with H(2)O(2) resulted in an 50% loss of the mitochondrial calcein fluorescence, suggesting substantial activation of the mPTP. Consistent with the reported role of CypD in mPTP activation, CypD null (CypD(-/-)) MEFs exhibited significantly less mPTP opening. Addition of a nitric oxide donor, GSNO, to WT but not CypD(-/-) MEFs prior to H(2)O(2) attenuated mPTP opening. To test whether Cys-203 is required for this protection, we infected CypD(-/-) MEFs with a C203S-CypD vector. Surprisingly, C203S-CypD reconstituted MEFs were resistant to mPTP opening in the presence or absence of GSNO, suggesting a crucial role for Cys-203 in mPTP activation. To determine whether mutation of C203S-CypD would alter mPTP in vivo, we injected a recombinant adenovirus encoding C203S-CypD or WT CypD into CypD(-/-) mice via tail vein. Mitochondria isolated from livers of CypD(-/-) mice or mice expressing C203S-CypD were resistant to Ca(2+)-induced swelling as compared with WT CypD-reconstituted mice. Our results indicate that the Cys-203 residue of CypD is necessary for redox stress-induced activation of mPTP.
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WebPage:
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