| http://purl.uniprot.org/citations/16551620 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16551620 | http://www.w3.org/2000/01/rdf-schema#comment | "The permeability transition pore is involved in the mitochondrial pathway of apoptosis. Cyclophilin D, a pore component, has catalytic activity as a peptidyl prolyl cis, trans-isomerase (PPIase), which is essential to the pore opening. It has been reported that cyclophilin D overexpression suppresses apoptosis in cancer cells. To clarify the mechanism of this effect, we generated glioma cells overexpressing wild-type or a PPIase-deficient mutant of cyclophilin D. Interestingly, we found that the PPIase-dependent apoptosis suppression by cyclophilin D correlated with the amounts of mitochondrial-bound hexokinase II, which has anti-apoptotic activity. Inactivation of endogenous cyclophilin D by small interference RNA or a cyclophilin inhibitor was found to release hexokinase II from mitochondria and to enhance Bax-mediated apoptosis. The anti-apoptotic effects of cyclophilin D were canceled out by the detachment of hexokinase II from mitochondria, demonstrating that mitochondrial binding of hexokinase II is essential to the apoptosis suppression by cyclophilin D. Furthermore, cyclophilin D dysfunction appears to abrogate hexokinase II-mediated apoptosis suppression, indicating that cyclophilin D is required for the anti-apoptotic activity of hexokinase II. Based on the above, we propose here that cyclophilin D suppresses apoptotic cell death via a mitochondrial hexokinase II-dependent mechanism in cancer cells."xsd:string |
| http://purl.uniprot.org/citations/16551620 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m513297200"xsd:string |
| http://purl.uniprot.org/citations/16551620 | http://purl.uniprot.org/core/author | "Ohta Y."xsd:string |
| http://purl.uniprot.org/citations/16551620 | http://purl.uniprot.org/core/author | "Osada H."xsd:string |
| http://purl.uniprot.org/citations/16551620 | http://purl.uniprot.org/core/author | "Machida K."xsd:string |
| http://purl.uniprot.org/citations/16551620 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/16551620 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
| http://purl.uniprot.org/citations/16551620 | http://purl.uniprot.org/core/pages | "14314-14320"xsd:string |
| http://purl.uniprot.org/citations/16551620 | http://purl.uniprot.org/core/title | "Suppression of apoptosis by cyclophilin D via stabilization of hexokinase II mitochondrial binding in cancer cells."xsd:string |
| http://purl.uniprot.org/citations/16551620 | http://purl.uniprot.org/core/volume | "281"xsd:string |
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| http://purl.uniprot.org/uniprot/#_P52789-mappedCitation-16551620 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16551620 |
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| http://purl.uniprot.org/uniprot/#_E5KN55-mappedCitation-16551620 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16551620 |
| http://purl.uniprot.org/uniprot/#_E5KN59-mappedCitation-16551620 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16551620 |
| http://purl.uniprot.org/uniprot/#_Q53QX9-mappedCitation-16551620 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16551620 |
| http://purl.uniprot.org/uniprot/#_Q53SG7-mappedCitation-16551620 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16551620 |
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| http://purl.uniprot.org/uniprot/#_Q09LL6-mappedCitation-16551620 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16551620 |
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| http://purl.uniprot.org/uniprot/#_Q6FGM6-mappedCitation-16551620 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16551620 |
| http://purl.uniprot.org/uniprot/#_Q7Z7Q6-mappedCitation-16551620 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/16551620 |