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http://purl.uniprot.org/citations/25837584http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25837584http://www.w3.org/2000/01/rdf-schema#comment"Cyclophilin-D (Cyp-D) is a mitochondrial matrix peptidyl-prolyl isomerase. Because cyclophilins can regulate nuclear gene expression, we examined whether Cyp-D could regulate mitochondrial gene expression. We demonstrated in HEK 293T cells that transfected Cyp-D interacts with mitochondrial transcription factors B1 and B2 (TFB2M) but not with mitochondrial transcription factor A. We also demonstrated that Cyp-D interacts in vivo with TFB2M. Genetic silencing of Cyp-D and pharmacologic inhibition of Cyp-D markedly reduced mitochondrial transcription to 18 ± 5% (P < 0.05) and 24 ± 3% (P < 0.05) of respective controls. The level of interaction between Cyp-D and TFB2M correlated with the level of nascent mitochondrial RNA intensity (r = 0.896; P = 0.0156). Cyp-D silencing down-regulated mitochondrial transcripts initiated from the heavy strand promoter 2 [i.e., NADH dehydrogenase 1 (ND1) by 11-fold, P < 0.005; cytochrome oxidase 1 (COX1) by 4-fold, P < 0.001; and ATP synthase subunit 6 (ATP6) by 6.5-fold, P < 0.005); but not NADH dehydrogenase 6 (ND6)], which is initiated from the light strand promoter. Cyp-D silencing reduced mitochondrial membrane potential and cellular oxygen consumption (from 59 ± 5 to 34 ± 1 µmol oxygen/min/10(6) cells, P < 0.001); the latter without a statistically significant reversal after uncoupling electron transport from ATP synthesis, consistent with down-regulation of electron transport complexes. Accordingly, these studies provide novel evidence that Cyp-D could play a key role in regulating mitochondrial gene expression."xsd:string
http://purl.uniprot.org/citations/25837584http://purl.org/dc/terms/identifier"doi:10.1096/fj.14-263855"xsd:string
http://purl.uniprot.org/citations/25837584http://purl.uniprot.org/core/author"Chandran B."xsd:string
http://purl.uniprot.org/citations/25837584http://purl.uniprot.org/core/author"Radhakrishnan J."xsd:string
http://purl.uniprot.org/citations/25837584http://purl.uniprot.org/core/author"Bazarek S."xsd:string
http://purl.uniprot.org/citations/25837584http://purl.uniprot.org/core/author"Gazmuri R.J."xsd:string
http://purl.uniprot.org/citations/25837584http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25837584http://purl.uniprot.org/core/name"FASEB J"xsd:string
http://purl.uniprot.org/citations/25837584http://purl.uniprot.org/core/pages"2734-2748"xsd:string
http://purl.uniprot.org/citations/25837584http://purl.uniprot.org/core/title"Cyclophilin-D: a resident regulator of mitochondrial gene expression."xsd:string
http://purl.uniprot.org/citations/25837584http://purl.uniprot.org/core/volume"29"xsd:string
http://purl.uniprot.org/citations/25837584http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25837584
http://purl.uniprot.org/citations/25837584http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25837584
http://purl.uniprot.org/uniprot/#_B2R6X6-mappedCitation-25837584http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25837584
http://purl.uniprot.org/uniprot/#_P30405-mappedCitation-25837584http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25837584
http://purl.uniprot.org/uniprot/#_Q6UWC4-mappedCitation-25837584http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25837584
http://purl.uniprot.org/uniprot/B2R6X6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25837584
http://purl.uniprot.org/uniprot/P30405http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25837584
http://purl.uniprot.org/uniprot/Q6UWC4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25837584