Project description:RNA Sequencing of transmitochondrial cybrids revealed a downregulation of oxidative phosphorylation and nicotinamide metabolism in cybrids with patient mitochondria
Project description:This dataset investigates the transcriptional effect of mitochondrial 12S rRNA hypermethylation, both by overexpressing the mitochondrial methyltransferase mtTFB1 in HeLa cells and by using A1555G cybrids, where the 12S rRNA is hypermethylated. HeLa cells overexpressing a methyltransferase-deficient mtTFB1 (mtTFB1[G65A]) and wild-type A1555A cybrids were used as controls.
Project description:Transcriptome profiling is a sensitive strategy to uncover the change of mitochondrial to nucleus signaling due to the minor alternation of mitochondrial OXPHOS function. Therefore, we hypothesized that even a minor alternation of OXPHOS function can also remold transcriptome profiles in m.14487T>C mutant cybrid when compared with control cybrids. Our data suggest that a comparable mitochondrial OXPHOS function between m.14487T and m.14487C cybrids is not because of compensatory boost of mitochondrial biogenesis in m.14487C cybrids.
Project description:This dataset investigates the transcriptional effect of mitochondrial 12S rRNA hypermethylation, both by overexpressing the mitochondrial methyltransferase mtTFB1 in HeLa cells and by using A1555G cybrids, where the 12S rRNA is hypermethylated. HeLa cells overexpressing a methyltransferase-deficient mtTFB1 (mtTFB1[G65A]) and wild-type A1555A cybrids were used as controls. four samples with 12S rRNA hypermethylation (two cell lines, with two biological replicates each) versus four samples with basal 12S rRNA methylation (two cell lines, with two biological replicates each)
Project description:We used a transmitochondrial cybrid (cybrids)-based discovery approach to identify mitochondria-regulated cancer pathways in TN BCa. Cybrids were generated under a moderately metastatic TN BCa cell line SUM159 as the common nuclear background with mitochondria from benign breast epithelium (A1N4) and moderately metastatic (SUM159) TN BCa cells. In vitro and in vivo studies suggested that even under the common moderately cancerous nuclear background, mitochondria from benign cells inhibit and metastatic cell induce cancer properties of a moderately aggressive TN BCa cell. Gene expression studies identified c-Src onco-pathway as one of the major cancer pathways altered according to the mitochondria status of the cybrids.
Project description:We used a transmitochondrial cybrid (cybrids)-based discovery approach to identify mitochondria-regulated cancer pathways in TN BCa. Cybrids were generated under a moderately metastatic TN BCa cell line SUM159 as the common nuclear background with mitochondria from benign breast epithelium (A1N4) and moderately metastatic (SUM159) TN BCa cells. In vitro and in vivo studies suggested that even under the common moderately cancerous nuclear background, mitochondria from benign cells inhibit and metastatic cell induce cancer properties of a moderately aggressive TN BCa cell. Gene expression studies identified c-Src onco-pathway as one of the major cancer pathways altered according to the mitochondria status of the cybrids. SUM159 Ï0 cells were used as nuclear donor and A1N4 and SUM 159 cells were used as mitochondrial donor cells. The two groups were profiled for gene expression using microarrays. two group comparison (159/SUM159 vs A1/SUM159)
Project description:We selected humann intervertebral disc samples to perform proteomics analysis. There were 1 case of grade I , 1 case of grade II, 3 cases of grade Ⅲ and 3 cases of grade Ⅳ according to Pfirrmann classfication. RNA seqencing analysis and single-cell RNA sequencing were integrated with proteomics data to identify the hub genes for intervertebral disc degeneration using bioinformatic method.
Project description:Mitochondrial respiratory chain (MRC) complexes I, III and IV are associated into large molecular structures named supercomplexes (SCs) or respirasomes, whose functional roles remain to be fully understood. Biochemical analyses in a diversity of OXPHOS-deficient cellular and animal models support the idea that one of the SCs function is to confer stability to individual MRC complexes, in particular to complex I (CI). To gain insight into the mechanisms that regulate the structural interdependences among MRC complexes, we performed complexome profiling of human cybrids laking mitochondrial genes Cox1 or Cox2 and compared protein assemblies and intermediates to control 143B cells.