Project description:Human iPSCs and NSCs were engineered by AAVS1 and/or C13 safe-harbor TALENs which mediated targeted integration of various reporter genes at single or dual safe-harbor loci. Multiple clones of targeted human iPSCs were used to compare with parental untargeted NCRM5 iPSCs. Polyclonal targeted human NSCs were used to compare with their parental untargeted NCRM1NSCs or H9NSCs. Total RNA obtained from targeted human iPSCs or NSCs compared to untargeted control iPSCs or NSCs.
Project description:To comprehensively elucidate the possible mechanism of short-term administration of emodin on the metabolic disturbance in vivo, our study utilized both LC/MS and NMR platforms for untargeted metabolomics studies. These analyses aimed to identify potential biomarkers associated with emodin-induced metabolic disturbances in mice. Subsequently, we delved into lipidomics to explore lipid metabolism systematically and determined the position of C=C double bonds in unsaturated lipids.
Project description:We performed integrated targeted lipidomics and untargeted metabolomics on patients' plasma (n = 81) from MPXV without HIV (MPLWOH), MPXV with HIV (MPLWH), HIV-positive without MPXV (PLWH) and healthy. Exosome proteomics and cytokine profiling complemented lipidome/metabolome analyses for functional interpretation.
Project description:To detect miRNAs in microglia derived from AD mice (5xFAD) brain we single cell sorted Cd11b+ and Cd45+ cells divided by Methoxy-X04 staining (Ab aggregates) positivity We performed differentially expression analysis of RNA-seq of wild-type microglia (Me-X04 neg), non-phagocytic AD microglia (Me-X04 neg), phagocytic AD microglia (Me-X04 positive)
Project description:Persister cancer cells (PSs) are implicated in minimal residual disease from which cancer relapse occurs. PSs are sensitive to and present a critical point through which identification and targeting of PSs may be possible. To identify biomarkers for such cells, the drivers of ferroptosis sensitivity in PSs should be identified. Here, we first derived PSs from the lung carcinoma cell line PC9 (PSPC9), performed transcriptomic analysis, and observed enrichment of lipid and sugar metabolism gene expression in PSPC9. We performed untargeted and targeted lipidomics, revealing enrichment within PSPC9 for ferroptosis-driving diPUFA phospholipids (diPUFA-PL), as well as polyunsaturated free fatty acids (PUFA FFAs). Upon PSPC9 reversion to the ferroptosis-resistant parental state (PC9PS -> PC9), this lipid signature reverted. We generated two additional PS-like cell models: PS-like prostate carcinoma (PSLNCaP) from LNCaP and PS-like fibrosarcoma (PSHT1080) from HT1080. These PS-like models individually had features consistent with PS, including increased labile-iron pool, reversibility, and enhanced ferroptosis sensitivity. We performed lipidomics in these cell models, and identified lipid features consistent with those in PSPC9. Finally, we found that in PSHT1080, mitochondrial elimination partially abrogated ferroptosis sensitivity and altered the PSHT1080 lipid profile. In summary, we found that lipidomic changes dependent on the presence of mitochondria are key for the ferroptosis sensitivity of drug-tolerant persister cancer cells.