Project description:We conducted transcriptome analysis of TFAM-depleted HepG2 cells and HeLa cells as a mitochondrial stress model. We found that mitochondrial dysfunction upregulated unique secretory proteins such as amphiregulin (AREG) and thrombospondin 1 in hepatic cells.
Project description:ChIP-seq data characterizing the occupancy of TFAM over the mitochondrial and nuclear genomes in HeLa cells. Characterization of mitochondrial and nuclear genome-wide TFAM binding in HeLa cells
Project description:Transcriptome analysis of LSD2-depleted HepG2 cells revealed that many of the target genes were related to lipid metabolism. We found that LSD2 is an important epigenetic regulator of hepatic lipid metabolism. We depleted LSD2 in HepG2 human hepatic cells using three different siRNAs, and then carried out an expression microarray experiment.
Project description:Purpose: The goal of this study is to compare the transcriptome changes between Negative control, UBR5 depleted and MYC depleted HeLa cells Methods: Gene expression profiles of Negative control, UBR5 depleted and MYC depleted HeLa cells were generated by deep sequencing, in triplicate. Results:The data were analyzed, and we sucessfully detected global differences in the gene expression between the given groups. Conclusions: UBR5 depletion induces gene expression changes that are partly overlapping with gene expression changes induced by MYC depletion
Project description:We generated a HeLa cell model of mucopolysaccharidosis IIIB (MPSIIIB) by depleting NAGLU. MPSIIIB-associated cell defects were prominent in NAGLU-depleted cells. We explored alterations of metabolic pathways in NAGLU-depleted cells versus non-depleted control cells by performing gene expression profiling. Exon array transcriptome analysis showed 96 transcripts with increased expression level and 38 transcripts with decreased expression level in NAGLU-depleted versus non-depleted cells.
Project description:ChIP-seq analyses were used to examine the effect of TFAM inhibition on mono-methylated H3K4 (H3K4me1) and acetylated H3K27 (H3K27ac), which are histone marks characteristic of enhancer activity. Our study revealed that c-JUN-mediated enhancer activation shapes the mitochondrial stress-associated secretory phenotype.
Project description:We generated a HeLa cell model of mucopolysaccharidosis IIIB (MPSIIIB) by depleting NAGLU. MPSIIIB-associated cell defects were prominent in NAGLU-depleted cells. We explored alterations of metabolic pathways in NAGLU-depleted cells versus non-depleted control cells by performing gene expression profiling. Exon array transcriptome analysis showed 96 transcripts with increased expression level and 38 transcripts with decreased expression level in NAGLU-depleted versus non-depleted cells. Total RNA was extracted from two independent cultures of non-depleted cells and NAGLU-depleted cells. We considered a minimal fold change of 1.5 fold and a corrected P value lower than 0.05.