Similar Datasets
Project description:A novel Sox9/lncRNA H19 axis contributes to hepatocyte death and liver fibrosis
| PRJNA627486 | ENA
Project description:Homo sapiens H19, H19 imprinted maternally expressed transcript [Source:HGNC Symbol;Acc:HGNC:4713], is differentially expressed in 119 experiment(s);
| ENSG00000130600 | ExpressionAtlas
Project description:Homo sapiens H19, H19 imprinted maternally expressed transcript [Source:HGNC Symbol;Acc:HGNC:4713], is expressed in 35 baseline experiment(s);
| ENSG00000130600 | ExpressionAtlas
Project description:Mus musculus H19, H19, imprinted maternally expressed transcript [Source:MGI Symbol;Acc:MGI:95891], is differentially expressed in 99 experiment(s);
| ENSMUSG00000000031 | ExpressionAtlas
Project description:Mus musculus H19, H19, imprinted maternally expressed transcript [Source:MGI Symbol;Acc:MGI:95891], is expressed in 25 baseline experiment(s);
| ENSMUSG00000000031 | ExpressionAtlas
Project description:We generated the HepG2 subline stably expressing Sox9 (HepG2-Sox9) and performed transcriptome RNA sequence.
2021-05-28 | GSE175627 | GEO
Project description:Dystrophin proteomic regulation in Muscular Dystrophies (MD) remains unclear. We report that a long noncoding RNA (lncRNA) H19 associates with dystrophin. To investigate the biological roles of this interaction in vivo, we performed mass spectrometry analysis of dystrophin and its associated proteins in H19-proficient and -deficient C2C12 myotubes. Mass spectrometry data indicated that in H19-proficient myotubes, dystrophin associates with components of dystrophin-associated protein complex (DPC); however, in H19-deficient myotubes, dystrophin associated with UBA1, UB2G1, TRIM63 ubiquitin E3 ligase and ubiquitin. In H19-deficient myotubes, dystrophin was post-translationally modified with K48-linked poly-ubiquitination at Lys3577 (referred to as Ub-DMD). This mass spectrometry study demonstrated that lncRNA H19, associates with dystrophin and inhibits E3 ligase-dependent Ub-DMD formation and its subsequent proteasomal degradation. Based on this study, H19 RNA oligonucleotides conjugated with a muscle homing ligand Agrin (referred to as AGR-H19) and Nifenazone, a TRIM63-specific small molecule inhibitor, reverses the dystrophin degradation in iPSC-derived skeletal muscle cells from Becker Muscular Dystrophy patients. Furthermore,treatment of mdx mice with exon-skipping reagent, in combination with either AGR-H19 or Nifenazone, dramatically stablized dystrophin, preserved skeletal/cardiac muscle histology, and improved strength/heart function. In summary, this mass spectrometry study paves the way to meaningful targeted therapeutics for BMD and certain DMD patients.
2020-08-19 | PXD020566 | Pride
Project description:Galangin, a natural flavonoid, derived from honey and Alpinia officinarum Hance (Zingiberaceae) has excellent was anti-tumor and anti-inflammatory properties. w It has been extensively studied as a novel therapeutic agent forhich was widely used in the treatment of various cancers. However, the effect of galangin in HCC remains elusive. Using RNA sequencing, the differential expression of LncRNA in MHCC97H cells treated with galangin was investigated in the present study. Furthermore, the expression of H19 was also determined in MHCC97H cells following treatment with galangin. And the effect of knockdown and overexpression of H19 on cell apoptosis, cell cycle, migration and invasion of HCC cells was also evaluated. Moreover, the in vivo effect of galangin on tumor development was also determined in nude mice. This study identified aT total of 50 LncRNAs were to be significantly differentially expressed by RNA-seq analysis in MHCC97H cells treated with galangin. It has been demostreated that noncoding RNA H19 are abnormally expressed in different cancers. Our results showed that Besides, the expression of H19 was markedly reduced after following treatment with galangin treatment in MHCC97H cells. In addition, galangin could increase the occurrence of cell apoptosis. Moreover, compared to the Control group, the galangin-treated group inhibited cell migration and invasion in MHCC97H cells.To further investigated if H19 expression pattern affect cell apoptosis, migration and invasion, knock down and overexpression of H19 vector were constructed. The results of the knockdown of H19 expression showed knock down of H19 expression increased cell apoptosis and decreasedinhibited invasion. In addition, RNA-seq data showed also identified 161 mRNA which were was significantly differentially expressed after following treatment withof galangin. To further determine the underlying mechanism,confirmed cell apoptosis, p53 protein and its related proteins were was analyzed through micor RNA 675-3p (miR675-3p) which was in the H19 locus. Notably, Tthe results indicatedshowed that reduced knockdown of H19 and miR675 induced the protein expression of p53, eventually promoting cell apoptosis expression of H19 and miR675-3p increased p53 expression in MHCC97H cells. These results indicated that galangin promoted cell apoptosis through the regulation of H19 and miR675 expression in MHCC97H cells. Furthermorely, galangin was used to treated in nude mice. Tthe in vivo result showed that compared to the Control group, inhibited tumor growth was remarkably suppressed and reduced expression of H19 in galangin-treated group. Taken together, these results indicated that galangin regulated cell apoptosis which associate with p53 protein through H19 and miR675 expression in MHCC97H cells.Collectively, our data suggested that galangin plays a role in hepatocarcinogenesis through regulation of H19 expression pattern.
2020-08-12 | GSE142680 | GEO
Project description:Treatment of pathological cardiac remodeling and subsequent heart failure represents an unmet clinical need. The well conserved lncRNA H19 shows as powerful therapeutic potential in the treatment of pathological cardiac hypertrophy. H19 is strongly repressed in failing hearts from mice, pigs and humans. Gene therapy using murine but also human H19 strongly attenuated heart failure even when cardiac hypertrophy was already established. Using microarray , GSEA and ChIP-Seq we identified a link between H19 and NFAT signalling. H19 physically interacts with PRC2 to epigenetically induced Tescalcin repression which in turn leads to reduced NFAT expression and activity.
2020-08-01 | GSE153344 | GEO
Project description:Long non-coding RNAs (lncRNAs) regulate diverse cellular processes and are associated with many age-associated diseases. However, the function of lncRNAs in cellular senescence remains largely unknown. Here we characterize the role of lncRNA H19 in senescence. We show that H19 levels decline as cells undergo senescence, and depletion of H19 results in premature senescence. We find that repression of H19 is triggered by the loss of CTCF and prolonged activation of p53 as part of the senescence pathway. Mechanistically, the loss of H19 drives senescence via increased let7b mediated targeting of EZH2. We further demonstrate that H19 is required for senescence inhibition by the mTOR inhibitor rapamycin, where it maintains lncRNA H19 levels throughout the cellular lifespan and thus prevents the reduction of EZH2 that would otherwise lead to cellular senescence. Therefore, lncRNA H19 is crucial in maintaining the balance between sustained cell growth and the onset of senescence.
2022-11-30 | GSE211157 | GEO