MiR-1,miR-122,miR-124 overexpression in 293T cells
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ABSTRACT:
PROVIDER: PRJNA508297 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To identify miR-1, miR-122 and miR-124 target genes in 293T cells using RNA-seq.
2019-09-18 | GSE123311 | GEO
Project description:This time course analysis is to study the targets and functions of miR-124. MiR-124 was overexpressed and the effect of miR-124 overexpression was compared to negative controls to identify downregulated genes and potential miRNA targets. Keywords: time course
2006-11-03 | GSE6207 | GEO
Project description:We aimed to determine whether overexpression of endoderm-specific miRNA may affect hESC differentiation. To this end, we analyzed the effect of lentiviral-based overexpression of liver-specific miR-122 on hESC differentiation, using genomewide gene microarrays. Stable overexpression of endoderm-specific miR-122 in hESC resulted in increased expression of a few endodermal markers in spontaneously-differentiating hESC, but had no clear effect on directing differentiation towards an endodermal fate; rather, it delayed the general differentiation of hESC.
2008-11-05 | GSE13460 | GEO
Project description:The liver-specific microRNA, miR-122, is an essential host factor for replication of hepatitis C virus (HCV), an important infectious cause of chronic liver disease and hepatocellular carcinoma. miR-122 stabilizes the positive-strand HCV RNA genome and promotes viral RNA synthesis by binding two closely spaced sites (S1 and S2) near the 5’ end of the genome in association with Ago2. Ago2 is essential for both host factor activities, but whether other host proteins are involved is unknown. Using a quantitative proteomics approach, we identified TNRC6A (GW182) and its paralogs (TNRC6B and TNRC6C), as functionally important components of the miR-122/Ago2 host factor complex binding HCV RNA. Depletion of any two TNRC6 proteins reduced HCV replication in Huh-7.5 cells,but did not reduce viral RNA stability or translational activity, but rather dampened miR-122 stimulation of viral RNA synthesis. However, TNRC6 depletion had no effect on replication of HCV in which S2 was mutated so that miR-122 binds only S1, whereas it significantly enhanced replication when S1 was mutated and only S2 bound by miR-122. Consistent with this, we found that TNRC6 proteins preferentially associate with the S1 site, and that the association of Ago2 with S2 is increased in TNRC6-depleted cells. Collectively, these data suggest a model in which TNRC6 proteins, which are known to interact with Ago2, preferentially direct the miR-122/Ago2 complex to S1 while restricting its association with S2, thereby fine tuning the spatial organization of miR-122/Ago2 complexes bound to the viral RNA.
2019-04-24 | PXD013054 | Pride
Project description:We aimed to determine whether overexpression of endoderm-specific miRNA may affect hESC differentiation. To this end, we analyzed the effect of lentiviral-based overexpression of liver-specific miR-122 on hESC differentiation, using genomewide gene microarrays. Stable overexpression of endoderm-specific miR-122 in hESC resulted in increased expression of a few endodermal markers in spontaneously-differentiating hESC, but had no clear effect on directing differentiation towards an endodermal fate; rather, it delayed the general differentiation of hESC. Experiment Overall Design: Lentiviral vectors encoding either wt or mutant (control) hsa-miR-122 were transduced into hES cells (line HES2). The cells differentiated spontaneously in KO medium without feeder cells for 2 weeks, and the gene expression profile of wt- vs mutant-expressing miR-122 was compared. We used for this study 3 arrays for control (mutant miR) and 2 arrays for the treatment (wt miRNA).
2008-11-15 | E-GEOD-13460 | biostudies-arrayexpress
Project description:This time course analysis is to study the targets and functions of miR-124. MiR-124 was overexpressed and the effect of miR-124 overexpression was compared to negative controls to identify downregulated genes and potential miRNA targets. Experiment Overall Design: one array for each time point of miR-124 and negative control transfections
2007-11-01 | E-GEOD-6207 | biostudies-arrayexpress
Project description:The aim of this study was to identify at genome-wide level, the effect of miR-122 on the distribution of its responsive genes on the polyribosomes. For this purpose human hepatoma cells Huh-7 were transfected for 48 hrs with LNA-based miR-122 inhibitors (122-PM) or miR-122 mimics (122-MIM). Following the treatment with cycloheximide, cells were lysed and layered on a 10-50% sucrose gradient. Following ultracetrifigation the polyribosomes were separated in 12 different fractions
2023-06-14 | GSE234690 | GEO
Project description:Hepatitis C virus uniquely requires the liver specific microRNA-122 for replication, yet global effects on endogenous miRNA targets during infection are unexplored. Here, high-throughput sequencing and crosslinking immunoprecipitation (HITS-CLIP) experiments of human Argonaute (Ago) during HCV infection showed robust Ago binding on the HCV 5’UTR, at known and predicted miR-122 sites. On the human transcriptome, we observed reduced Ago binding and functional mRNA de-repression of miR-122 targets during virus infection. This miR-122 “sponge” effect could be relieved and redirected to miR-15 targets by swapping the miRNA tropism of the virus. Single-cell expression data from reporters containing miR-122 sites showed significant de-repression during HCV infection depending on expression level and number of sites. We describe a quantitative mathematical model of HCV induced miR-122 sequestration and propose that such miR-122 inhibition by HCV RNA may result in global de-repression of host miR-122 targets, providing an environment fertile for the long-term oncogenic potential of HCV.
2015-01-06 | GSE64679 | GEO
Project description:Hepatitis C virus uniquely requires the liver specific microRNA-122 for replication, yet global effects on endogenous miRNA targets during infection are unexplored. Here, high-throughput sequencing and crosslinking immunoprecipitation (HITS-CLIP) experiments of human Argonaute (Ago) during HCV infection showed robust Ago binding on the HCV 5’UTR, at known and predicted miR-122 sites. On the human transcriptome, we observed reduced Ago binding and functional mRNA de-repression of miR-122 targets during virus infection. This miR-122 “sponge” effect could be relieved and redirected to miR-15 targets by swapping the miRNA tropism of the virus. Single-cell expression data from reporters containing miR-122 sites showed significant de-repression during HCV infection depending on expression level and number of sites. We describe a quantitative mathematical model of HCV induced miR-122 sequestration and propose that such miR-122 inhibition by HCV RNA may result in global de-repression of host miR-122 targets, providing an environment fertile for the long-term oncogenic potential of HCV. AGO HITS-CLIP libraries were generated from single cell clones of miR-122 deleted Huh7.5 cells using CRISPR (KO), unedited controls (WT), or cells transfected with GFP instead of CRISPR. Libraries were generated with a 4nt index read, a common priming sequence, followed by a 5nt degenerate barcode terminiating in a G. Files have been demultiplexed such that the 5nt degenerate barcode has been appended as the first 5 nucleotides of the read.
2015-01-06 | E-GEOD-64679 | biostudies-arrayexpress
Project description:Hepatic injury is often accompanied by pulmonary inflammation and tissue damage, but the underneath mechanism is not fully elucidated. Here we identify hepatic miR-122 as a culprit of pulmonary inflammation induced by various liver injuries. Analyses of acute and chronic liver injury mouse models confirm that liver dysfunction can cause pulmonary inflammation and tissue damage. Injured livers release large amounts of miR-122 in a microvesicle-independent manner into the circulation compared to normal livers. Circulating miR-122 is then preferentially transported to mouse lungs and taken up by alveolar macrophages, in which it binds toll-like receptor 7 (TLR7) and activates inflammatory responses. Depleting plasma miR-122 largely abolishes liver injury-induced pulmonary inflammation and tissue damage. Furthermore, alveolar macrophage activation by miR-122 is blocked by mutating the TLR7-binding UG-rich sequence on miR-122 or knocking out macrophage TLR7. Our findings reveal a novel causative role of hepatic miR-122 in liver injury-induced pulmonary dysfunction.
2018-12-27 | GSE124360 | GEO