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MRNA-seq data for DDX3 knockdown in murine hepatocytes in vivo and in vitro

ABSTRACT: mRNA-seq data for DDX3 knockdown in murine hepatocytes in vivo and in vitro

PROVIDER: PRJNA739730 | ENA |

REPOSITORIES: ENA

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mRNA-seq data for DDX3 knockdown in murine hepatocytes in vivo and in vitro

Project description:A transcriptome analysis was performed to estimate a primary response of the hepatocytes to depletion of DDX3 RNA helicase both in vitro and in vivo. We used two siRNAs with different efficacy and demonstrated protein level-dependent effects on DDX3 RNA helicase depletion in the murine liver. We found that strong reduction of DDX3 protein (>85%) leads to similar changes in vitro and in vivo – we observed deregulation of cell cycle, Wnt and cadherin pathways. However, more modest downregulation of DDX3 protein (60-65%) resulted in discordant results between gene expression in vitro and in vivo – in vitro data were close to those under strong reduction, while in vivo phenotype was weak. These results demonstrate that the level of active DDX3 protein can dramatically influence on the phenotype in vivo, which should be taken into account during drug development.

2021-06-29 | GSE178618 | GEO

Level of Murine DDX3 RNA Helicase Determines Phenotype Changes of Hepatocytes In Vitro and In Vivo.

Project description: Not available

| S-EPMC8269429 | biostudies-literature

Microarray expression profile from YAP1 knockdown in DDX3-overexpressing colorectal cancer cells

Project description:To identify which genes could be modulated by the DDX3-YAP1 axis in SW48 cells.

2016-10-18 | GSE88851 | GEO

Effect of long non-coding RNA LL35/Falcor depletion on gene expression in murine hepatocytes in vivo and in vitro

Project description:To determine and compare a functional role of long non-coding RNA LL35/Falcor in murine hepatocytes in vitro and in vivo we performed a transcriptome analysis of AML12 hepatocytes cell line and murine liver after LL35 depletion.

2022-06-10 | GSE203431 | GEO

StemNet - in vitro differentiation of human hepatocytes

Project description:Integrative epigenomic and transcriptomic characterization of hepatocyte-like cells differentiated in vitro from human induced pluripotent stem cells in comparison with primary human hepatocytes. This study comprises single cell RNA-seq, bulk mRNA-seq, ATAC-seq and RRBS.

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Genome wide analysis of mRNA expression and polysome profiling in DDX3 knockdown SAS cells

Project description:By analyzing the RNAseq and RIBOseq results, we identified potential pathways for DDX3 to remodel tumor microenviroment.

2020-11-05 | GSE160803 | GEO

In vitro differentiation of hepatoblasts into hepatocytes

Project description:In vitro differentiation of hepatoblasts into hepatocytes

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In vitro differentiation of hepatoblasts into hepatocytes

Project description:We differentiated primary mouse E14.5 Dlk1+ hepatoblasts in vitro into hepatocyte-like cells that recapitulated morphological features of hepatocytes. To assess the level of differentiation, we performed RNA-seq analysis and compared gene expression profiles of hepatobalsts, in vitro differentiated hepatocytes and mature hepatocytes isolated from adult mouse livers as a control.

2021-07-26 | GSE176069 | GEO

Effect of DDX3 inhibitors on CD4+ T cells

Project description:An innovative approach to eliminate HIV-1-infected cells emerging out of latency, the major hurdle to HIV-1 cure, is to pharmacologically reactivate viral expression and concomitantly trigger intracellular pro-apoptotic pathways in order to selectively induce cell death (ICD) of infected cells, without reliance on the extracellular immune system. In this work we demonstrate the effect of DEAD-box polypeptide 3, X-Linked (DDX3) inhibitors on selectively inducing cell death in latent HIV-1-infected cell lines, primary CD4+ T cells and in CD4+ T cells from cART-suppressed people living with HIV-1 (PLWHIV). RNA sequencing analysis revealed that while overall gene expression was minimally dysregulated, DDX3 inhibition in independent donor CD4+ T cells led to significant downregulation of BIRC5 and HSPB1A, genes critical to cell survival during HIV-1 infection. We used single-cell FISH-Flow technology to characterise latency reversal and the contribution of viral RNA to inducing cell death; pharmacological targeting of DDX3 induced HIV-1 RNA expression, resulting in phosphorylation of IRF3, upregulation of IFNβ and selective induction of apoptosis in viral RNA-expressing CD4+ T cells from PLWHIV but not bystander cells. DDX3 inhibitor treatment of CD4+ T cells from PLWHIV in an in vitro culture model over five days resulted in an approximately 50% reduction of the inducible latent HIV-1 reservoir as determined by quantitation of CA HIV-1 RNA, by TILDA, as well as by FISH-Flow technology. Our data support the translation of DDX3 inhibitor class compounds into HIV-1 curative strategies and provide proof of concept for pharmacological reversal of latency coupled to induction of apoptosis towards elimination of the inducible reservoir.

2021-02-26 | GSE167553 | GEO

A new role for the DEAD-box RNA helicase DDX3 in co-translational protein quality control

Project description:DEAD-box RNA helicases are central players in RNA metabolism, however, their role in translation regulation is largely unexplored in parasitic protozoa. Here, we have investigated the role of DDX3 RNA helicase in ribosome-associated protein quality control in Leishmania. We show that ribosomes move more slowly and de novo polypeptide synthesis is reduced in cells lacking DDX3. In accordance with the slowing of ribosome speed, DDX3 depleted cells exhibit higher levels of ribosome-associated ubiquitination. Especially, ubiquitination of nascent polypeptides is enhanced upon DDX3 loss as determined by the isolation of ribosome-associated nascent chains modified either by HA-Ubiquitin or by endogenous ubiquitin using biotinylated-puromycin labeling. Consistent with increased co-translational ubiquitination, quantitative proteomics analysis revealed higher recruitment of E3 ubiquitin ligases and proteasomal components to DDX3 knockout ribosomes to eliminate aberrant nascent polypeptides. In addition, we show that cells lacking DDX3 accumulate cytosolic aggregates. This along with the higher recruitment of ribosome-associated chaperones and the improvement of translation by increasing HSP70 availability suggests that co-translational control of nascent polypeptides is impaired in the absence of DDX3. Altogether, these results highlight an important role for DDX3 in ribosome-associated quality control by reducing co-translational ubiquitination and proteotoxicity, hence allowing optimal ribosome movement and translation elongation.

2021-07-23 | PXD020667 | Pride

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