HuR knockdown in humanized and wildtype mice liver samples
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ABSTRACT:
PROVIDER: PRJNA678342 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:HuR shRNA adenoviruses were delivered into WT or humanized mice intravenously at 2 × 109 pfu/mouse for both control virus and HuR shRNA virus . After seven days, liver tissue samples were harvested after a four hours fasting and stored immediately in liquid nitrogen till further analysis.The frozen liver tissue samples were homogenized in Trizol reagent (Invitrogen) using TissueLyser LT system (Qiagen). The isolated RNA was purified by MagMAX RNA Extraction Kit (ThermoFisher) and the construction of strand specific sequencing libraries using TruSeq Stranded Total RNA Prep kit (Illumina) and the sequencing was performed at NHLBI DNA Sequencing and Genomics Core using Illumina HiSeq 3000 paired-end sequencing platform.
2021-01-04 | GSE161462 | GEO
Project description:Integrative regulatory mapping indicates that the RNA-binding protein HuR (ELAVL1) couples pre-mRNA processing and mRNA stability In this dataset, we employed two distinct experiments. 1) HuR RIP-chip to identify mRNA targets of HuR. 2) HuR knockdown to identify mRNAs whose expression are dependent on HuR. All 12 samples were normalized with PLIER using Affymetrix power tools. To identify RNA targets of HuR, HuR RIP samples were compared to Mock RIP samples. To identify RNA regulated by HuR, HuR knockdown samples were compared to mock knockdown samples.
2011-08-18 | E-GEOD-29778 | biostudies-arrayexpress
Project description:Integrative regulatory mapping indicates that the RNA-binding protein HuR (ELAVL1) couples pre-mRNA processing and mRNA stability In this dataset, we employed two distinct experiments. 1) HuR RIP-chip to identify mRNA targets of HuR. 2) HuR knockdown to identify mRNAs whose expression are dependent on HuR.
2011-08-19 | GSE29778 | GEO
Project description:We report the HuR-RNA interactions in the liver by performing RNA-immunoprecipitation sequencing (RIP-seq). RIP-seq was performed in healthy livers of wildtype (WT) mice using a HuR antibody. We found that 1380 cytoplasmic-target mRNAs bound to HuR, as assessed by the comparison between the HuR-specific antibody and the IgG control
2021-09-15 | GSE143703 | GEO
Project description:HuR is known to regulate mRNA stability and translatability in cytoplasm. In several human tumors, the level of HuR expression has been shown to correlate with poor disease outcome. In meningioma, however, the prognostic value and the potential pro-oncogenic properties of HuR remain obscure. To clarify these, transcriptome-wide analyses in IOMM-Lee cells were performed to pinpoint the detailed molecular consequences of HuR knockdown. In IOMM-Lee cells, transcriptomic analyses revealed that HuR knockdown deregulated the signaling pathway of HIF1A and upregulated the expression of genes for cytoplasmic mRNA processing body assembly, poly(A)-specific ribonuclease activity, positive regulation of apoptosis, negative regulation of RNA splicing, global genome nucleotide-excision repair, and positive regulation of cell cycle arrest. Interestingly, HuR knockdown under hypoxic culture condition potentiated further the effects of HuR knockdown on cell growth, apoptosis, and HIF1A expression.
2017-05-11 | GSE95212 | GEO
Project description:We aimed to identify genes that are altered upon deletion of HuR in hepatocytes under steady state conditions.
2021-09-15 | GSE143358 | GEO
Project description:Sequencing of liver RNA from HuR WT and HuR KO mice
| PRJNA600219 | ENA
Project description:The 3’ UTR of messenger RNAs serves as the regulatory region that mediates post-transcriptional control by microRNAs and RNA-binding proteins (RBPs). Aside from individual sequence-specific binding and regulation, examples of interaction between these factors at particular 3’ UTR sites have emerged in recent studies. However, the whole picture of such higher-order regulatory modules across the transcriptome is lacking. Here, we investigate the interactions between HuR, a ubiquitous RBP, and Ago2, a core effector of the miRNA pathway, at the transcriptome-wide level. Using HITS-CLIP, we map HuR and miRNA binding sites on human 3’UTRs and assess their co-occurrence. Additionally, we demonstrate global effects of HuR knockdown on Ago2 occupancy, suggesting a co-regulatory relationship. Focusing on sites of Ago2-HuR overlap, 13 candidates were screened in luciferase reporter assays, compared to miRNA site mutant controls. Eleven of the sites showed a repressive activity, which displayed significant de-repression upon subsequent testing of the reporters in Dicer-null cells, substantiating miRNA dependence. To experimentally test for HuR’s role in co-regulation, we tested the reporters in CRISPR-generated HuR KO cells. Three of the miRNA sites demonstrated altered activities, indicating that HuR has an effect on miRNA repression at those sites. Our study presents an efficient search and validation system for studying miRNA-HuR interactions, which expands our understanding of the combinatorial post-transcriptional control of gene expression at the 3’ UTR.
2018-01-19 | GSE102320 | GEO
Project description:Human antigen R (HuR) protein, a RNA binding protein (RBP), has been reported to regulate essential steps in RNA metabolism and immune response in a variety of cell types, but its function in metabolism remains unclear. This study identifies HuR as a major repressor during adipogenesis. Knockdown and overexpression of HuR in primary adipocyte culture enhances and inhibits adipogenesis in vitro, respectively. Fat-specific knockout of HuR significantly enhances adipogenic gene program in all three major adipose tissues including epidydimal, inguinal white and brown adipose tissue, accompanied with systemic glucose intolerance and insulin resistance. Conversely, transgenic overexpression of HuR in adipose tissue prevents the HFD induced obesity by repressing adipogenesis. Mechanistically, HuR may inhibit adipogenesis by recognizing and modulating the stability of hundreds of adipocyte transcripts, including the mRNA of Insig1, a negative regulator during adipogenesis. Taken together, our work establishes HuR as a novel posttranscriptional regulator of adipogenesis and provides a new insight into how RNA processing contributes to adipocyte development.
2019-09-09 | GSE124278 | GEO
Project description:Human antigen R (HuR) protein, a RNA binding protein (RBP), has been reported to regulate essential steps in RNA metabolism and immune response in a variety of cell types, but its function in metabolism remains unclear. This study identifies HuR as a major repressor during adipogenesis. Knockdown and overexpression of HuR in primary adipocyte culture enhances and inhibits adipogenesis in vitro, respectively. Fat-specific knockout of HuR significantly enhances adipogenic gene program in all three major adipose tissues including epidydimal, inguinal white and brown adipose tissue, accompanied with systemic glucose intolerance and insulin resistance. Conversely, transgenic overexpression of HuR in adipose tissue prevents the HFD induced obesity by repressing adipogenesis. Mechanistically, HuR may inhibit adipogenesis by recognizing and modulating the stability of hundreds of adipocyte transcripts, including the mRNA of Insig1, a negative regulator during adipogenesis. Taken together, our work establishes HuR as a novel posttranscriptional regulator of adipogenesis and provides a new insight into how RNA processing contributes to adipocyte development.
2019-09-09 | GSE124275 | GEO