Expression date from WT RAW264.7 and HuR-deficient RAW264.7 stimulated with poly(I:C) using lipofectamine
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE103459 | GEO | 2018/04/01
REPOSITORIES: GEO
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Project description:HuR Deficient and Control, Bone Marrow Derived Macrophages stimulated with Lipopolysaccharides, from Salmonella enteritidis, 100ng/ml for 0, 2 and 6 hours. RNA from 2.000.000 cells was extracted with the RiboPure kit.
2011-01-01 | E-MEXP-2904 | biostudies-arrayexpress
Project description:ionPurpose: The goal of this study is to investigate how HuR regulates NASH progression. Methods: The hepatic mRNA profiles of HuR flox/flox and hepatocyte-specific HuR knockout (HKO) mice (n=3 for each group) fed with an MCD for 3 weeks were generated by deep sequencing using an Illumina Novaseq platform. Paired-end clean reads were aligned to the mouse reference genome(Ensemble_GRCm38.p6) with TopHat (version 2.0.12), and the aligned reads were used to quantify mRNA expression by using HTSeq-count (version 0.6.1). Conclusion: Our study represents the first detailed analysis of hepatic mRNA profiles in HuR flox/flox and hepatocyte-specific HuR knockout (HKO) mice fed with an MCD for 3 weeks, generated by RNA-seq technology. Our results show that 353 genes were upregulated and 422 genes were downregulated. Gene Ontology (GO) analysis showed that genes related to leukocyte migration, leukocyte chemotaxis, cell chemotaxis, neutrophil migration and Fc receptor signaling pathway were significantly decreased, which contributes to the protective effects of NASH progression in HKO mice.
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Project description:To study the neuron-specific function of HuR, we generated inducible, neuron-specific HuR-deficient mice of both sexes. These mice developed a phenotype consisting of poor balance, decreased movement, and decreased strength Genome-wide microarray and RT-PCR analysis further indicated that HuR deficiency in neurons resulted in altered expression of genes in the brain involved in cell growth The additional enriched GO terms in the brain tissues of neuron-specific HuR-deficient mice were largely related to inflammation, including interferon-induced genes and complement components.
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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.
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Project description:The aim of the current study was to investigate the response of in vitro differentiated trout macrophages, a primary cell culture system widely used in fish immunology research, to lipopolysaccharide (LPS) and to the analog viral ds(RNA) Poly I:C. To that end we have used a salmonid-specific microarray platform enriched with immune-related genes. The results clearly suggest that the molecular mechanisms involved in the response of macrophages to LPS and Poly (I:C) are specific in some signaling pathways related to cell communication, signal transduction and kinase cascades. Nevertheless, macrophages stimulated with bacterial or viral PAMPs also activate common transcription factors.
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Project description:Although neurogenesis in the adult brain recapitulates processes that occur during embryonic development, adult neurogenesis exhibits distinct characteristics from its embryonic counterpart. However, the intrinsic mechanism underlying the differential regulation of neurogenesis between these two stages remains unclear. Herein, we show that the ablation of RNA-binding protein HuR in neural stem cells (NSCs) impairs adult, but not embryonic, neurogenesis. HuR is predominantly expressed in the cytoplasm of embryonic NSCs but translocates into the nucleus of adult NSCs. Transcriptomic analysis of HuR-deficient adult NSCs revealed that nuclear HuR primarily regulates alternative splicing of numerous premRNA transcripts, including focal adhesion kinase (FAK). HuR-deficient adult NSCs generate increased FAK mRNA isoforms with shorter 5’ UTRs, leading to enhanced FAK mRNA translation and hyperactivated FAK signaling, and inhibition of FAK ameliorates defective adult neurogenesis and impaired hippocampus-dependent learning in HuR-deficient mice. Taken together, these findings reveal novel mechanistic insights into the differential regulation of embryonic and adult neurogenesis through developmental cytoplasmic-to-nuclear translocation of HuR in NSCs.
2019-11-04 | GSE137323 | GEO
Project description:RNA-binding proteins coordinate the fates of multiple RNAs, but the principles underlying these global interactions remain poorly understood. We elucidated regulatory mechanisms of the RNA-binding protein HuR, by integrating data from diverse high-throughput targeting technologies, specifically PAR-CLIP, RIP-chip, and whole-transcript expression profiling. The number of binding sites per transcript, degree of HuR-association, and degree of HuR-dependent RNA stabilization were positively correlated. Pre-mRNA and mature mRNA containing both intronic and 3' UTR binding sites were more highly stabilized than transcripts with only 3' UTR or only intronic binding sites, suggesting that HuR couples pre-mRNA processing with mature mRNA stability. We also observed HuR-dependent splicing changes and substantial binding of HuR in poly-pyrimidine tracts of pre-mRNAs. Comparison of the spatial patterns surrounding HuR and miRNA binding sites provided functional evidence for HuR-dependent antagonism of proximal miRNA-mediated repression. We conclude that HuR coordinates gene expression outcomes at multiple interconnected steps of RNA processing. HuR (ELAVL1) PAR-CLIP
2011-08-19 | E-GEOD-29779 | biostudies-arrayexpress
Project description:RNA-binding proteins coordinate the fates of multiple RNAs, but the principles underlying these global interactions remain poorly understood. We elucidated regulatory mechanisms of the RNA-binding protein HuR, by integrating data from diverse high-throughput targeting technologies, specifically PAR-CLIP, RIP-chip, and whole-transcript expression profiling. The number of binding sites per transcript, degree of HuR-association, and degree of HuR-dependent RNA stabilization were positively correlated. Pre-mRNA and mature mRNA containing both intronic and 3' UTR binding sites were more highly stabilized than transcripts with only 3' UTR or only intronic binding sites, suggesting that HuR couples pre-mRNA processing with mature mRNA stability. We also observed HuR-dependent splicing changes and substantial binding of HuR in poly-pyrimidine tracts of pre-mRNAs. Comparison of the spatial patterns surrounding HuR and miRNA binding sites provided functional evidence for HuR-dependent antagonism of proximal miRNA-mediated repression. We conclude that HuR coordinates gene expression outcomes at multiple interconnected steps of RNA processing.
2011-08-19 | GSE29779 | GEO
Project description:Lipopolysaccharide exposure to macrophages induces an inflammatory response that is heavily regulated at the post-transcriptional level. HuR, ELAVL1, is an RNA binding protein that binds and regulate the maturation and half-life of AU/U rich elements (ARE) containing cytokines and chemokines transcripts, mediating the LPS induced response. Here we investigated to what extent small molecules inhibiting HuR-RNA interaction, called tanshinone mimics, counteract the LPS induced macrophage response. We show that tanshinone mimics are present in solution in a keto-enolic tautomerism and that, by molecular dynamic calculations, the ortho quinone form is the preferred species interacting with HuR and favoring the closure of its conformation to a no-binding mode. The protection of the enolic status with diacetate caused the loss of activity of tanshinone mimics in vitro but active in vivo. Murine macrophages cell line RAW264.7 was treated with LPS and tanshinone mimics and the modulation of the LPS induced response was monitored by RNA and Ribonucleoprotein immunoprecipitation sequencing. Correlation analyses indicated that LPS induced a strong coupling between differentially expressed genes and HuR-bound genes and that tanshinone mimics reduced the interaction. Functional annotation addressed a specific set of genes, as Cxcl10, Il1b, Cd40, Fas, involved in chemotaxis and immune response whose association with HuR decreased and led to a reduction of their protein level and secretion. The same effect was observed in primary murine bone marrow derived macrophages and in vivo in a LPS induced peritonitis model, in which the serum level of Cxcl10 and Il1b was strongly reduced, endowing tanshinone mimics with anti-inflammatory properties in vivo.
2023-03-01 | GSE198605 | 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.
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