Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA310647 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We generated a genome wide map of instances where the long noncoding RNA, Tug1, binds to DNA in cultured mouse podocytes under normal glucose conditions using Chromatin-RNA Precipitation coupled with high throughput sequencing (ChIRP-Seq) 48 alternating (even, odd) biotynilated probes were designed to span the full length of Tug1 RNA. Chromatin was prepared from gluteraldehyde crosslinked nuclei from early passage podocytes. Chromatin extracts were duplicated with either even or odd probes. Duplicate samples for Input DNA, Even pulldown (PD) and Odd PD DNA was purified following incubation and supplied for Illumina sequencing by ArrayStar (Rockville, MD).
2016-10-24 | E-GEOD-77493 | biostudies-arrayexpress
Project description:We generated a genome wide map of instances where the long noncoding RNA, Tug1, binds to DNA in cultured mouse podocytes under normal glucose conditions using Chromatin-RNA Precipitation coupled with high throughput sequencing (ChIRP-Seq)
2016-10-24 | GSE77493 | GEO
Project description:We generated two mouse podocyte cell lines stably transduced with either a shControl lentiviral construct or a shRNA lentiviral construct designed to target Tug1 RNA to investigate the consequences on the gene expression profile of Tug1 knockdown in differentiated mouse podocytes
2016-10-24 | GSE77506 | GEO
Project description:Genome wide map of long noncoding RNA Tug1 binding sites in cultured mouse podocytes
| PRJNA310632 | ENA
Project description:Hepatic injury provoked by cold storage is a major problem affecting liver transplantation, as exposure to cold induces apoptosis in hepatic tissues. Long noncoding RNAs (lncRNAs) are increasingly understood to regulate apoptosis, but the contribution of lncRNAs to cold-induced liver injury remains unknown. Using RNA-seq, we determined the differential lncRNA expression profile in mouse livers after cold storage and found that expression of the lncRNA TUG1 was significantly down-regulated. Over-expression of TUG1 attenuated cold-induced apoptosis in mouse hepatocytes and liver sinusoidal endothelial cells LSECs, in part by blocking mitochondrial apoptosis and ER stress pathways. Moreover, TUG1 attenuated apoptosis, inflammation and oxidative stress in vivo in livers subjected to cold storage. Over-expression of TUG1 also improved hepatocyte function and prolonged hepatic graft survival rates in mice. These results suggest that the lncRNA TUG1 exerts a protective effect against cold-induced liver damage by inhibiting apoptosis in mice, and suggests a potential role for TUG1 as a target for the prevention of cold-induced liver damage in liver transplantation.
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Project description:We report trancriptional changes between wildtype mouse immortalized podocytes and compared to podocytes with shRNA-knockdown of Pdss2.
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Project description:Hepatocellular carcinoma (HCC) remains the third leading cause of cancer deaths; however, its therapeutic options are limited. Understanding the molecular mechanisms of HCC could shed light on new therapies. Emerging studies indicate the important role of long-noncoding RNAs (lncRNAs) in the pathogenesis of HCC. One of the early discovered lncRNAs, taurine-upregulated gene 1 (TUG1), has been up-regulated in HCC tissues, but its impact on HCC cells’ transcriptomics remains unexplored. We established TUG1-knockdown HCC cells and performed RNA-seq analysis. KEGG analysis revealed the significant enrichment of downregulated genes involved in glycolysis. Accordingly, TUG1-depleted HCC cells showed impairments in glucose uptake, ATP synthesis, and lactate production. Clinical HCC tissue data revealed positive gene expression correlations between TUG1 and glycolysis genes identified by RNA-seq. To identify a molecular function of TUG1 in glycolysis, we explored the competing endogenous (ceRNA) model and identified five microRNAs (miRNAs) with the highest number of TUG1 binding sites using bioinformatic tools. Amongst these miRNAs, microRNA-122-5p (miR-122-5p) displayed an inverse relationship for gene expression with most TUG1-regulated glycolysis genes, including PKM, ALDOA, ENO2, and PFKM. Dual luciferase assays confirmed the direct interaction between TUG1 and miR-122-5p and between miR-122-5p and the 3’ untranslated regions (3’UTR) of PKM and ALDOA. We further showed that inhibition of miR-122-5p alleviated the suppression of glycolysis induced by TUG1 depletion. Together, our RNA-seq analysis of TUG1-depleted HCC cells in combination with clinical data reveals the crucial function of TUG1 in promoting glycolysis via sponging miR-122-5p, which is a negative regulator of multiple glycolytic enzymes.
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Project description:To determine the biological mechanisms underlying the oncogenic properties of YAP in ccRCC the human ccRCC cell line MZ1774 was transduced with lentivirus containing a shRNA-cassette targeting YAP-mRNA. Expression profiles of MZ1774 YAP knockdown cells were compared to mock-transduced control cells. Total RNA from MZ1774 cells stably expressing shRNA directed against YAP compared to mock-transduced MZ1174 cells
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Project description:Metastasis is a complex process involving loss of adhesion, migration, invasion and proliferation of cancer cells. Cell adhesion molecules play a pivotal role in this phenomenon by regulating cell-cell and cell-matrix interactions. CD146 (MCAM) is associated with advanced tumor stage in melanoma, prostate and ovarian cancers. For this study, the MDA-MB-231 cell line was used as a prototypic mesenchymal and invasive cell line, spontaneously expressing high levels of CD146. Using whole-genome DNA microarrays, we investigated genes for which expression was modified by CD146 down-regulation, obtained by siRNA or shRNA technology Experiment Overall Design: Expression profiles of two cell lines transfected by two differents ShRNA directed against CD146 were compared with expression profiles of 3 control cell lines (i.e. native cell line, empty plasmid and shRNA directed against GFP)
2008-10-21 | E-GEOD-11951 | biostudies-arrayexpress