Mouse Liver Raly knockdown
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE77805 | GEO | 2016/03/31
SECONDARY ACCESSION(S): PRJNA311591
REPOSITORIES: GEO
Similar Datasets
Project description:Effects of Raly knockdown on hepatic gene expression Mouse livers treated with adenoshRaly or control
2016-03-31 | E-GEOD-77805 | biostudies-arrayexpress
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of gene expression and alternative RNA splicing. The goals of this study are to compare alternative splicing in RALY knock-down cells to identify the function of RALY in alternative splicing transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Methods: mRNA profiles of RALY knock-dowed HCT 116 cells and non-silencing shRNA treated HCT 116 cells generated by deep sequencing, in duplicate, using Illumina Hiseq 2500. Results: Using an we mapped about more than 60 million reads per sample to the human genome (GRCh38) and identified 58,884 transcripts in WT and RALY knock-downed HCT 116 cells with Hisat2. rMATS analysis of RNA-seq data demonstrate significant effects of RALY on 4,046 skipped exon splicing and other alternative splicing events. Conclusions: Our study represents the first detailed analysis of transcriptomes in RALY KD cells, with biologic duplicates, generated by RNA-seq technology. The splicing analysis workflows reported here should provide a framework for the RALY function in the splicing.
2022-11-30 | GSE141283 | GEO
Project description:We applied a HeLa cell model with enforced expression of RALY and studied the effect of RALY on cancer cell proliferation and apoptosis. We then obtained RNA-seq transcriptomes from the normal cells and those with RALY overexpression, followed by analysis of the deregulation of alternative splicing and gene expression that were mediated by RALY overexpression.
2023-01-11 | GSE157125 | GEO
Project description:To investigate the effect of depletion of RALY on gene expression of A549 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq.
2023-05-24 | GSE209920 | GEO
Project description:Liver-specific Knockdown of JNK1 Up-regulates Proliferator-activated Receptor Coactivator 1 and Increases Plasma Triglyceride despite Reduced Glucose and Insulin Levels in Diet-induced Obese Mice. The c-Jun N-terminal kinases (JNKs) have been implicated in the development of insulin resistance, diabetes, and obesity. Genetic disruption of JNK1, but not JNK2, improves insulin sensitivity in diet-induced obese (DIO) mice. We applied RNA interference to investigate the specific role of hepatic JNK1 in contributing to insulin resistance in DIO mice. Adenovirus-mediated delivery of JNK1 short-hairpin RNA (Ad-shJNK1) resulted in almost complete knockdown of hepatic JNK1 protein without affecting JNK1 protein in other tissues. Liver-specific knockdown of JNK1 resulted in significant reductions in circulating insulin and glucose levels, by 57 and 16%, respectively. At the molecular level, JNK1 knockdown mice had sustained and significant increase of hepatic Akt phosphorylation. Furthermore, knockdown of JNK1 enhanced insulin signaling in vitro. Unexpectedly, plasma triglyceride levels were robustly elevated upon hepatic JNK1 knockdown. Concomitantly, expression of proliferator-activated receptor coactivator 1, glucokinase, and microsomal triacylglycerol transfer protein was increased. Further gene expression analysis demonstrated that knockdown of JNK1 up-regulates the hepatic expression of clusters of genes in glycolysis and several genes in triglyceride synthesis pathways. Our results demonstrate that liver-specific knockdown of JNK1 lowers circulating glucose and insulin levels but increases triglyceride levels in DIO mice. Keywords: Treatment Response
2007-10-02 | GSE7648 | GEO
Project description:We observed that Ildr2 knockdown via adenovirally-delivered shRNA (Adv-Ildr2 shRNA) causes hepatic steatosis in mice. Acute, liver-specific Ildr2 knockout mice generated by infecting C57BL/6J mice segregating for a floxed allele of Ildr2 with adenoviral Cre recombinase (Adv-Cre) do not develop hepatic steatosis. However, administration of Adv-Ildr2 shRNA to Ildr2 knockout mice (Ildr2floxed; albumin-cre) did cause hepatic steatosis, indicating that the Adv-Ildr2 shRNA had apparent “off-target” effects on gene(s) other than Ildr2. To determine additional targets of Ildr2 shRNA that may regulate hepatic lipid metabolism, we performed RNA sequencing on liver samples from (1) Adv-Ildr2 shRNA knockdown mice, (2) Adv-lacZ shRNA control mice, and (3) Adv-Cre Ildr2 knockout mice. For the purposes of our study, we sought to identify genes downregulated by Adv-Ildr2 shRNA, but unchanged in Adv-lacZ shRNA control or Adv-Cre Ildr2 knockout mice. The hepatic steatosis observed in Adv-Ildr2 shRNA knockdown mice was likely due to shRNA targeting of other “off-target” genes. We propose that the genes candidates identified in this sequencing experiment may lead to identification of novel regulators of hepatic lipid metabolism.
2018-05-11 | GSE114289 | GEO
Project description:Cytochrome P450 oxidoreductase (POR) is involved in the oxidative metabolism of xenobiotics and endogenous compounds like fatty acid and cholesterol. While effects of diminished Por were extensively studied in mouse models, studies in human models are still missing. We used previously established CRISPR/Cas9-mediated POR knockdown in HepaRG cells as a human hepatic cell model to investigate the effects of POR knockdown on global protein expression levels.
2021-11-04 | PXD028577 | Pride
Project description:Effect of depletion of RALY on gene expression of A549 cells.
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Project description:To study the role of Rab35 in the formation of bile canaliculi, primary mouse hepatoblasts were acquired, cultured in matrigel, and subjected to Rab35 knockdown by siRNA with scrambled control (4 biol. replicates each, block-randomised). Samples were subjected to S-trap protein digest and label-free quantification by staggered DIA demultiplexed with MSConvert and processed with DIA-NN, followed by differential expression and gene set enrichment analysis.
2023-03-06 | MSV000091413 | MassIVE
Project description:This study sought to interrogate the effects of lipids and lipid metabolites on the hepatic proteome. Protein expression and tyrosine phosphorylation in high-fat diet (HFD) mouse livers vs. livers of normal chow fed (NC) mice were investigated using multiplexed quantitative LC-MS/MS (TMT labeling). Additionally, the rat hepatoma cell line H4IIE was used to monitor the effects of free fatty acids on tyrosine signaling, gene expression and the levels of reactive oxygen species. These data were used to inform potential points of intervention and chemical perturbations and their effects on phenotypic and signaling output in the cell line, and included small molecule inhibtors of Src-family kinases and antioxidants. Based on the in vitro effects, HFD mice were fed an antioxidant and phenotypic and tyrosine signaling changes were measured.
2019-07-08 | PXD011458 | Pride