Mouse Liver Raly knockdown
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE77805 | GEO | 2016/03/31
SECONDARY ACCESSION(S): PRJNA311591
REPOSITORIES: GEO
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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.
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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:Monodelphis domestica RALY, RALY heterogeneous nuclear ribonucleoprotein [Source:NCBI gene;Acc:100032338], is expressed in 2 baseline experiment(s);
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Project description:Danio rerio raly, RALY heterogeneous nuclear ribonucleoprotein [Source:ZFIN;Acc:ZDB-GENE-041010-127], is differentially expressed in 1 experiment(s);
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Project description:Danio rerio raly, RALY heterogeneous nuclear ribonucleoprotein [Source:ZFIN;Acc:ZDB-GENE-041010-127], is expressed in 1 baseline experiment(s);
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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
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Project description:Genome-wide effects of Pbcas4 knockdown
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