Next Generation Sequencing of CD8+ cells from Wild Type and miR-144/451 knockout mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA835147 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19088071_1.fastq.gz | Fastqsanger.gz | |||
| SRR19088071_2.fastq.gz | Fastqsanger.gz | |||
| SRR19088072_1.fastq.gz | Fastqsanger.gz | |||
| SRR19088072_2.fastq.gz | Fastqsanger.gz | |||
| SRR19088073_1.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the function miR-144/451 on the function of CD8+ cells, we sorted the CD8a+ cells from wild type and miR-144/451 knockout mice, and then performed gene expression profiling analysis using data obtained from RNA-seq.
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Project description:microRNA miR-144/451 is highly expressed during erythropoiesis. We deleted the miR-144/451 gene locus in mice and compared the transcriptomes of miR-144/451-null bone marrow erythroid precursors to stage-matched wild-type control cells.
2010-07-15 | GSE21041 | GEO
Project description:microRNA miR-144/451 is highly expressed during erythropoiesis. We deleted the miR-144/451 gene locus in mice and compared the transcriptomes of miR-144/451-null bone marrow erythroid precursors to stage-matched wild-type control cells. Ter119+/CD71+/FSC-high bone marrow erythroblasts were sorted directly into Trizol LS reagent. Total RNAs extracted from three miR-144/451 knock-out and three wide type mice were analyzed using Affymetrix Mouse Genome 430 2.0 Arrays.
2010-07-15 | E-GEOD-21041 | biostudies-arrayexpress
Project description:Tto investigate whether ablation of miR-144/451 is deleterious for th3+/- mice, we crossed miR-144/451 knockout (mKO) mice (with mild anemia at baseline)13 with th3+/- mice (with severe anemia). We found that mKO/th3+/- double-mutant mice exhibited dramatic improvement in anemia. To explore the mechanism of anemia improvement in mKO/th3+/- mice, we fractionated erythroblasts from bone marrow of four genotypes mice, including WT,mKO, th3+/-,mKO/th3+/- mice,for microarray analysis.
2023-01-13 | GSE208608 | GEO
Project description:MicroRNAs inhibit gene expression by recruiting the RNA-induced silencing complex (RISC) to mRNAs in a process termed RNA interference (RNAi). While it is generally accepted that RNAi modulates gene expression pervasively, the number of mRNAs bound and repressed by miRNAs in vivo in individual cell types remains unknown, with estimates ranging from a few hundred genes to many thousands. We examined microRNA activities in primary cells by combining genetic loss of function with RNA-sequencing, quantitative proteomics and High-Throughput Sequencing of RNA isolated by Crosslinking Immunoprecipitation (HITS-CLIP), focusing on miR-144/451, the most highly expressed microRNA locus during red blood cell (RBC) formation. We show that Argonaute (Ago) protein binds over one thousand different mRNAs in a miR-144/451-dependent manner, accounting for one third of all Ago-bound mRNAs. However, only about 100 mRNAs are stabilized in RBC precursors after ablation of the miR-144/451 locus. Thus, Ago-miRNA complexes destabilize only a small subset of bound mRNAs, probably no more than a few hundred in erythroblasts under physiological conditions. Our integrated approach identified more than 50 new miR-144/451 target mRNAs, including Cox10, which facilitates assembly of the mitochondrial cytochrome c oxidase (COX) electron transport complex. Loss of miR-144/451 resulted in increased Cox10 expression, accumulation of the COX complex, and increased mitochondrial membrane potential with no change in mitochondrial mass. Thus, miR-144/451 represses mitochondrial respiration during erythropoiesis by inhibiting Cox10.
2018-10-01 | GSE104447 | GEO
Project description:MicroRNAs inhibit gene expression by recruiting the RNA-induced silencing complex (RISC) to mRNAs in a process termed RNA interference (RNAi). While it is generally accepted that RNAi modulates gene expression pervasively, the number of mRNAs bound and repressed by miRNAs in vivo in individual cell types remains unknown, with estimates ranging from a few hundred genes to many thousands. We examined microRNA activities in primary cells by combining genetic loss of function with RNA-sequencing, quantitative proteomics and High-Throughput Sequencing of RNA isolated by Crosslinking Immunoprecipitation (HITS-CLIP), focusing on miR-144/451, the most highly expressed microRNA locus during red blood cell (RBC) formation. We show that Argonaute (Ago) protein binds over one thousand different mRNAs in a miR-144/451-dependent manner, accounting for one third of all Ago-bound mRNAs. However, only about 100 mRNAs are stabilized in RBC precursors after ablation of the miR-144/451 locus. Thus, Ago-miRNA complexes destabilize only a small subset of bound mRNAs, probably no more than a few hundred in erythroblasts under physiological conditions. Our integrated approach identified more than 50 new miR-144/451 target mRNAs, including Cox10, which facilitates assembly of the mitochondrial cytochrome c oxidase (COX) electron transport complex. Loss of miR-144/451 resulted in increased Cox10 expression, accumulation of the COX complex, and increased mitochondrial membrane potential with no change in mitochondrial mass. Thus, miR-144/451 represses mitochondrial respiration during erythropoiesis by inhibiting Cox10.
2018-10-01 | GSE104441 | GEO
Project description:MicroRNAs inhibit gene expression by recruiting the RNA-induced silencing complex (RISC) to mRNAs in a process termed RNA interference (RNAi). While it is generally accepted that RNAi modulates gene expression pervasively, the number of mRNAs bound and repressed by miRNAs in vivo in individual cell types remains unknown, with estimates ranging from a few hundred genes to many thousands. We examined microRNA activities in primary cells by combining genetic loss of function with RNA-sequencing, quantitative proteomics and High-Throughput Sequencing of RNA isolated by Crosslinking Immunoprecipitation (HITS-CLIP), focusing on miR-144/451, the most highly expressed microRNA locus during red blood cell (RBC) formation. We show that Argonaute (Ago) protein binds over one thousand different mRNAs in a miR-144/451-dependent manner, accounting for one third of all Ago-bound mRNAs. However, only about 100 mRNAs are stabilized in RBC precursors after ablation of the miR-144/451 locus. Thus, Ago-miRNA complexes destabilize only a small subset of bound mRNAs, probably no more than a few hundred in erythroblasts under physiological conditions. Our integrated approach identified more than 50 new miR-144/451 target mRNAs, including Cox10, which facilitates assembly of the mitochondrial cytochrome c oxidase (COX) electron transport complex. Loss of miR-144/451 resulted in increased Cox10 expression, accumulation of the COX complex, and increased mitochondrial membrane potential with no change in mitochondrial mass. Thus, miR-144/451 represses mitochondrial respiration during erythropoiesis by inhibiting Cox10.
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Project description:Expression data of ECa9706 over expressing miR-144/451 cluster
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Project description:Antiviral responses must be regulated to rapidly defend against infection while minimizing inflammatory damage, but the mechanisms for establishing the magnitude of response within an infected cell are not well understood. miRNAs are small non-coding RNAs that negatively regulate protein levels by binding target sequences on their cognate mRNA. Here we identify miR-144 as a negative regulator of the host antiviral response. Ectopic expression of miR-144 resulted in increased replication of three RNA viruses, influenza, EMCV, and VSV, in primary mouse lung epithelial cells. To elucidate the mechanism whereby miR-144 increases influenza replication within lung epithelial cells, immortalized murine Type I epithelial cells (Let1 cells) stably over-expressing miR-144 were infected with influenza A for 1 or 18 hours and the transcriptional profile was compared with those of infected control cells. This systems biology approach identified the transcriptional network regulated by miR-144 and demonstrated that it controls the TRAF6/IRF7 antiviral response by post-transcriptionally suppressing TRAF6 levels. In vivo ablation of miR-144 reduced influenza replication within the lung. 16 RNA samples from immortalized murine Type I airway epithelial cells (Let1 cells) were analyzed using Agilent microarrays. Cells expressing miR-144, miR-451, or a vector control (GFP) were analyzed after infection with PR8 influenza virus (MOI=5) for 1 or 18 hours.
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