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Mus musculus

ABSTRACT: Loss of a mammalian circular RNA locus causes miRNA deregulation and affects brain function [miRNA-seq]

PROVIDER: PRJNA360107 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5144160.fastq.gz	Fastqsanger.gz
	SRR5144170.fastq.gz	Fastqsanger.gz
	SRR5144161.fastq.gz	Fastqsanger.gz
	SRR5144171.fastq.gz	Fastqsanger.gz
	SRR5144162.fastq.gz	Fastqsanger.gz

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Loss of a mammalian circular RNA locus causes miRNA deregulation and affects brain function

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Loss of a mammalian circular RNA locus causes miRNA deregulation and affects brain function [rRNA-depleted RNA-Seq]

Project description:Hundreds of circular RNAs (circRNAs) are highly abundant in the mammalian brain, often with conserved expression. Here we show that the circRNA Cdr1as is massively bound by the microRNAs (miRNAs) miR-7 and miR-671 in human and mouse brains. When the Cdr1as locus was removed from the mouse genome, knockout animals displayed impaired sensorimotor gating-a deficit in the ability to filter out unnecessary information-which is associated with neuropsychiatric disorders. Electrophysiological recordings revealed dysfunctional synaptic transmission. Expression of miR-7 and miR-671 was specifically and posttranscriptionally misregulated in all brain regions analyzed. Expression of immediate early genes such as Fos, a direct miR-7 target, was enhanced in Cdr1as-deficient brains, providing a possible molecular link to the behavioral phenotype. Our data indicate an in vivo loss-of-function circRNA phenotype and suggest that interactions between Cdr1as and miRNAs are important for normal brain function.

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Loss of a mammalian circular RNA locus causes miRNA deregulation and affects brain function [miRNA-seq]

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Loss of a mammalian circular RNA locus causes miRNA deregulation and affects brain function [RNA-seq]

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Huntingtin loss-of-function contributes to transcriptional deregulation in Huntington’s disease (miRNA-Seq)

Project description:Huntingtin loss-of-function contributes to transcriptional deregulation in Huntington’s disease (miRNA-Seq)

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Synthetic circular RNA functions as a miR-21 sponge to suppress gastric carcinoma cell proliferation

Project description:MicroRNA (miRNA) sponges containing miRNA complementary binding sites constitute a potentially useful strategy for miRNA-inhibition therapeutics in cancer patients. Recently, naturally occurring circular RNAs (circRNAs) have been revealed to function as efficient microRNA sponges. We hypothesized that synthetic circRNA sponges targeting oncomiRs could be constructed and used to achieve potentially therapeutic microRNA loss of function. In this study, linear RNA molecules containing five miR-21 binding sites were transcribed in vitro. After dephosphorylation by calf intestinal phosphatase and phosphorylation by T4 polynucleotide kinase, circRNA sponges were circularized using 5’-3’ end ligation by T4 RNA ligase 1. Synthetic circular sponge stability was assayed in the presence of RNase R or fetal bovine serum. Luciferase reporter and cell proliferation assays were performed to assess competitive inhibition of miR-21 activity by circRNA sponges in NCI-N87 gastric cancer cells. Tandem Mass Tag (TMT) labeling proteomics analysis and Western blotting were performed to delineate effects of circRNA sponges on miR-21 downstream targeted proteins. Our experiments revealed that artificial circRNA sponges can be synthesized using enzymatic ligation. These synthetic circRNA sponges are more resistant than their linear RNA counterparts to nuclease degradation in vitro. They effectively suppress the activity of miR-21 on its downstream protein targets, including the important cancer protein DAXX. Finally, they also inhibit gastric cancer cell proliferation. Our results suggest that synthetic circRNA sponges represent a rapid, effective, convenient strategy to achieve loss of miRNA function in vitro, with potential future therapeutic application in vivo.

2018-10-22 | PXD008584 | Pride

Project description:Frameshift mutation of a mammalian circRNA PVT1 locus causes the loss of PVT1-68aa coding function and promote organic aging.

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H3K4me3 chromatin profiling in SUMOylation-competent and -deficient bone marrow derived dendritic cells unstimulated or stimulated with LPS

Project description:Purpose: To determine H3K4me3 chromatin profile in UBC9WT and UBC9KO BMDC before and after LPS stimulation. Methods: H3K4me3 chromatin profile was determined by sequencing UBC9 WT and UBC9 KO BMDC chromatin immunoprecipitated with antibody specific for H3K4me3. Results: We show differential chromatin profile for H3K4me3 on the ifnb1 locus between UBC9 KO cells and UBC9 WT. Conclusions: Loss of SUMOylation causes a deregulation of ifnb1 transcription activation mark. A study of H3K4me3 chromatin profile in UBC9 WT and UBC9 KO Bone Marrow derived Dendritic Cells.

2015-12-14 | E-GEOD-66338 | biostudies-arrayexpress

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