Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of HEK293T total RNA treated with 40 nM pre-miR-124/pre-miR-132 against mock treated control samples

ABSTRACT: RNA-seq of HEK293T total RNA treated with 40 nM pre-miR-124/pre-miR-132 against mock treated control samples

PROVIDER: PRJEB35440 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

RNA-seq of HEK293T total RNA treated with 40 nM pre-miR-124/pre-miR-132 against mock treated control samples

Project description:The expression of different RNAs in miR-124/miR-132 transfected HEK293T cells were compared to mock treated samples in order to describe fold change of transcripts assigned as miRNA targets by different tools or experiments.

2020-11-23 | E-MTAB-8516 | biostudies-arrayexpress

RNA-seq of miR-CLIP double purified, miR-124/miR-132 miR-CLIP probe treated HEK293T cells and corresponding mock treated and intermediate samples

Project description:Targetome of miR-124/miR-132 was enriched in HEK293T cells, a cell line which lacks the expression of these miRNA. The targetome was captured using miR-CLIP, a transfection-based double-purification crosslinking and immunoprecipitation (CLIP) method. Therefore HEK293T cells were transfected with miR-124/miR-132 miR-CLIP probes, which are trioxsalen, biotin bis-modified pre-miRNAs. Unspecific RNA-protein and trioxsalen mediated RNA-RNA crosslinking were induced by UV-irradiation before cell lysis. Total RNA (input samples) was enriched for AGO2-bound RNA using AGO2 immunoprecipitation, by depleting non-RISC associated RNAs. A second enrichment for specific targets of the transfected miRNA is performed using magnetic streptavidin-beads. This step relies on the interaction of the biotinylated probe, on which the RNA target is crosslinked, with the beads. The method was shown to deliver high-quality miRNA targetomes of both 5p and 3p miRNAs.

2020-11-23 | E-MTAB-8517 | biostudies-arrayexpress

Therapeutic miR-132 inhibition reverses heart failure

Project description:Despite some success of pharmacotherapies targeting primarily neurohormonal dysregulation, heart failure is a growing global pandemic with increasing burden. Treatments that improve the disease by reversing heart failure at the cardiomyocyte level are lacking. MicroRNAs (miRNA) are transcriptional regulators of gene expression, acting through complex biological networks, and playing thereby essential roles in disease progression. Adverse structural remodelling of the left ventricle due to myocardial infarction (MI) is a common pathological feature leading to heart failure. We previously demonstrated increased cardiomyocyte expression of the miR-212/132 family during pathological cardiac conditions. Transgenic mice overexpressing the miR-212/132 cluster (miR-212/132-TG) develop pathological cardiac remodelling and die prematurely from progressive HF. Using both knockout and antisense strategies, we have shown miR-132 to be both necessary and sufficient to drive the pathological growth of cardiomyocytes in a murine model of left ventricular pressure overload. Based on the findings, we proposed that miR-132 may serve as a therapeutic target in heart failure therapy. Here we provide novel mechanistic insight and translational evidence for the therapeutic efficacy in small and large animal models (n=135) of heart failure. We demonstrate strong PK/PD relationship, dose-dependent efficacy and high clinical potential of a novel optimized synthetic locked nucleic acid phosphorothioate backbone antisense oligonucleotide inhibitor of miR-132 (antimiR-132) as a next-generation heart failure therapeutic.

2020-01-09 | PXD015337 | Pride

RNA-seq of miR-CLIP double purified, miR-124/miR-132 miR-CLIP probe treated HEK293T cells and corresponding mock treated and intermediate samples

Project description:RNA-seq of miR-CLIP double purified, miR-124/miR-132 miR-CLIP probe treated HEK293T cells and corresponding mock treated and intermediate samples

| PRJEB35442 | ENA

Functional Involvement of Septal miR-132 in Extinction and Oxytocin-mediated Reversal of Social Fear

Project description:Social interactions are critical components for the survival of mammalian biology and evolution. Dysregulation of social behavior often leads to psychopathologies such as social anxiety disorder, which is characterized by an intense fear and avoidance of social situations. Using the social fear conditioning (SFC) paradigm, we analyzed expression levels of miR-132-3p and miR-124-3p within the septum, a brain region essential for social behavior and fear, after acquisition and extinction of social fear. Functional in vivo approaches using pharmacology, functional inhibition of miR-132-3p, viral miR-132 overexpression and shRNA-mediated knockdown of miR-132-3p within oxytocin receptor positive neurons confirmed septal miR-132-3p to be involved in social fear extinction and the oxytocin-mediated reversal of social fear. Moreover, Argonaute-RNA-co-immunoprecipitation-microarray analysis and further target mRNA quantification, depicted growth differentiation factor-5 (GDF-5) to be involved in miR-132-3p-mediated regulation of social fear extinction. Local application of GDF-5 resulted in impaired social fear extinction, an effect which seems to be mediated by miR-132-3p. In summary, we show that septal miR-132-3p is functionally involved in social fear extinction learning and oxytocin-mediated reversal of social fear.

2023-11-08 | GSE211449 | GEO

A global transcriptome analysis of skin wounds of diabetic mice (db/db) treated with miR-132 or control mimics

Project description:MiR-132 is one of the most upregulated miRNAs in human skin wounds at the inflammatory phase of healing. MiR-132 inhibits inflammation but promotes growth of epidermal keratinocytes, indicating that it may facilitate the inflammatory-proliferative phase transition during wound repair. Following this line of research, here we evaluated the therapeutic potential of miR-132 in chronic wound using mouse in vivo wound model. We performed a global transcriptome analysis of skin wounds of leptin receptor-deficient (db/db) mice treated with miR-132 or control mimics. Db/db mouse has been used as a type 2 diabetic model with impaired wound healing capacity.

2017-02-01 | GSE92409 | GEO

Impact of miR-132 and miR-381 on endogenous forskolin responsive CREB targets in HEK293T cells

Project description:Expression profiling of HEK293T cells transfected with miR-neg (negative control), miR-132 or miR-381 mimics and treated with forskolin for 0, 1 or 4hrs.

2011-07-01 | GSE24812 | GEO

Effect of HIC1 and miR-212/132 expression on MCF7 cells

Project description:To identify the target of miR-212, miR-132 and HIC1, we have employed whole genome microarray expression profiling on the human breast cancer MCF7 cells. To generate miR-212/132 or HIC1 inducible MCF7 cells, doxycycline-dependent miR-212/132 or HIC1 gene expression system was used. Either Tet-ON miR-212/132 MCF7 or Tet-ON HIC1 MCF7 were treated with 1μg/ml of Doxycycline for 36 hours with EMEM containing 0.01 mg/ml bovine insulin and 10% FCS. Two independent experiments were performed.

2014-07-29 | E-GEOD-37945 | biostudies-arrayexpress

A global transcriptome analysis of keratinocytes upon overexpression of microRNA-132

Project description:MiR-132 is one of the most upregulated miRNAs in keratinocytes of human skin wounds during the inflammatory phase of healing; however its biological role during skin wound healing has not been studied. To study the genes regulated by miR-132, we transfected miR-132 mimics (pre-miR-132) into primary human keratinocytes to overexpress miR-132. We performed a global transcriptome analysis of keratinocytes upon overexpression of miR-132 using Affymetrix arrays.

2014-12-30 | GSE61139 | GEO

miR-132 mediates renal fibrosis

Project description:miR-132 mediates renal fibrosis

| PRJNA307696 | ENA