Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The miR-183/96/182 cluster is a checkpoint for resident immune cells and shapes the cellular landscape of the cornea.

ABSTRACT: The miR-183/96/182 cluster is a checkpoint for resident immune cells and shapes the cellular landscape of the cornea.

PROVIDER: PRJNA1048937 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27089338_1.fastq.gz	Fastqsanger.gz
	SRR27089338_2.fastq.gz	Fastqsanger.gz
	SRR27089339_1.fastq.gz	Fastqsanger.gz
	SRR27089339_2.fastq.gz	Fastqsanger.gz
	SRR27089340_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

The miR-183/96/182 cluster is a checkpoint for resident immune cells and shapes the cellular landscape of the cornea.

Project description:The conserved miR-183/96/182 cluster (miR-183C) regulates both corneal sensory innervation and corneal resident immune cells (CRICs). This study is to uncover its role in CRICs and in shaping the corneal cellular landscape at a single-cell (sc) level.

2024-01-10 | GSE249384 | GEO

The microRNA cluster miR-183/96/182 contributes to long-term memory in a protein phosphatase 1 dependent manner

Project description:Memory formation is a complex cognitive function regulated by coordinated synaptic and nuclear processes in neurons. In mammals, it is controlled by multiple molecular activators and suppressors, including the key signaling regulator protein phosphatase 1 (PP1). Here, we show that memory control by PP1 involves the miR-183/96/182 cluster, which is selectively regulated during memory formation. Inhibiting nuclear PP1 in mice brain or training in object recognition task similarly increases miR-183/96/182 expression in the hippocampus. Mimicking this increase by overexpressing miR-183/96/182 enhances object memory, while suppressing endogenous level of the cluster reduces it. This effect involves the modulation of many plasticity-related genes, and we identified HDAC9 as one of the functional targets. Further, PP1 controls miR-183/96/182 in a transcription-independent manner influencing processing of their precursors. These findings provide novel evidence for the role of miRNAs in memory formation and suggest the implication of PP1 in miRNAs processing in the adult brain.

2016-09-20 | GSE83707 | GEO

Modulation of the microRNA cluster miR-183-96-182 expression by the Epstein-Barr virus latent membrane protein 1

Project description:Epstein-Barr virus (EBV) is an oncogenic human herpesvirus involved in the pathogenesis of Burkitt’s lymphoma (BL) and various other lymphoproliferative disorders. In BL, EBV protein expression is restricted to the EBNA-1, but small non-coding RNAs such as the EBERs and micro (mi)RNAs can also be detected. miRNAs play major roles in crucial processes such as proliferation, differentiation and cell death. It has recently become clear that alteration in the expression profile of miRNAs contribute to the pathogenesis of a number of malignancies. During latent infection, EBV expresses 25 viral pre-miRNAs and modulates the expression of specific cellular miRNAs, such as miR-155 and miR-146, which potentially play a role in oncogenesis. Here, we established the small RNA expression profiles of three BL cell lines. Using large-scale sequencing coupled to northern blot and real-time RT-PCR analysis validation, we demonstrated the differential expression of some cellular and viral miRNAs. High-level expression of the miR-183-96-182 cluster and EBV miR-BART cluster was significantly associated with EBV type I latency. This expression was not affected by viral reactivation since TGF-ß1 stimulation did not significantly change the miRNA profiles. However, the expression of latent membrane protein (LMP)-1 triggered down-regulation of the expression of the miR-183-96-182 cluster. We further show that this effect involves the AKT signaling pathway.

2015-09-25 | GSE65752 | GEO

Regulation of Th17 cell pathogenic function by miR-183/96/182

Project description:Th17 cells are key players in autoimmune diseases. However, the roles of non-coding RNAs in Th17 cells are largely unknown. Here, we show that deletion of the Dicer gene specifically in Th17 cells protects from experimental autoimmune encephalomyelitis (EAE). Th17 cells highly express the miR-183/96/182 cluster (miR-183C), in response to IL-6/STAT3 signaling. Moreover, miR-183C regulates pathogenic cytokine expression during Th17 development. Furthermore, transcription factor Foxo1 is one of functional targets of miR-183C in Th17 cells: Foxo1 negatively regulates the pathogenicity of Th17 cells and miR-183C represses Foxo1 expression. Collectively, our results demonstrate one of crucial roles for miR-183C cluster in regulation of Th17 cell function in autoimmune diseases.

2016-06-21 | GSE78505 | GEO

A mouse model of miR-96, miR-182 and miR-183 misexpression implicates miRNAs in cochlear cell fate and homeostasis

Project description:Transgenic FVB/NCrl-Tg(GFAP-Mir183,Mir96,Mir182)MDW1 mice (Tg1MDW) overexpress this neurosensory-specific miRNA cluster in the inner ear and were developed as a model system to identify target genes and biologic processes regulated by the miR-183 cluster. Affymetrix mRNA microarray data analysis revealed that downregulated genes in P5 Tg1MDW/1MDW cochlea are statistically enriched for evolutionarily conserved predicted miR-96, miR-182 or miR-183 target sites.

2018-02-28 | GSE95579 | GEO

The miR-183/96/182 Cluster Regulates Sensory Innervation, Resident Myeloid Cells and Functions of the Cornea Through Cell type-specific Target Genes

Project description:The miR-183/96/182 cluster (miR-183C) is specifically expressed in sensory neurons and immune cells and modulates corneal immune/inflammatory response to bacterial infection. To uncover the roles of miR-183C in corneal homeostasis through its regulation of sensory neurons of the trigeminal ganglia (TG) and innate myeloid cells, we created miR-183C conventional knockout (KO), and sensory nerve-specific (SNS-CKO) and myeloid cell-specific conditional knockout (MS-CKO) mice. We performed 3'RNA sequencing in the TG and corneas of these knockout mice and their wild type (WT)-control littermates. To study specific functions of miR-183C in corneal resident myeloid cells (CRMCs), we isolated Csf1r-EGFP+ CRMCs from conventional KO and MS-CKO and their WT control mice. By comparison of the gene expression profiles of the KO or CKO vs their corresponding WT mice, we identified a series of differentially expressed genes. Bioinformatic analyses uncovered tissue- and/or cell-type-specific target genes of miR-183C. Functional annotation of the target genes revealed functions of miR-183C in TG and CRMCs.

2023-12-20 | GSE250213 | GEO

The miR-183/96/182 Cluster Regulates Sensory Innervation, Resident Myeloid Cells and Functions of the Cornea Through Cell type-specific Target Genes

Project description:The miR-183/96/182 Cluster Regulates Sensory Innervation, Resident Myeloid Cells and Functions of the Cornea Through Cell type-specific Target Genes

| PRJNA1052678 | ENA

Expression data from the RWPE-1 prostate epithelial cell line overexpressing the miR-183 family cluster

Project description:The full genomic miR-183 cluster (4.8kb) was cloned into lentiviral vector CD511B-1 with polycistronic GFP. RWPE-1 were transduced with a lentivirus from this vector (RWPE-1 183FC), or a CD511B-1 scrambled control with polycistronic GFP (RWPE-1 control). RWPE-1 were FACS sorted by GFP expression and expanded in culture. In RWPE-1 183FC, the miR-183 family members, miR-182, miR-96, and miR-183 were confirmed to be over-expressed at physioloically relevent levels, similar to the increased expression observed in prostate cancer epithelium.

2017-05-23 | GSE99134 | GEO

MicroRNA-183/96/182 cluster in immunity and autoimmunity.

Project description:MicroRNAs (miRNAs) are crucial post-transcriptional regulators of gene expression in ubiquitous biological processes, including immune-related pathways. This review focuses on the miR-183/96/182 cluster (miR-183C), which contains three miRNAs, miR-183, -96, and -182, having almost identical seed sequences with minor differences. The similarity among seed sequences allows these three miRNAs to act cooperatively. In addition, their minor differences permit them to target distinct genes and regulate unique pathways. The expression of miR-183C was initially identified in sensory organs. Subsequently, abnormal expression of miR-183C miRNAs in various cancers and autoimmune diseases has been reported, implying their potential role in human diseases. The regulatory effects of miR-183C miRNAs on the differentiation and function of both innate and adaptive immune cells have now been documented. In this review, we have discussed the complex role of miR-183C in the immune cells in both normal and autoimmune backgrounds. We highlighted the dysregulation of miR-183C miRNAs in several autoimmune diseases, including systemic lupus erythematosus (SLE), multiple sclerosis (MS), and ocular autoimmune disorders, and discussed the potential for utilizing miR-183C as biomarkers and therapeutic targets of specific autoimmune diseases.

| S-EPMC9986322 | biostudies-literature

Gene expression profiling of miR-183/96 knock out mouse cochlea

Project description:Transcriptome analysis of P16 cochlea from wild type and miR-183/96 Knock out mice Gene expression analysis of miR-183/96 KO cochlea revealed a set of hair cell-relevant differentially expressed genes that could adversely impact hair cell physiology and contribute to the observed phenotype.

2018-05-01 | GSE106599 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data