Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

XbCteSpea

ABSTRACT: Ctena cf. galapagana NHMUK 20210086

PROVIDER: PRJEB85220 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	xbCteSpea1.metagenome.1.primary.fa.gz	Other
	xbCteSpea1.Rhodococcus_qingshengii_1.1.primary.fa.gz	Other
	xbCteSpea1.Spirochaetaceae_2.1.primary.fa.gz	Other
	ERR14209200.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 14

Similar Datasets

xbCteSpea

Project description:Ctena cf. galapagana NHMUK 20210086, genomic and transcriptomic data

| PRJEB85219 | ENA

xbCteSpea1.metagenome

Project description:Ctena cf. galapagana NHMUK 20210086 mollusc metagenome assembly, xbCteSpea1.metagenome

| PRJEB85485 | ENA

xbCteDecu

Project description:Ctena decussata

| PRJEB65003 | ENA

xbCteImbr

Project description:Ctena imbricatula

| PRJEB82726 | ENA

Ctena imbricatula

Project description:Ctena imbricatula overview

| PRJNA1208655 | ENA

Ctena decussata

Project description:Ctena decussata overview

| PRJNA1095106 | ENA

miR-146a is overexpressed and contributes to dampen IL-6 production in cystic fibrosis macrophages

Project description:In this study, we investigated whether miRNA deregulation might underlie the functional abnormalities of cystic fibrosis (CF) macrophages. To this aim we performed miRNA profiling in macrophages from CF and non-CF macrophages. This led to the identification of a panel of differentially expressed miRNAs in CF macrophages compared to non-CF cells.

2020-04-14 | GSE134702 | GEO

miRNA repertoires of ex-vivo bronchial, nasal, and polyps cells cultured from healthy and CF donors

Project description:Cystic fibrosis (CF), a genetic disorder, is characterized by chronic lung disease. Small non-coding RNAs are key regulators of gene expression and participate in various processes, which are dysregulated in CF; however, they remain poorly studied. Here, we determined the complete microRNAs (miRNAs) expression pattern in three CF ex-vivo models. The miRNA profiles of air-liquid interface cultures of airway epithelia (bronchi, nasal cells, and nasal polyps) samples from patients with CF and non-CF controls were obtained by deep sequencing. Compared with non-CF controls, several miRNAs were deregulated in CF samples, for instance miR-181a-5p and the miR-449 family were upregulated. Moreover, mature miRNAs often showed variations (i.e., isomiRs) relative to their reference sequence, such as miR-101, suggesting that miRNAs consist of heterogeneous repertoires of multiple isoforms with different effects on gene expression. Analysis of miR-181a-5p and miR-101-3p roles indicated that they regulate the expression of WISP1, a key component of cell proliferation/migration programs. We showed that miR-101 and miR-181a-5p participated in aberrant recapitulation of wound healing programs by controlling WISP1 mRNA and protein level. Our miRNA expression data bring new insights into CF physiopathology and define new potential therapeutic targets in CF

2020-10-21 | GSE159708 | GEO

TGF-β1 alter the SARS-CoV2 pathogenesis and modulates ACE2 expression by miRNA dependent mechanism

Project description:We studied miRNAs and their gene targets affecting SARS-CoV-2 pathogenesis in CF airway epithelial cell models in response to TGF-β1. Small RNAseq in CF human bronchial epithelial cell line treated with TGF-β1 and miRNA profiling characterized TGF-β1 effects on the SARS-CoV-2 pathogenesis pathways. Among the effectors, we identified and validated two miRNAs targeting ACE2 mRNA using different CF and non-CF human bronchial epithelial cell models. We have shown that TGF-β1 inhibits ACE2 expression by miR-136-3p and miR-369-5p. ACE2 levels were higher in cells expressing F508del-CFTR, compared to wild-type(WT)-CFTR and TGF-β1 inhibited ACE2 in both cell types. The ACE2 protein levels were still higher in CF, compared to non-CF cells after TGF-β1 treatment. TGF-β1 prevented the functional rescue of F508del-CFTR by ETI in primary human bronchial epithelial cells while ETI did not prevent the TGF-β1 inhibition of ACE2 protein. Finally, TGF-β1 reduced binding of ACE2 to the recombinant monomeric spike RBD. Our results may help to explain, at least in part, the role of TGF-β1 on the SARS-CoV-2 entry via ACE2 in the CF and non-CF airway.

2023-04-01 | GSE226758 | GEO

xbCteDecu1

Project description:Ctena decussata genome assembly, xbCteDecu1

| PRJEB73778 | ENA