Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: The airway metagenome of monozygous cystic fibrosis twins

PROVIDER: PRJEB41644 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR4900042.fastq.gz	Fastqsanger.gz
	ERR4900043.fastq.gz	Fastqsanger.gz
	ERR4900044.fastq.gz	Fastqsanger.gz
	ERR4900045.fastq.gz	Fastqsanger.gz
	ERR4900046.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Longitudinal tracking of the cystic fibrosis airway metagenome

Project description:Cystic fibrosis airway metagenome

| PRJEB50802 | ENA

Transcriptional analysis of cystic fibrosis airways at single-cell resolution reveals altered epithelial cell states and composition

Project description:Single cell sequencing of human airway epithelium from normal and cystic fibrosis lungs.

2021-03-10 | GSE150674 | GEO

Cystic_fibrosis_airway

Project description:The cystic fibrosis upper and lower airway metagenome

| PRJEB28553 | ENA

A microRNA network regulates expression and biosynthesis of CFTR and CFTR-M-NM-^TF508.

Project description:Production of functional proteins requires multiple steps including gene transcription and post-translational processing. MicroRNAs (miRNA) can regulate individual stages of these processes. Despite the importance of the cystic fibrosis transmembrane conductance regulator (CFTR) channel for epithelial anion transport, how its expression is regulated remains uncertain. We discovered that microRNA-138 regulates CFTR expression through its interactions with the transcriptional regulatory protein SIN3A. Treating airway epithelia with a miR-138 mimic increased CFTR mRNA and also enhanced CFTR abundance and transepithelial Cl- permeability independently of elevated mRNA levels. A miR-138 anti-miR had the opposite effects. Importantly, miR-138 altered the expression of many genes encoding proteins that associate with CFTR and may influence its biosynthesis. The most common CFTR mutation, M-NM-^TF508, causes protein misfolding, degradation, and cystic fibrosis. Remarkably, manipulating the miR-138 regulatory network also improved biosynthesis of CFTR-M-NM-^TF508 and restored Cl- transport to cystic fibrosis airway epithelia. This novel miRNA-regulated network directs gene expression from the chromosome to the cell membrane, indicating that an individual miRNA can control a cellular process broader than previously recognized. This discovery also provides new therapeutic avenues for restoring CFTR function to cells affected by the most common cystic fibrosis mutation. 12 samples of Calu-3 cells representing different interventions.

2012-09-04 | E-GEOD-38956 | biostudies-arrayexpress

Gene expression of immortalized cystic fibrosis and non-cystic fibrosis airway epithelial cells

Project description:Our laboratory has held a long interest in the glycosylation changes seen on the surface of airway epithelia of patients with the disease cystic fibrosis (CF). Experiments from our laboratory have detailed a CF glycosylation phenotype of increased Fuca1,3/4 and decreased Fuca1,2 and sialic acid on the surfaces of immortalized and primary CF cells compared to non-CF cells. Further, we have shown that gene transfer and subsequent expression of a wild type CF plasmid in CF airway cells results in correction or reversal of this glycosylation phenotype. We hypothesize that the changes in glycosylation seen in CF cells are key in the pathophysiology of the cystic fibrosis airway disease. For example, it has been shown that Pseudomonas aeruginosa, a bacterium that has a predilection for colonizing CF airways, adheres to asialylated glycolipids and glycoconjugates with terminal Fuca1,3/4. One focus of our laboratory is to elucidate the etiology of the glycosylation changes seen in CF cells and the mechanism by which these changes are reversed by wild type CFTR gene transfer. We propose to study the gene expression of immortalized and primary CF and non-CF airway epithelial cells: 1. CF/T43 vs. BEAS-2B cells. These are two widely used immortalized airway cell lines that we have used extensively in the past. 2. C38 cells; C38 cells are IB3 cells expressing wtCFTR. The experimental focus is to elucidate the etiology of the glycosylation changes seen in Cystic Fibrosis (CF) cells and the mechanism by which these changes are reversed by wild type CFTR gene transfer. To do so, the gene expression of immortalized and primary CF and non-CF airway epithelial cells were compared and studied. Cell lines used were CF/T43 and BEAS-2B, both widely used immortalized airway cell lines. Other cell lines studied included C38 cell lines (clonal derivatives of IB3 cells expressing wtCFTR).

2011-01-07 | E-GEOD-26482 | biostudies-arrayexpress

E-GEOD-39843

Project description:Expression data of cystic fibrosis and non-cystic fibrosis airway cell lines under oxidative stress

2015-09-30 | E-GEOD-39843 | ExpressionAtlas

Time course of respiratory syncytial virus (RSV) infection in healthy and cystic fibrosis (CF) human airway epithelial cell cultures

Project description:The goal of this study was to examine changes in gene expression over time in healthy and cystic fibrosis (CF) human airway epithelia infected with RSV.

2023-11-08 | GSE247298 | GEO

CF airways metagenome

Project description:The cystic fibrosis upper and lower airway metagenome - data update

| PRJEB52317 | ENA

Airway metagenome

Project description:Airway metagenome of healthy infants and infants with cystic fibrosis

| PRJEB38221 | ENA

Homo sapiens

Project description:Gene expression of immortalized cystic fibrosis and non-cystic fibrosis airway epithelial cells

| PRJNA136507 | ENA