Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lung expression of human ACE2 sensitizes the mouse to SARS-CoV2 infection

ABSTRACT: Lung expression of human ACE2 sensitizes the mouse to SARS-CoV2 infection

PROVIDER: PRJNA663882 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

MDM2 influences ACE2 stability and SARS-Cov2 uptake

Project description:The Angiotensin-converting enzyme 2 (ACE2) receptor is the central entry point for SARS-Cov2. Several SAR-Cov2 substrains have developed mutations in their spike protein to maximize their use of ACE2, e.g. to strengthen ACE2 binding for increased uptake or adapt to specific amino acid properties of ACE2 to cross the species barrier. But little is known about the effect of host regulators on ACE2 and subsequently their impact on SARS-Cov2 infection. Here we identify the E3 ligase MDM2 as a ACE2 modulator. The knockout of MDM2 induced a strong pro-viral effect specific for SARS-Cov2 and we could see the increase of ACE2 levels. This effect is likely dependent on the ubiquitination site Lysine 788, which MDM2 uses to induce proteasomal degradation of ACE2. Substituting this amino acid led to increased ACE2 levels and increased SARS-CoV2 infection facilitated by enhanced SARS-Cov2 uptake.

2023-09-08 | PXD040891 | Pride

IL-9 exacerbates SARS-CoV2 infection and associated airway inflammation

Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus diseases 2019 (COVID-19) and broncho-alveolar inflammation (Merad and Martin, 2020). IL-9 induces airway inflammation and bronchial hyper responsiveness in respiratory viral illnesses and allergic inflammation (Temann et al., 1998). However, the role of IL-9 is not yet identified in SARS-CoV2 infection. Here we show that IL-9 promotes SARS-CoV2 infection and airway inflammation in K18-hACE2 transgenic (ACE2.Tg) mice, as IL-9 blockade reduces SARS-CoV2 infection and suppressed airway inflammation. Foxo1 is essential for the induction of IL-9 in helper T (Th) cells (Malik et al., 2017). While ACE2.Tg mice with Foxo1-deficiency in CD4+ T cells were performed to be resistant to SARS-CoV2 infection associated with reduced IL-9 production, exogenous IL-9 made Foxo1-deficient mice susceptible to SARS-CoV2 infection with increased airway inflammation. Collectively, we identify a mechanistic insight of IL-9-mediated regulation of antiviral and inflammatory pathways in SARS-CoV2 infection, and unravel a principle for the development of host-directed therapeutics to mitigate disease severity.

2022-07-22 | GSE209550 | GEO

Promoter Capture Hi-C performed on A549 cells in a SARS-CoV2 infection timecourse

Project description:Here, A549 cells expressing the ACE2 receptor were infected with SARS-CoV2, and pCHi-C was performed at 0 (mock), 8 and 24 hours post-infection. This repository provides the raw pCHi-C sequence reads and downstream processed CHiCAGO data (Rds files).

2021-05-10 | GSE164533 | GEO

Bulk RNA-seq of an ALI (Air-lung interface) model of SARS-CoV2

Project description:This dataset looks at the transcriptome of in vitro-differentiated primary lung cells infected with SARS-CoV2. Some cells have been treated with the drug Enzalutamide.

2022-05-04 | E-MTAB-10687 | biostudies-arrayexpress

Transcriptomics analysis of SARS-CoV2-induced changes in human lung epithelial Calu-3 cells

Project description:RNA-Seq was carried out in order to obtain the time dependent expression dynamics of SARS-CoV2 (Trondheim strain)-induced transcriptome changes in human lung epithelial Calu-3 cells.

2022-10-25 | E-MTAB-12134 | biostudies-arrayexpress

ChIP-seq in Calu3 cells upon SARS-CoV2 infection

Project description:This study addresses the question how host cells transcriptionally respond to SARS-CoV2 infection.

2023-12-02 | GSE162492 | GEO

Slam-seq in Calu3 cells upon SARS-CoV2 infection

Project description:This study addresses the question how host cells transcriptionally respond to SARS-CoV2 infection.

2023-12-02 | GSE162491 | GEO

Total RNA-seq in Calu3 cells upon SARS-CoV2 infection

Project description:This study addresses the question how host cells transcriptionally respond to SARS-CoV2 infection.

2023-12-02 | GSE162494 | GEO

Single-cell RNA-seq of an ALI (Air-lung interface) model of SARS-CoV2

Project description:This dataset looks at the transcriptome of in vitro-differentiated primary lung cells during an infection time course of SARS-CoV2. Some cells have been treated with the drug Enzalutamide. Cells from one man and one female were mixed to minimize the technical variability, and can be separated by SNPs (SNPs not included, but the calculated cell-donor associations are provided).

2023-04-01 | E-MTAB-10697 | biostudies-arrayexpress

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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