Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell RNA-seq in AT1 cell-ablated mouse lungs

ABSTRACT: We performed single-cell RNA-seq analysis using Drop-seq S3 method in mouse lungs following AT1 cell ablation

ORGANISM(S): Mus musculus

PROVIDER: GSE218666 | GEO | 2023/11/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Single-cell RNA-seq in AT2 cell-ablated mouse lungs

Project description:We performed single-cell RNA-seq using the chemistry of 10x Genomic Chromium v3.1 in mouse lungs following AT2 cell ablation.

2022-09-14 | GSE173878 | GEO

Tgfb in AT1 cells

Project description:Premature birth disrupts normal lung development and places infants at risk for bronchopulmonary dysplasia (BPD), a disease increasing in incidence which disrupts lung health throughout the lifespan. The TGFβ superfamily has been implicated in BPD pathogenesis, however, what cell lineage it impacts remains unclear. We show that the primary TGFβ receptor, Tgfbr2, is critical for AT1 cell fate maintenance and function. Loss of Tgfbr2 in AT1 cells during late lung development leads to AT1-AT2 cell reprogramming and altered pulmonary architecture, which persists into adulthood. Restriction of fetal lung stretch and associated AT1 cell spreading through a model of oligohydramnios enhances AT1-AT2 reprogramming. Transcriptomic and proteomic analysis reveal that expression of extracellular matrix components by AT1 cells is attenuated with loss of Tgfbr2. Cell spreading assays shows that TGFβ signaling regulates integrin transcription to alter AT1 cell morphology, which further impacts ECM expression through changes in mechanotransduction. These data reveal the cell intrinsic necessity of TGFβ signaling to maintain AT1 fate and define this cell lineage as a major orchestrator of the alveolar matrisome, which, if altered, may predispose to BPD.

2024-03-04 | GSE230268 | GEO

N-Acetylation of secreted proteins is widespread in Apicomplexa and independent of acetyl-CoA transporter AT1

Project description:Acetyl-CoA critically participates in post-translational modification of proteins, central carbon and lipid metabolism in several compartments of eukaryotic cells. In mammals, the acetyl-CoA transporter 1 (AT1) facilitates the flux of cytosolic acetyl-CoA into the endoplasmic reticulum (ER) enabling the acetylation of proteins of the secretory pathway in concert with dedicated acetyltransferases including Nat8. Homologues of AT1 and Nat8 were identified in the apicomplexan parasites Toxoplasma gondii and Plasmodium berghei. However, the implication of acetyl-CoA pool influx into the ER in acetylation of ER-transiting proteins and their relevance throughout the parasites’ life cycle is unknown. Here, we report proteome-wide analyses, which revealed unprecedented widespread N-terminal acetylation marks of secreted proteins in both parasites. Deletion of the gene coding for AT1 in both parasites, resulted in global loss of fitness and in addition to retardation in erythrocytic development, malaria parasites are blocked in transmission to mosquitoes. However, in absence of AT1 proteome wide lysine and N-terminal acetylation modifications remain unaltered. This highlights a role of AT1 in parasite development uncoupled to acetylation capacity, indicative of an unusually active acetylation machinery occurring in the ER of Apicomplexa.

2022-06-20 | PXD029616 | Pride

Drop-seq analysis of bleomycin-treated and control mouse lung single-cell suspensions

Project description:Cell suspensions were prepared from mouse lungs dissociated at baseline or 14 days after intratracheal bleomycin injury, and single cell mRNA-seq libraries were generated with Drop-seq.

2018-10-25 | E-MTAB-7142 | biostudies-arrayexpress

Hypercapnia impairs AT2 cell progenitor activity and promotes differentiation to AT1 cells

Project description:Hypercapnia has deleterious effects on cell function, including inhibition of alveolar epithelial cells (AEC) and fibroblast proliferation without causing cell death. Classical studies and lineage-trace models demonstrated that surfactant-producing AT2 cells can serve as stem cells for the structurally and functionally distinct alveolar type 1 cells (AT1) This AT2 reprogramming depends on Wnt/βcat signaling, a pathway that plays critical roles in tissue development and homeostasis throughout the organism lifespan. We found that high CO2 inhibits AT2 cell proliferation and self renewal, and promote their differentiation to ATEC and AT1 cells

2021-12-31 | GSE139426 | GEO

Characterization of lysine acetylation in Toxoplasma gondii proteome lacking acetyl-CoA transporter 1 (AT1).

Project description:Acetyl-CoA participates in post-translational modification of proteins, central carbon and lipid metabolism in several cell compartments. In mammals, the acetyl-CoA transporter 1 (AT1) facilitates the flux of cytosolic acetyl-CoA into the endoplasmic reticulum (ER), enabling the acetylation of proteins of the secretory pathway, in concert with dedicated acetyltransferases including Nat8. However, the implication of the ER acetyl-CoA pool in acetylation of ER-transiting proteins and their relevance throughout the parasites’ life cycle is unknown. Here, we evaluated the impact of blocking putative cytosolic acetyl-CoA import on acetylation of proteins through KO of the homologue of AT1 in the parasite Toxoplasma gondii.

2022-07-25 | PXD030932 | Pride

Profiling AT1 and AT2 cells throughout alveolar development

Project description:This experiment profiled the transcriptomes of developing AT1 and AT2 cells from the beginning of embryonic alveolar development through the end of alveologenesis at 6 weeks of age.

2021-05-20 | GSE148487 | GEO

Drop-seq analysis of bleomycin-treated and control mouse lung single-cell suspensions

2018-10-24 | GSE111664 | GEO

Transcription profiling of mouse AT1 transgenics undergoing cardiac failure, cardiac hypertrophy and wild type aged matched controls

Project description:Analysis of cardiac specific AT1 transgenic mice undergoing cardiac failure, cardiac hypertrophy and wild type aged matched controls. For detailed description of the AT1 Tg mice please refer to:; Paradis P, Dali-Youcef N, Paradis FW, Thibault G, Nemer M. Overexpression of angiotensin II type I receptor in cardiomyocytes induces cardiac hypertrophy and remodeling. Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):931-6. PMID: 10639182 [PubMed - indexed for MEDLINE]

2008-06-12 | E-GEOD-2355 | biostudies-arrayexpress

Single cell RNA sequencing profiles of human iPSC-derived AT1-like cells in 3D cultures [SPC2B2_LDCI]

Project description:Comparison of differentiation of human iPSC derived alveolar epitheilal type 2 cells (iAT2s) into AT1-like cells (iAT1s) using a defined "LDCI" medium vs. lentiviral forced over-expression of activated nuclear YAP (YAP5SA)

2023-08-08 | GSE221343 | 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