Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ScRNAseq analysis in control and Goblet-Y/T-Scgb1a1CreERT mouse lung tissues.

ABSTRACT: This experiment aims to examine the global cellular response in the lung tissues of Goblet-Y/T-Scgb1a1CreERT mice. Depletion of Yap and Taz in airway secretory cells resulted in goblet cell metaplasia. To elucidate the underlying cellular response, we utilized scRNA sequencing of lung tissues.

ORGANISM(S): Mus musculus

PROVIDER: GSE275465 | GEO | 2025/08/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

CD45+ Epcam- poluation scRNAseq analysis in control and Goblet-Y/T-Scgb1a1CreERT mouse lung tissues.

Project description:The gole of this experiment is to get an in depth understanding of the immune population responses in mouse lungs presented with goblet cell metaplasia in the airway upon Yap/Taz deletion in Scgb1a1+ cells.

2025-08-20 | GSE275467 | GEO

Yap/Taz inhibit goblet cell fate to maintain lung epithelial homeostasis

Project description:Proper lung function relies on precisely balanced numbers of specialized epithelial cell types that work together and are maintained in homeostasis. We describe essential roles for the transcriptional regulators Yap and Taz, which are key effectors of Hippo pathway signaling, in maintaining lung epithelial homeostasis. We report that conditional deletion of Yap1/Yap and Wwtr1/Taz in the lung epithelium of adult mice results in severe defects with consequent animal lethality. Phenotypes associated with Yap/Taz deletion include alveolar defects and a striking development of goblet cell metaplasia throughout the airways. We performed gene expression analysis of wild type and Yap/Taz null primary mouse airway epithelial cells in order to define Yap/Taz controlled gene expression.

2021-08-09 | GSE156525 | GEO

Yap/Taz inhibit goblet cell fate to maintain lung epithelial homeostasis (ChIP-seq)

Project description:Proper lung function relies on precisely balanced numbers of specialized epithelial cell types that work together and are maintained in homeostasis. In this study we have described essential roles for the transcriptional regulators YAP and TAZ, which are key effectors of Hippo pathway signaling, in maintaining lung epithelial homeostasis. Phenotypes associated with Yap/Taz deletion include alveolar defects and a striking development of goblet cell metaplasia throughout the airways. Knockdown of YAP and TAZ in HBECs similarly drives mucin expression. The TEAD family of transcription factors are well characterized partners of the YAP/TAZ transcriptional effectors, and we have found that knockdown of TEAD1-4 similarly drives elevated mucin expression. In order to further understand the role of the TEAD transcription factors in human lung epithelial cell fate, we conducted TEAD Chromatin Immunopreciptitation (ChIP)-Sequencing.

2021-08-19 | GSE158306 | GEO

Yap/Taz inhibit goblet cell fate to maintain lung epithelial homeostasis (RNA-seq)

Project description:Proper lung function relies on precisely balanced numbers of specialized epithelial cell types that work together and are maintained in homeostasis. In this study we have described essential roles for the transcriptional regulators YAP and TAZ, which are key effectors of Hippo pathway signaling, in maintaining lung epithelial homeostasis. Phenotypes associated with Yap/Taz deletion include alveolar defects and a striking development of goblet cell metaplasia throughout the airways. Knockdown of YAP and TAZ in HBECs similarly drives mucin expression. The TEAD family of transcription factors are well characterized partners of the YAP/TAZ transcriptional effectors, and we have found that knockdown of TEAD1-4 similarly drives elevated mucin expression. In order to further understand the role of the TEAD transcription factors in human lung epithelial cell fate, we conducted TEAD Chromatin Immunopreciptitation (ChIP)-Sequencing.

2021-08-19 | GSE158305 | GEO

RNA sequencing of flow sorted Scgb1a1 lineage traced Control and Yap/Taz knockout lung epithelial cells

Project description:Proper lung function relies on precisely balanced numbers of specialized epithelial cell types that work together and are maintained in homeostasis. In this study we have described essential roles for the transcriptional regulators YAP and TAZ, which are key effectors of Hippo pathway signaling, in maintaining lung epithelial homeostasis. Phenotypes associated with Yap/Taz deletion include alveolar defects and a striking development of goblet cell metaplasia throughout the airways. Lineage specific deletion of Yap and Taz in Scgb1a1+ cells leads to increased Mucin production within the knockout cells in vivo. In order better characterize the in vivo transcriptional changes associated with Yap/Taz knockout in these cells, we have isolated Scgb1a1 lineage traced cells from control and yap/taz cNull mice and performed bulk RNA sequencing.

2021-08-09 | GSE171712 | GEO

Effects of HSP90 inhibitors on airway goblet cell metaplasia

Project description:Goblet cell metaplasia and mucus hypersecretion are disabling hallmarks of chronic lung diseases for which no curative treatments are available. Therapies targeting specific upstream drivers of asthma have had variable results. We hypothesized that an a priori-knowledge independent approach would point to new therapies for airway goblet cell metaplasia. We analyzed the transcriptome of an organotypic model of human goblet cell metaplasia. We combined our data with previously published datasets from IL13-exposed in vitro and asthmatic in vivo human airway epithelial cells. The drug perturbation-response connectivity approach identified the heat shock protein 90 (HSP90) inhibitor geldanamycin as a candidate for reverting airway goblet cell metaplasia. We found that geldanamycin not only prevented but reverted IL13-induced goblet cell metaplasia. Geldanamycin did not induce goblet cell death, did not solely block mucin synthesis, and did not block IL13 receptor-proximal signaling. Moreover, the transcriptional effects of geldanamycin were absent in unstimulated cells and became evident only after stimulation with IL13. The predicted mechanism of action suggested that geldanamycin should also revert IL17-induced goblet cell metaplasia, a prediction confirmed by our data. Our findings suggest HSP90 activity may be required for persistence of goblet cell metaplasia driven by various mechanisms in chronic lung diseases.

2019-02-07 | GSE116927 | GEO

Transcription profiling of mouse lung from individuals with airway hyperactivity and goblet cell metaplasia post-Sendai virus infection

Project description:Mice representing phenotypic extremes of airway hyperreactivity and goblet cell metaplasia post-Sendai virus infection were identified from a 500 mouse F2 cohort (CB6F2/J). Whole lung RNA from 3 mice at each extreme was analyzed via microarray for gene expression. Subsequent pairwise comparisons between arrays allowed the identification of genes differentially expressed with respect to the disease phenotypes (airway hyperreactivity and goblet cell metaplasia).

2007-07-06 | E-GEOD-3925 | biostudies-arrayexpress

Yap/Taz inhibit goblet cell fate to maintain lung epithelial homeostasis

Project description:Yap/Taz inhibit goblet cell fate to maintain lung epithelial homeostasis

| PRJNA658249 | ENA

Yap/Taz inhibit goblet cell fate to maintain lung epithelial homeostasis

Project description:Yap/Taz inhibit goblet cell fate to maintain lung epithelial homeostasis

| PRJNA664777 | ENA

Virus Induced Airway Hyperreactivity and Goblet Cell Metaplasia Phenotypic Extremes (CB6F2/J)

2006-03-30 | GSE3925 | GEO