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Gene expression profile at single cell level of hiPSC-derived lung airways epithelial cells upon knock-out of EHF in normoxia and in hypoxia

GSE220784 Homo sapiens Expression profiling by high throughput sequencing 4 samples Submitted 2025/06/05 Platform GPL24676
Summary
Cystic Fibrosis (CF) is caused by mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene coding for a chloride- and bicarbonate-ion channel. Deficient or dysfunctional CFTR changes ion composition resulting in abnormal mucus, affecting transport and fluid’s homeostasis in multiple epithelia. Lung disease is responsible for the majority of patients’ morbimortality. Intriguingly, more than half of its phenotype is not due to CFTR mutations, but to the environment and genetic modifiers. Genome-Wide Association Studies (GWAS) have identified Single Nucleotide Polymorphisms (SNPs) that could be genetic modifiers. One of the regions outlined (11q13) is located close by an epithelium-specific gene named ETS Homologous Factor (EHF). Here, we hypothesized EHF may be impacted by these variants and may play a crucial role in the airway epithelium. We used human-induced Pluripotent Stem Cells (hiPSC)- derived Airway Epithelial Cells (AECs) to study the knock-out of EHF in normoxia and in hypoxia.
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Also filed as BioProject PRJNA911318 and SRA study SRP412611. Searching any of these in the dataset finder brings you back here.

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