![]() EHF activates expression of the SAM pointed domain-containing ETS transcription factor, which contributes to goblet cell hyperplasia. Furthermore, changes in gene expression impact cell phenotype because EHF depletion alters epithelial secretion of a neutrophil chemokine and slows wound closure in HBE cells. Using EHF ChIP followed by deep sequencing (ChIP-seq) and RNA sequencing after EHF depletion, we show that EHF targets in HBE cells are enriched for genes involved in inflammation and wound repair. Here we determine the functions of EHF in primary human bronchial epithelial (HBE) cells and relevant airway cell lines. EHF, which has altered expression in inflammatory states, maps to the 5′ end of an intergenic region on Chr11p13 that is implicated as a modifier of cystic fibrosis airway disease. Ets homologous factor (EHF) is a key member of the transcription factor network that regulates gene expression in the airway epithelium in response to endogenous and exogenous stimuli. Epithelial dysfunction is critical in the pathology of many respiratory diseases, including cystic fibrosis. The airway epithelium forms a barrier between the internal and external environments. ![]()
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