NIH R01 · 2025
Transmembrane Protein 178 as a Novel Endogenous Inhibitory Mechanism in Asthma
PROJECT SUMMARY Asthma is characterized by chronic, non-resolving lung inflammation; however, there are endogenous inhibitory mechanisms that normally promote the resolution of lung inflammation. The long-term objective of our research is to understand the bronchial epithelial cell (BEC)-mediated inhibition of lung inflammation in asthma. Transmembrane protein 178 (Tmem178) mediates a novel endogenous inhibitory mechanism in asthma. Our preliminary data showed that TMEM178 gene expression in BECs decreased as asthma severity increased. In addition, we found that Tmem178 inhibits adenosine triphosphate- and allergen-induced [Ca2+]i responses, store- operated calcium entry (SOCE), and…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.