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- W2023751898 abstract "Increased mucus production is a common cause of morbidity and mortality in inflammatory airway diseases, including asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis. However, the precise molecular mechanisms for pathogenic mucus production are largely undetermined. Accordingly, there are no specific and effective anti-mucus therapeutics. Here, we define a signaling pathway from chloride channel calcium-activated 1 (CLCA1) to MAPK13 that is responsible for IL-13-driven mucus production in human airway epithelial cells. The same pathway was also highly activated in the lungs of humans with excess mucus production due to COPD. We further validated the pathway by using structure-based drug design to develop a series of novel MAPK13 inhibitors with nanomolar potency that effectively reduced mucus production in human airway epithelial cells. These results uncover and validate a new pathway for regulating mucus production as well as a corresponding therapeutic approach to mucus overproduction in inflammatory airway diseases." @default.
- W2023751898 created "2016-06-24" @default.
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- W2023751898 date "2012-11-26" @default.
- W2023751898 modified "2023-10-13" @default.
- W2023751898 title "IL-13–induced airway mucus production is attenuated by MAPK13 inhibition" @default.
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- W2023751898 doi "https://doi.org/10.1172/jci64896" @default.
- W2023751898 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3533556" @default.
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- W2023751898 hasPublicationYear "2012" @default.
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