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- W2034162419 abstract "Mucus hypersecretion is an important characteristic feature of the pathogenesis of allergy. Although interleukin (IL)-4 is known to be an inflammatory mediator in respiratory diseases, the mechanism by which IL-4 induces MUC5AC gene expression has not been fully explored. The aim of this study was to investigate the mechanism by which IL-4 induces MUC5AC gene expression in the airway. We examined the role of mitogen-activated protein kinase (MAPK) signaling on MUC5AC gene expression in airway epithelium. We showed that phosphorylation of ERK1/2 increased after treatment of cells with IL-4, whereas phosphorylation of p38 and JNK was not detected. In addition, pharmacologic and genetic inhibition of ERK1/2 abolished IL-4-induced MUC5AC gene expression. Moreover, we investigated the activation of p90 ribosomal S6 kinase 1 (RSK1) as a downstream signaling target of ERK1/2 in IL-4 signaling. The activation of RSK1 was prevented by pretreatment with PD98059 or plasmid expressing a MEK1 dominant-negative mutant. We also found that RSK1 mediated the IL-4-induced phosphorylation of cAMP response element-binding protein (CREB) and the transcription of MUC5AC. Furthermore, the cAMP-response element (CRE) in the MUC5AC promoter appears to be important for IL-4-induced MUC5AC gene expression in NCI-H292 cells." @default.
- W2034162419 created "2016-06-24" @default.
- W2034162419 creator A5033615399 @default.
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- W2034162419 date "2009-08-28" @default.
- W2034162419 modified "2023-10-10" @default.
- W2034162419 title "Upregulation of<i>MUC5AC</i>gene expression by IL-4 through CREB in Human airway epithelial cells" @default.
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- W2034162419 doi "https://doi.org/10.1002/jcb.22330" @default.
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