{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ma J"],"funding":["Ministry of Education - Singapore"],"pagination":["e66596"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8291973"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10"],"pubmed_abstract":["Epithelial tissues are primed to respond to insults by activating epithelial cell motility and rapid inflammation. Such responses are also elicited upon overexpression of the membrane-bound protease, Matriptase, or mutation of its inhibitor, Hai1. Unrestricted Matriptase activity also predisposes to carcinoma. How Matriptase leads to these cellular outcomes is unknown. We demonstrate that zebrafish <i>hai1a</i> mutants show increased H<sub>2</sub>O<sub>2</sub>, NfκB signalling, and IP<sub>3</sub>R -mediated calcium flashes, and that these promote inflammation, but do not generate epithelial cell motility. In contrast, inhibition of the Gq subunit in <i>hai1a</i> mutants rescues both the inflammation and epithelial phenotypes, with the latter recapitulated by the DAG analogue, PMA. We demon"],"journal":["eLife"],"pubmed_title":["Matriptase activation of Gq drives epithelial disruption and inflammation via RSK and DUOX."],"pmcid":["PMC8291973"],"funding_grant_id":["2015-T1-001-035","MOE2016-T3-1-005"],"pubmed_authors":["Marsay KS","Amaya E","Ho YN","Zhang W","Mahabaleshwar H","Partridge LJ","Scott CA","Carney TJ","Tergaonkar V","Teow CK","Roy S","Ma J","Zhang C","Ng SS"],"additional_accession":[]},"is_claimable":false,"name":"Matriptase activation of Gq drives epithelial disruption and inflammation via RSK and DUOX.","description":"Epithelial tissues are primed to respond to insults by activating epithelial cell motility and rapid inflammation. Such responses are also elicited upon overexpression of the membrane-bound protease, Matriptase, or mutation of its inhibitor, Hai1. Unrestricted Matriptase activity also predisposes to carcinoma. How Matriptase leads to these cellular outcomes is unknown. We demonstrate that zebrafish <i>hai1a</i> mutants show increased H<sub>2</sub>O<sub>2</sub>, NfκB signalling, and IP<sub>3</sub>R -mediated calcium flashes, and that these promote inflammation, but do not generate epithelial cell motility. In contrast, inhibition of the Gq subunit in <i>hai1a</i> mutants rescues both the inflammation and epithelial phenotypes, with the latter recapitulated by the DAG analogue, PMA. We demon","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jun","modification":"2026-06-11T04:04:22.86Z","creation":"2022-02-10T22:15:56.317Z"},"accession":"S-EPMC8291973","cross_references":{"pubmed":["34165081"],"doi":["10.7554/eLife.66596"]}}