{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(1)"],"submitter":["Chen L"],"pubmed_abstract":["SARS-CoV-2, the culprit pathogen of COVID-19, elicits prominent immune responses and cytokine storms. Intracellular Cl<sup>-</sup> is a crucial regulator of host defense, whereas the role of Cl<sup>-</sup> signaling pathway in modulating pulmonary inflammation associated with SARS-CoV-2 infection remains unclear. By using human respiratory epithelial cell lines, primary cultured human airway epithelial cells, and murine models of viral structural protein stimulation and SARS-CoV-2 direct challenge, we demonstrated that SARS-CoV-2 nucleocapsid (N) protein could interact with Smad3, which downregulated cystic fibrosis transmembrane conductance regulator (CFTR) expression via microRNA-145. The intracellular Cl<sup>-</sup> concentration ([Cl<sup>-</sup>]<sub>i</sub>) was raised, resulting in p"],"journal":["Signal transduction and targeted therapy"],"pagination":["255"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9328007"],"repository":["biostudies-literature"],"pubmed_title":["SARS-CoV-2 nucleocapsid protein triggers hyperinflammation via protein-protein interaction-mediated intracellular Cl<sup>-</sup> accumulation in respiratory epithelium."],"pmcid":["PMC9328007"],"pubmed_authors":["Huang ZX","Lun ZR","Huang ZY","Ye KN","Chen L","Lei TL","Bai X","Qu S","Guan WJ","Zhong NS","Zhang YL","Hou XC","Xu JB","Qiu ZE","Zhu YX","Zhou WL","Zhao J","Sun J"],"additional_accession":[]},"is_claimable":false,"name":"SARS-CoV-2 nucleocapsid protein triggers hyperinflammation via protein-protein interaction-mediated intracellular Cl<sup>-</sup> accumulation in respiratory epithelium.","description":"SARS-CoV-2, the culprit pathogen of COVID-19, elicits prominent immune responses and cytokine storms. Intracellular Cl<sup>-</sup> is a crucial regulator of host defense, whereas the role of Cl<sup>-</sup> signaling pathway in modulating pulmonary inflammation associated with SARS-CoV-2 infection remains unclear. By using human respiratory epithelial cell lines, primary cultured human airway epithelial cells, and murine models of viral structural protein stimulation and SARS-CoV-2 direct challenge, we demonstrated that SARS-CoV-2 nucleocapsid (N) protein could interact with Smad3, which downregulated cystic fibrosis transmembrane conductance regulator (CFTR) expression via microRNA-145. The intracellular Cl<sup>-</sup> concentration ([Cl<sup>-</sup>]<sub>i</sub>) was raised, resulting in p","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jul","modification":"2025-05-31T23:03:29.194Z","creation":"2022-08-03T07:05:23.275Z"},"accession":"S-EPMC9328007","cross_references":{"pubmed":["35896532"],"doi":["10.1038/s41392-022-01048-1"]}}