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dc.contributor.authorBaker, Biancaen
dc.contributor.authorGeng, Shuoen
dc.contributor.authorChen, Keqiangen
dc.contributor.authorDiao, Naen
dc.contributor.authorYuan, Ruoxien
dc.contributor.authorXu, Xiguangen
dc.contributor.authorDougherty, Seanen
dc.contributor.authorStephenson, Carolineen
dc.contributor.authorXiong, Huabaoen
dc.contributor.authorChu, Hong Weien
dc.contributor.authorLi, Liwuen
dc.date.accessioned2021-04-26T13:58:15Zen
dc.date.available2021-04-26T13:58:15Zen
dc.date.issued2015-01-13en
dc.identifier.urihttp://hdl.handle.net/10919/103122en
dc.description.abstractBackground: Super-low-dose endotoxemia contributes to cell stress and low-grade inflammation. Results: Super-low-dose LPS removed Tollip from late endosomes/lysosomes and blocked lysosome fusion with endosomes or autophagosomes. Tollip knock-out mice had impaired wound healing. Conclusion: Super-low-dose LPS leads to cell stress through clearing Tollip and blocking lysosome fusion. Significance: Our data reveal molecular dynamics of innate immunity regulation.en
dc.language.isoen_USen
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Incen
dc.rightsAttribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.titleAlteration of Lysosome Fusion and Low-grade Inflammation Mediated by Super-low-dose Endotoxinen
dc.typeArticle - Refereeden
dc.title.serialJournal of Biological Chemistryen
dc.identifier.doihttps://doi.org/10.1074/jbc.M114.611442en
dc.identifier.volume290en
dc.identifier.issue10en


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Attribution 4.0 International
License: Attribution 4.0 International