{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Vijayan M"],"funding":["NIAID NIH HHS","NIGMS NIH HHS"],"pagination":["677-687"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5528153"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["199(2)"],"pubmed_abstract":["Sphingosine 1-phosphate (S1P) lyase (SPL) is an intracellular enzyme that mediates the irreversible degradation of the bioactive lipid S1P. We have previously reported that overexpressed SPL displays anti-influenza viral activity; however, the underlying mechanism is incompletely understood. In this study, we demonstrate that SPL functions as a positive regulator of IKKε to propel type I IFN-mediated innate immune responses against viral infection. Exogenous SPL expression inhibited influenza A virus replication, which correlated with an increase in type I IFN production and IFN-stimulated gene accumulation upon infection. In contrast, the lack of SPL expression led to an elevated cellular susceptibility to influenza A virus infection. In support of this, SPL-deficient cells were defective"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["Sphingosine 1-Phosphate Lyase Enhances the Activation of IKKε To Promote Type I IFN-Mediated Innate Immune Responses to Influenza A Virus Infection."],"pmcid":["PMC5528153"],"funding_grant_id":["R56 AI108861","R01 GM110776","R01 AI091797"],"pubmed_authors":["Hiscott J","Vijayan M","Fox TE","Hahm B","Ngo H","Johnson MC","Alexander S","Kester M","Drews K","Xia C","Song YE","Studstill CJ"],"additional_accession":[]},"is_claimable":false,"name":"Sphingosine 1-Phosphate Lyase Enhances the Activation of IKKε To Promote Type I IFN-Mediated Innate Immune Responses to Influenza A Virus Infection.","description":"Sphingosine 1-phosphate (S1P) lyase (SPL) is an intracellular enzyme that mediates the irreversible degradation of the bioactive lipid S1P. We have previously reported that overexpressed SPL displays anti-influenza viral activity; however, the underlying mechanism is incompletely understood. In this study, we demonstrate that SPL functions as a positive regulator of IKKε to propel type I IFN-mediated innate immune responses against viral infection. Exogenous SPL expression inhibited influenza A virus replication, which correlated with an increase in type I IFN production and IFN-stimulated gene accumulation upon infection. In contrast, the lack of SPL expression led to an elevated cellular susceptibility to influenza A virus infection. In support of this, SPL-deficient cells were defective","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Jul","modification":"2025-04-04T02:58:27.974Z","creation":"2019-03-26T23:46:21Z"},"accession":"S-EPMC5528153","cross_references":{"pubmed":["28600291"],"doi":["10.4049/jimmunol.1601959"]}}