{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cai C"],"funding":["National Natural Science Foundation of China"],"pagination":["11535-11545"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7576308"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(19)"],"pubmed_abstract":["Early type I interferon is essential for antagonizing against malaria infection, which remains a significant global infectious disease. After Plasmodium yoelii YM infection, the activation of MAVS-, STING- and inflammasome-IRF3-mediated pathway could trigger the Socs1 expression to inhibit the TLR7-MyD88-IRF7-induced type I interferon production. However, the dynamic regulatory mechanisms of type I interferon response to YM infection and delicate cross-regulation of these signalling are far from clear. In current study, we established a mathematical model to systematically demonstrate that the MAVS-, STING- and inflammasome-mediated signalling pathways play distinct roles in regulating type I interferon response after YM infection; and the YM dose could significantly affect the difference "],"journal":["Journal of cellular and molecular medicine"],"pubmed_title":["A mathematic model to reveal delicate cross-regulation between MAVS/STING, inflammasome and MyD88-dependent type I interferon signalling."],"pmcid":["PMC7576308"],"funding_grant_id":["81960292","81801579"],"pubmed_authors":["Cai C","Yu X"],"additional_accession":[]},"is_claimable":false,"name":"A mathematic model to reveal delicate cross-regulation between MAVS/STING, inflammasome and MyD88-dependent type I interferon signalling.","description":"Early type I interferon is essential for antagonizing against malaria infection, which remains a significant global infectious disease. After Plasmodium yoelii YM infection, the activation of MAVS-, STING- and inflammasome-IRF3-mediated pathway could trigger the Socs1 expression to inhibit the TLR7-MyD88-IRF7-induced type I interferon production. However, the dynamic regulatory mechanisms of type I interferon response to YM infection and delicate cross-regulation of these signalling are far from clear. In current study, we established a mathematical model to systematically demonstrate that the MAVS-, STING- and inflammasome-mediated signalling pathways play distinct roles in regulating type I interferon response after YM infection; and the YM dose could significantly affect the difference ","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Oct","modification":"2025-04-18T20:45:16.265Z","creation":"2020-10-29T14:51:48Z"},"accession":"S-EPMC7576308","cross_references":{"pubmed":["32885594"],"doi":["10.1111/jcmm.15768"]}}