{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chengyue W"],"funding":["National Natural Science Foundation of China","Natural Science Foundation of Jiangsu Province"],"pagination":["84"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11225307"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["55(1)"],"pubmed_abstract":["Pseudorabies virus (PRV) has evolved multiple strategies to evade host antiviral responses to benefit virus replication and establish persistent infection. Recently, tripartite motif 26 (TRIM26), a TRIM family protein, has been shown to be involved in a broad range of biological processes involved in innate immunity, especially in regulating viral infection. Herein, we found that the expression of TRIM26 was significantly induced after PRV infection. Surprisingly, the overexpression of TRIM26 promoted PRV production, while the depletion of this protein inhibited virus replication, suggesting that TRIM26 could positively regulate PRV infection. Further analysis revealed that TRIM26 negatively regulates the innate immune response by targeting the RIG-I-triggered type I interferon signalling "],"journal":["Veterinary research"],"pubmed_title":["TRIM26 facilitates PRV infection through NDP52-mediated autophagic degradation of MAVS."],"pmcid":["PMC11225307"],"funding_grant_id":["32002231","BK20201005"],"pubmed_authors":["Mengdong W","Liumei S","Zhendong Z","Yeping C","Hao L","Chengyue W","Jianle R","Xiaoquan W"],"additional_accession":[]},"is_claimable":false,"name":"TRIM26 facilitates PRV infection through NDP52-mediated autophagic degradation of MAVS.","description":"Pseudorabies virus (PRV) has evolved multiple strategies to evade host antiviral responses to benefit virus replication and establish persistent infection. Recently, tripartite motif 26 (TRIM26), a TRIM family protein, has been shown to be involved in a broad range of biological processes involved in innate immunity, especially in regulating viral infection. Herein, we found that the expression of TRIM26 was significantly induced after PRV infection. Surprisingly, the overexpression of TRIM26 promoted PRV production, while the depletion of this protein inhibited virus replication, suggesting that TRIM26 could positively regulate PRV infection. Further analysis revealed that TRIM26 negatively regulates the innate immune response by targeting the RIG-I-triggered type I interferon signalling ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2025-04-04T23:54:15.074Z","creation":"2025-04-04T23:54:15.074Z"},"accession":"S-EPMC11225307","cross_references":{"pubmed":["38965634"],"doi":["10.1186/s13567-024-01336-4"]}}