{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sariyer IK"],"funding":["National Institute of Allergy and Infectious Diseases","NIAID NIH HHS","NIMH NIH HHS","NINDS NIH HHS","NCI NIH HHS","National Institutes of Health"],"pagination":["e0156819"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4892494"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(6)"],"pubmed_abstract":["<h4>Objective</h4>PML is a rare and fatal demyelinating disease of the CNS caused by the human polyomavirus, JC virus (JCV), which occurs in AIDS patients and those on immunosuppressive monoclonal antibody therapies (mAbs). We sought to identify mechanisms that could stimulate reactivation of JCV in a cell culture model system and targeted pathways which could affect early gene transcription and JCV T-antigen production, which are key steps of the viral life cycle for blocking reactivation of JCV. Two important regulatory partners we have previously identified for T-antigen include Pur-alpha and SRSF1 (SF2/ASF). SRSF1, an alternative splicing factor, is a potential regulator of JCV whose overexpression in glial cells strongly suppresses viral gene expression and replication. Pur-alpha has "],"journal":["PloS one"],"pubmed_title":["Pur-Alpha Induces JCV Gene Expression and Viral Replication by Suppressing SRSF1 in Glial Cells."],"pmcid":["PMC4892494"],"funding_grant_id":["P30 MH092177","R21 NS081447","R01AI101192","P30 CA006927","P30MH092177","R01 AI101192","R21NS081447"],"pubmed_authors":["Sariyer IK","Otte J","Gordon J","Sariyer R"],"additional_accession":[]},"is_claimable":false,"name":"Pur-Alpha Induces JCV Gene Expression and Viral Replication by Suppressing SRSF1 in Glial Cells.","description":"<h4>Objective</h4>PML is a rare and fatal demyelinating disease of the CNS caused by the human polyomavirus, JC virus (JCV), which occurs in AIDS patients and those on immunosuppressive monoclonal antibody therapies (mAbs). We sought to identify mechanisms that could stimulate reactivation of JCV in a cell culture model system and targeted pathways which could affect early gene transcription and JCV T-antigen production, which are key steps of the viral life cycle for blocking reactivation of JCV. Two important regulatory partners we have previously identified for T-antigen include Pur-alpha and SRSF1 (SF2/ASF). SRSF1, an alternative splicing factor, is a potential regulator of JCV whose overexpression in glial cells strongly suppresses viral gene expression and replication. Pur-alpha has ","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016","modification":"2025-04-22T21:34:44.644Z","creation":"2019-03-26T22:53:55Z"},"accession":"S-EPMC4892494","cross_references":{"pubmed":["27257867"],"doi":["10.1371/journal.pone.0156819"]}}