{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang X"],"funding":["Natural Science Foundation of Beijing Municipality (Beijing Natural Science Foundation)","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["4529"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12081701"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["Latent HIV-1 presents a formidable challenge for viral eradication. HIV-1 transcription and latency reversal require interactions between the viral promoter and host proteins. Here, we perform the dCas9-targeted locus-specific protein analysis and discover the interaction of human arginine methyltransferase 3 (PRMT3) with the HIV-1 promoter. This interaction reverses latency in cell line models and primary cells from latently infected persons by increasing the levels of H4R3Me2a and transcription factor P-TEFb at the viral promoter. PRMT3 is found to promote chromatin accessibility and transcription of HIV-1 and a small subset of host genes in regions harboring the classical recognition motif for another transcription factor TEAD4. This motif attracts TEAD4 and PRMT3 to the viral promoter "],"journal":["Nature communications"],"pubmed_title":["PRMT3 reverses HIV-1 latency by increasing chromatin accessibility to form a TEAD4-P-TEFb-containing transcriptional hub."],"pmcid":["PMC12081701"],"funding_grant_id":["31900132","32470588","7232052"],"pubmed_authors":["Yao K","Chong H","Zhou Q","Guo Y","Wan L","Fan M","Wang F","Liu R","Yu D","Chen C","Li L","Jia L","Song J","Xue Y","Li X","Lu L","He Y","Lin D","Xiang Z","Wang X","Han J","Gao X","Su W"],"additional_accession":[]},"is_claimable":false,"name":"PRMT3 reverses HIV-1 latency by increasing chromatin accessibility to form a TEAD4-P-TEFb-containing transcriptional hub.","description":"Latent HIV-1 presents a formidable challenge for viral eradication. HIV-1 transcription and latency reversal require interactions between the viral promoter and host proteins. Here, we perform the dCas9-targeted locus-specific protein analysis and discover the interaction of human arginine methyltransferase 3 (PRMT3) with the HIV-1 promoter. This interaction reverses latency in cell line models and primary cells from latently infected persons by increasing the levels of H4R3Me2a and transcription factor P-TEFb at the viral promoter. PRMT3 is found to promote chromatin accessibility and transcription of HIV-1 and a small subset of host genes in regions harboring the classical recognition motif for another transcription factor TEAD4. This motif attracts TEAD4 and PRMT3 to the viral promoter ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-06-01T23:01:41.492Z","creation":"2026-05-23T03:08:16.754Z"},"accession":"S-EPMC12081701","cross_references":{"pubmed":["40374607"],"doi":["10.1038/s41467-025-59578-5"]}}