{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rom S"],"funding":["NIMH NIH HHS","NIAAA NIH HHS","NINDS NIH HHS"],"pagination":["878"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4548080"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["6"],"pubmed_abstract":["Multifactorial mechanisms comprising countless cellular factors and virus-encoded transactivators regulate the transcription of HIV-1 (HIV). Since poly(ADP-ribose) polymerase 1 (PARP-1) regulates numerous genes through its interaction with various transcription factors, inhibition of PARP-1 has surfaced recently as a powerful anti-inflammatory tool. We suggest a novel tactic to diminish HIV replication via PARP-1 inhibition in an in vitro model system, exploiting human primary monocyte-derived macrophages (MDM). PARP-1 inhibition was capable to lessen HIV replication in MDM by 60-80% after 7 days infection. Tat, tumor necrosis factor α (TNFα), and phorbol 12-myristate 13-acetate (PMA) are known triggers of the Long Terminal Repeat (LTR), which can switch virus replication. Tat overexpressi"],"journal":["Frontiers in microbiology"],"pubmed_title":["The dual action of poly(ADP-ribose) polymerase -1 (PARP-1) inhibition in HIV-1 infection: HIV-1 LTR inhibition and diminution in Rho GTPase activity."],"pmcid":["PMC4548080"],"funding_grant_id":["R37 AA015913","R21 NS087385","R01 MH065151","R01 AA015913"],"pubmed_authors":["Persidsky Y","Rom S","Dykstra H","Reichenbach NL"],"additional_accession":[]},"is_claimable":false,"name":"The dual action of poly(ADP-ribose) polymerase -1 (PARP-1) inhibition in HIV-1 infection: HIV-1 LTR inhibition and diminution in Rho GTPase activity.","description":"Multifactorial mechanisms comprising countless cellular factors and virus-encoded transactivators regulate the transcription of HIV-1 (HIV). Since poly(ADP-ribose) polymerase 1 (PARP-1) regulates numerous genes through its interaction with various transcription factors, inhibition of PARP-1 has surfaced recently as a powerful anti-inflammatory tool. We suggest a novel tactic to diminish HIV replication via PARP-1 inhibition in an in vitro model system, exploiting human primary monocyte-derived macrophages (MDM). PARP-1 inhibition was capable to lessen HIV replication in MDM by 60-80% after 7 days infection. Tat, tumor necrosis factor α (TNFα), and phorbol 12-myristate 13-acetate (PMA) are known triggers of the Long Terminal Repeat (LTR), which can switch virus replication. Tat overexpressi","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015","modification":"2025-04-26T01:07:09.274Z","creation":"2019-03-27T01:57:15Z"},"accession":"S-EPMC4548080","cross_references":{"pubmed":["26379653"],"doi":["10.3389/fmicb.2015.00878"]}}