{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["1(3)"],"submitter":["Wen J"],"pubmed_abstract":["Alpha7 nicotinic acetylcholine receptor (α7 nAChR), a hub of the cholinergic anti-inflammatory pathway (CAP), is required for the treatment of inflammatory diseases. HIV-1 infection can upregulate the expression of α7 nAChR in T lymphocytes and affect the role of CAP. However, whether α7 nAChR regulates HIV-1 infection in CD4<sup>+</sup> T cells is unclear. In this study, we first found that activation of α7 nAChR by GTS-21 (an α7 nAChR agonist) can promote the transcription of HIV-1 proviral DNA. Then, through transcriptome sequencing analysis, we found that p38 MAPK signaling was enriched in GTS-21 treated HIV-latent T cells. Mechanistically, activation of α7 nAChR could increase reactive oxygen species (ROS), reduce <i>DUSP1</i> and <i>DUSP6</i>, and consequently enhance the phosphoryla"],"journal":["Cell insight"],"pagination":["100028"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10120325"],"repository":["biostudies-literature"],"pubmed_title":["Activation of α7 nicotinic acetylcholine receptor promotes HIV-1 transcription."],"pmcid":["PMC10120325"],"pubmed_authors":["Wen J","Zhao C","Chen J","Qi H","Song S","Lin Z","Wang J","Su X","Xie S"],"additional_accession":[]},"is_claimable":false,"name":"Activation of α7 nicotinic acetylcholine receptor promotes HIV-1 transcription.","description":"Alpha7 nicotinic acetylcholine receptor (α7 nAChR), a hub of the cholinergic anti-inflammatory pathway (CAP), is required for the treatment of inflammatory diseases. HIV-1 infection can upregulate the expression of α7 nAChR in T lymphocytes and affect the role of CAP. However, whether α7 nAChR regulates HIV-1 infection in CD4<sup>+</sup> T cells is unclear. In this study, we first found that activation of α7 nAChR by GTS-21 (an α7 nAChR agonist) can promote the transcription of HIV-1 proviral DNA. Then, through transcriptome sequencing analysis, we found that p38 MAPK signaling was enriched in GTS-21 treated HIV-latent T cells. Mechanistically, activation of α7 nAChR could increase reactive oxygen species (ROS), reduce <i>DUSP1</i> and <i>DUSP6</i>, and consequently enhance the phosphoryla","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jun","modification":"2025-04-19T06:41:27.99Z","creation":"2025-04-19T06:41:27.99Z"},"accession":"S-EPMC10120325","cross_references":{"pubmed":["37193048"],"doi":["10.1016/j.cellin.2022.100028"]}}