{"doi":"10.3389/fviro.2022.971293","title":"Altered recruitment of Sp isoforms to HIV-1 long terminal repeat between differentiated monoblastic cell lines and primary monocyte-derived macrophages","abstract":"Human immunodeficiency virus type 1 (HIV-1) transcription in cells of the monocyte-macrophage lineage is regulated by interactions between the HIV-1 long terminal repeat (LTR) and a variety of host cell and viral proteins. Binding of the Sp family of transcription factors (TFs) to the G/C box array of the LTR governs both basal as well as activated LTR-directed transcriptional activity. The effect of monocytic differentiation on Sp factor binding and transactivation was examined with respect to the HIV-1 LTR. The binding of Sp1, full-length Sp3 and truncated Sp3 to a high affinity HIV-1 Sp element was specifically investigated and results showed that Sp1 binding increased relative to the binding of the sum of full-length and truncated Sp3 binding following chemically-induced monocytic differentiation in monoblastic (U-937, THP-1) and myelomonocytic (HL-60) cells. In addition, Sp binding ratios from PMA-induced cell lines were shown to more closely approximate those derived from primary monocyte-derived macrophages (MDMs) than did ratios derived from uninduced cell lines. The altered Sp binding phenotype associated with changes in the transcriptional activation mediated by the HIV-1 G/C box array. Additionally, analysis of post-translational modifications on Sp1 and Sp3 revealed a loss of phosphorylation on serine and threonine residues with chemically-induced differentiation indicating that the activity of Sp factors is additionally regulated at the level of post-translational modifications (PTMs).","journal":"Frontiers in Virology","year":2022,"id":296014,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9524,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2022-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":299484,"name":"Satinder Dahiya","orcid":"0000-0002-2189-4846","position":1,"is_corresponding":false},{"id":855418,"name":"Rachel Berman","orcid":null,"position":2,"is_corresponding":false},{"id":854600,"name":"Mackenzie Collins","orcid":"0000-0003-1781-6367","position":3,"is_corresponding":false},{"id":365999,"name":"Michael R. Nonnemacher","orcid":"0000-0003-4299-3779","position":4,"is_corresponding":false},{"id":282163,"name":"Tricia H. Burdo","orcid":"0000-0002-4224-7381","position":5,"is_corresponding":false},{"id":365998,"name":"Brian Wigdahl","orcid":"0000-0002-5211-0936","position":6,"is_corresponding":false},{"id":982208,"name":"John McAllister","orcid":"0000-0002-4017-115X","position":0,"is_corresponding":true}],"reference_count":76,"raw_metadata":null,"created_at":"2026-07-19T00:31:12.531553Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}