{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gamez-Garcia A"],"funding":["Barncancerfonden (Swedish Childhood Cancer Foundation)","EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Skłodowska-Curie Actions (H2020 Excellent Science - Marie Skłodowska-Curie Actions)","Forskningsrådet om Hälsa, Arbetsliv och Välfärd (Swedish Research Council for Health, Working Life and Welfare)","Departament d'Innovació, Universitats i Empresa, Generalitat de Catalunya (Department of Innovation, Education and Enterprise, Government of Catalonia)","Fundación Científica Asociación Española Contra el Cáncer (Scientific Foundation, Spanish Association Against Cancer)","Ministry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación)"],"pagination":["2308-2319"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11588656"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(12)"],"pubmed_abstract":["B lymphopoiesis is orchestrated by lineage-specific transcription factors. In B cell progenitors, lineage commitment is mediated by Pax5, which is commonly mutated in B cell acute lymphoblastic leukemia. Despite its essential role in immunity, the mechanisms regulating Pax5 function remain largely unknown. Here, we found that the NAD<sup>+</sup>-dependent enzyme SIRT7 coordinates B cell development through deacetylation of Pax5 at K198, which promotes Pax5 protein stability and transcriptional activity. Neither Pax5<sup>K198</sup> deacetylated nor acetylated mimics rescued B cell differentiation in Pax5<sup>-/-</sup> pro-B cells, suggesting that B cell development requires Pax5 dynamic deacetylation. The Pax5<sup>K198</sup> deacetylation mimic restored lineage commitment in Pax5<sup>-/-</s"],"journal":["Nature immunology"],"pubmed_title":["A SIRT7-dependent acetylation switch regulates early B cell differentiation and lineage commitment through Pax5."],"pmcid":["PMC11588656"],"funding_grant_id":["MSC-2021-101065013","2021-SGR-01494","2022-0019","PROYE20042VAQU","FI_B 00293","2017-SGR-148","2021-02379","SAF2017-88975R","MSC-2020-895979","2021-SGR-01378","2016-BP-00250"],"pubmed_authors":["Gamez-Garcia A","Bueno-Costa A","Sigvardsson M","Alari-Pahissa E","Berenguer C","Tischfield JA","Esteller M","Espinosa-Alcantud M","De La Torre C","Bech JJ","Braun T","Vaquero A","Vazquez BN","Marazuela-Duque A","Thackray JK","Kumari P","Ray C","Ianni A","Serrano L","Sardina JL"],"additional_accession":[]},"is_claimable":false,"name":"A SIRT7-dependent acetylation switch regulates early B cell differentiation and lineage commitment through Pax5.","description":"B lymphopoiesis is orchestrated by lineage-specific transcription factors. In B cell progenitors, lineage commitment is mediated by Pax5, which is commonly mutated in B cell acute lymphoblastic leukemia. Despite its essential role in immunity, the mechanisms regulating Pax5 function remain largely unknown. Here, we found that the NAD<sup>+</sup>-dependent enzyme SIRT7 coordinates B cell development through deacetylation of Pax5 at K198, which promotes Pax5 protein stability and transcriptional activity. Neither Pax5<sup>K198</sup> deacetylated nor acetylated mimics rescued B cell differentiation in Pax5<sup>-/-</sup> pro-B cells, suggesting that B cell development requires Pax5 dynamic deacetylation. The Pax5<sup>K198</sup> deacetylation mimic restored lineage commitment in Pax5<sup>-/-</s","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Dec","modification":"2026-06-02T22:57:02.649Z","creation":"2025-04-21T21:42:49.289Z"},"accession":"S-EPMC11588656","cross_references":{"pubmed":["39424985"],"doi":["10.1038/s41590-024-01995-7"]}}