{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Guan J"],"funding":["山东省科学技术厅 | Natural Science Foundation of Shandong Province","The QILU Young Scholars Program of Shandong University","| Natural Science Foundation of Shandong Province ()","GDSTC | Basic and Applied Basic Research Foundation of Guangdong Province","MOST | National Natural Science Foundation of China (NSFC)","NIAID NIH HHS","GDSTC | Basic and Applied Basic Research Foundation of Guangdong Province ()","HHS | NIH | National Institute of Allergy and Infectious Diseases","MOST | National Natural Science Foundation of China","HHS | NIH | National Institute of Allergy and Infectious Diseases (NIAID)"],"pagination":["e2400657121"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11348272"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["121(34)"],"pubmed_abstract":["Microsporidia are intracellular eukaryotic pathogens that pose a substantial threat to immunocompromised hosts. The way these pathogens manipulate host cells during infection remains poorly understood. Using a proximity biotinylation strategy we established that microsporidian EnP1 is a nucleus-targeted effector that modifies the host cell environment. EnP1's translocation to the host nucleus is meditated by nuclear localization signals (NLSs). In the nucleus, EnP1 interacts with host histone H2B. This interaction disrupts H2B monoubiquitination (H2Bub), subsequently impacting p53 expression. Crucially, this inhibition of p53 weakens its control over the downstream target gene SLC7A11, enhancing the host cell's resilience against ferroptosis during microsporidian infection. This favorable condition promotes the proliferation of microsporidia within the host cell. These findings shed light on the molecular mechanisms by which microsporidia modify their host cells to facilitate their survival."],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Microsporidian EnP1 alters host cell H2B monoubiquitination and prevents ferroptosis facilitating microsporidia survival."],"pmcid":["PMC11348272"],"funding_grant_id":["32000106","2024A1515010685","AI124753","2023A1515110681","R01 AI124753","ZR2023QC236","81971960","21510082063092"],"pubmed_authors":["Guan J","Cong H","Qu H","Sabi MM","Xia T","Wang J","Zheng K","Tang L","Han B","Zhou C","Weiss LM","Wang Y","Fu M","Zhou H"],"additional_accession":[]},"is_claimable":false,"name":"Microsporidian EnP1 alters host cell H2B monoubiquitination and prevents ferroptosis facilitating microsporidia survival.","description":"Microsporidia are intracellular eukaryotic pathogens that pose a substantial threat to immunocompromised hosts. The way these pathogens manipulate host cells during infection remains poorly understood. Using a proximity biotinylation strategy we established that microsporidian EnP1 is a nucleus-targeted effector that modifies the host cell environment. EnP1's translocation to the host nucleus is meditated by nuclear localization signals (NLSs). In the nucleus, EnP1 interacts with host histone H2B. This interaction disrupts H2B monoubiquitination (H2Bub), subsequently impacting p53 expression. Crucially, this inhibition of p53 weakens its control over the downstream target gene SLC7A11, enhancing the host cell's resilience against ferroptosis during microsporidian infection. This favorable condition promotes the proliferation of microsporidia within the host cell. These findings shed light on the molecular mechanisms by which microsporidia modify their host cells to facilitate their survival.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Aug","modification":"2026-06-02T20:16:40.783Z","creation":"2025-04-07T07:53:30.303Z"},"accession":"S-EPMC11348272","cross_references":{"pubmed":["39141344"],"doi":["10.1073/pnas.2400657121"]}}