{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Knatko EV"],"funding":["Wellcome Trust"],"pagination":["4378-4390"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12447449"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(17)"],"pubmed_abstract":["Abstract
Ten-eleven translocation (TET) enzymes are epigenetic regulators important for the prevention of hematological malignancies. Proline and serine rich 1 (PROSER1), a known TET protein interactor, has a critical role in modulating TET-mediated DNA demethylation during development. However, the potential involvement of PROSER1 in the regulation of hematopoiesis and leukemogenesis remains unknown. Here, we demonstrate that the leukemia-suppressive functions of TET2 are preserved in the absence of PROSER1. Nonetheless, we find that loss of PROSER1 partially recapitulates the aberrant enhancer DNA methylation phenotype observed upon TET2 knockout, suggesting that PROSER1 and TET2 play both cooperative and distinct roles in the regulation of DNA methylation in hematopoiesis. Impor"],"journal":["Blood advances"],"pubmed_title":["The TET protein family interactor PROSER1 sustains hematopoietic stem cell function."],"pmcid":["PMC12447449"],"funding_grant_id":["22644/Z/22/Z"],"pubmed_authors":["Rasmussen KD","Li X","Fleming A","Knatko EV","Crawley P","Budriunaite I"],"additional_accession":[]},"is_claimable":false,"name":"The TET protein family interactor PROSER1 sustains hematopoietic stem cell function.","description":"Abstract
Ten-eleven translocation (TET) enzymes are epigenetic regulators important for the prevention of hematological malignancies. Proline and serine rich 1 (PROSER1), a known TET protein interactor, has a critical role in modulating TET-mediated DNA demethylation during development. However, the potential involvement of PROSER1 in the regulation of hematopoiesis and leukemogenesis remains unknown. Here, we demonstrate that the leukemia-suppressive functions of TET2 are preserved in the absence of PROSER1. Nonetheless, we find that loss of PROSER1 partially recapitulates the aberrant enhancer DNA methylation phenotype observed upon TET2 knockout, suggesting that PROSER1 and TET2 play both cooperative and distinct roles in the regulation of DNA methylation in hematopoiesis. Impor","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-07-15T05:50:25.374Z","creation":"2026-06-29T03:19:47.678Z"},"accession":"S-EPMC12447449","cross_references":{"pubmed":["40554416"],"doi":["10.1182/bloodadvances.2024015683"]}}