{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["136(2)"],"submitter":["Niederkorn M"],"pubmed_abstract":["Myelodysplastic syndromes (MDSs) are malignant hematopoietic stem and progenitor cell (HSPC) disorders that lead to ineffective blood production with poor outcomes. We previously showed that F-box only protein 11 (FBXO11) is downregulated in MDS, and here we report how this event contributes to disease progression. Integration of multiomics data revealed that the SCF-FBXO11 complex regulates spliceosome and ribosome components in a nucleophosmin 1 (NPM1)-centric network. FBXO11 facilitates the ubiquitylation of NPM1, whereby deletion of FBXO11 results in the reorganization of NPM1 and a de-repression of alternative splicing. Label-free total quantitative proteomics demonstrated that the FBXO11-NPM1 interactome was markedly downregulated in cells from patients with CD34+ MDS. In addition, w"],"journal":["The Journal of clinical investigation"],"pagination":["e193636"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12807477"],"repository":["biostudies-literature"],"pubmed_title":["FBXO11 suppression rewires an NPM1-centered interactome influencing the progression of myelodysplastic syndrome."],"pmcid":["PMC12807477"],"pubmed_authors":["Bezavada L","Cotton A","Pagala VR","Wu C","Fu Y","Verma A","Niederkorn M","Kang G","Pruett-Miller SM","Zhai J","Weiss M","Palmer LE","Xu P","Konada L","Crispino JD","Aminov S","Taylor AB","Hall T","Narina S","Ji P","Rampal RK","Schieber M","Schild A","High AA","Janke LJ","Yuan ZF","Steele JA","McGovern E","Gurbuxani S"],"additional_accession":[]},"is_claimable":false,"name":"FBXO11 suppression rewires an NPM1-centered interactome influencing the progression of myelodysplastic syndrome.","description":"Myelodysplastic syndromes (MDSs) are malignant hematopoietic stem and progenitor cell (HSPC) disorders that lead to ineffective blood production with poor outcomes. We previously showed that F-box only protein 11 (FBXO11) is downregulated in MDS, and here we report how this event contributes to disease progression. Integration of multiomics data revealed that the SCF-FBXO11 complex regulates spliceosome and ribosome components in a nucleophosmin 1 (NPM1)-centric network. FBXO11 facilitates the ubiquitylation of NPM1, whereby deletion of FBXO11 results in the reorganization of NPM1 and a de-repression of alternative splicing. Label-free total quantitative proteomics demonstrated that the FBXO11-NPM1 interactome was markedly downregulated in cells from patients with CD34+ MDS. In addition, w","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-07-15T06:35:11.415Z","creation":"2026-06-30T03:21:57.837Z"},"accession":"S-EPMC12807477","cross_references":{"pubmed":["41542766"],"doi":["10.1172/JCI193636"]}}