{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T22:34:00Z","timestamp":1793918040341,"version":"4.8.0"},"reference-count":68,"publisher":"American Society of Hematology","issue":"17","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,10,22]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>Leukemia stem cells (LSCs) drive acute myeloid leukemia (AML) initiation, relapse, and chemoresistance, yet the core posttranslational events sustaining LSC maintenance remain poorly defined. Here, through phosphoproteomic profiling of normal hematopoietic stem and progenitor cells (HSPCs) vs LSC-enriched populations, we identified DEK phosphorylation as a critical modification during leukemogenesis. Functional studies in MLL-AF9\u2013 and HOXA9\/MEIS1-driven AML mouse models, as well as patient-derived xenografts, demonstrate that DEK deficiency impairs LSC maintenance and AML progression. Moreover, DEK deletion enhances LSC chemosensitivity to the standard-of-care combination of azacitidine and venetoclax, whereas DEK overexpression confers robust chemoresistance. Mechanistically, DEK recruits the transcription factor GA repeat binding protein \u03b1 (GABPA) to upregulate the transcriptional cofactor PBX3, a key oncogenic driver in AML, thereby sustaining the leukemogenic transcriptional program. This DEK-GABPA interaction strictly depends on DEK phosphorylation at Ser301\/303\/306\/307 (the 4S sites), which stabilizes the conformation of the DEK-GABPA complex. We identify casein kinase 2 (CK2) as the upstream kinase that directly phosphorylates DEK-4S sites. Importantly, blockade of DEK phosphorylation via 4S site mutagenesis or treatment with the clinical-stage CK2 inhibitor CX-4945 selectively depletes LSCs while sparing normal HSPCs. Furthermore, combining CX-4945 with venetoclax promotes LSC apoptosis and represses the PBX3-driven leukemogenic transcriptional program, exhibiting synergistic anti-AML effects both in vitro and in vivo. Collectively, our findings uncover a previously unrecognized phosphorylation event (DEK-4S phosphorylation) that sustains LSCs and establish the CK2-DEK axis as a promising LSC-specific therapeutic strategy for AML.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2025032710","type":"journal-article","created":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T19:14:32Z","timestamp":1782846872000},"page":"2159-2175","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":8,"title":["Phosphorylated DEK sustains leukemia stem cells by enabling PBX3-driven transcriptional reprogramming"],"prefix":"10.1182","volume":"148","author":[{"given":"Yufei","family":"Lei","sequence":"first","affiliation":[{"name":"1Department of Hematology, The Second Affiliated Hospital of Chongqing Medical University, School of Basic Medical Sciences, Chongqing Medical University, Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanru","family":"Lai","sequence":"additional","affiliation":[{"name":"1Department of Hematology, The Second Affiliated Hospital of Chongqing Medical University, School of Basic Medical Sciences, Chongqing Medical University, Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5346-3098","authenticated-orcid":false,"given":"Yan","family":"Li","sequence":"additional","affiliation":[{"name":"2Department of Obstetrics and Gynecology, Women and Children's Hospital of Chongqing Medical University, Chongqing Health Center for Women and Children, Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuxia","family":"Wang","sequence":"additional","affiliation":[{"name":"3Department of Hematology, The First Affiliated Hospital of Chongqing Medical University, School of Basic Medical Sciences, Chongqing Medical University, Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haiqi","family":"Fan","sequence":"additional","affiliation":[{"name":"1Department of Hematology, The Second Affiliated Hospital of Chongqing Medical University, School of Basic Medical Sciences, Chongqing Medical University, Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-0724-1951","authenticated-orcid":false,"given":"Qiang","family":"Gong","sequence":"additional","affiliation":[{"name":"4Department of Clinical Hematology, Third Military Medical University (Army Medical University), Chongqing, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0570-4280","authenticated-orcid":false,"given":"Feng","family":"Wu","sequence":"additional","affiliation":[{"name":"1Department of Hematology, The Second Affiliated Hospital of Chongqing Medical University, School of Basic Medical Sciences, Chongqing Medical 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