{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T19:35:50Z","timestamp":1783625750827,"version":"3.55.0"},"update-to":[{"DOI":"10.1371\/journal.pgen.1010463","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2022,11,7]],"date-time":"2022-11-07T00:00:00Z","timestamp":1667779200000}}],"reference-count":50,"publisher":"Public Library of Science (PLoS)","issue":"10","license":[{"start":{"date-parts":[[2022,10,26]],"date-time":"2022-10-26T00:00:00Z","timestamp":1666742400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100005972","name":"Deutsche Krebshilfe","doi-asserted-by":"publisher","award":["109787"],"award-info":[{"award-number":["109787"]}],"id":[{"id":"10.13039\/501100005972","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Alfred and Angelika Gutermuth Foundation"},{"DOI":"10.13039\/501100003099","name":"FAZIT Stiftung","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003099","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Newton-Mosharafa Fund"},{"DOI":"10.13039\/501100004410","name":"Scientific and Technological Research Council of Turkey","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100004410","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Leukaemia and Myeloma Research UK"}],"content-domain":{"domain":["www.plosgenetics.org"],"crossmark-restriction":false},"short-container-title":["PLoS Genet"],"abstract":"<jats:p>The WHO classifies t(6;9)-positive acute myeloid leukemia (AML) as a subgroup of high-risk AML because of its clinical and biological peculiarities, such as young age and therapy resistance. t(6;9) encodes the DEK\/NUP214 fusion oncoprotein that targets only a small subpopulation of bone marrow progenitors for leukemic transformation. This distinguishes DEK\/NUP214 from other fusion oncoproteins, such as PML\/RAR\u03b1, RUNX1\/ETO, or MLL\/AF9, which have a broad target population they block differentiation and increase stem cell capacity. A common theme among most leukemogenic fusion proteins is their aberrant localization compared to their wild-type counterparts. Although the actual consequences are widely unknown, it seems to contribute to leukemogenesis most likely by a sequester of interaction partners. Thus, we applied a global approach to studying the consequences of the aberrant localization of t(6;9)-DEK\/NUP214 for its interactome. This study aimed to disclose the role of localization of DEK\/NUP214 and the related sequester of proteins interacting with DEK\/NUP214 for the determination of the biology of t(6;9)-AML. Here we show the complexity of the biological consequences of the expression of DEK\/NUP214 by an in-depth bioinformatic analysis of the interactome of DEK\/NUP214 and its biologically dead mutants. DEK\/NUP214\u2019s interactome points to an essential role for aberrant RNA-regulation and aberrant regulation of apoptosis and leukocyte activation as a significant determinant of the phenotype of t(6;9)-AML. Taken together, we provide evidence that the interactome contributes to the aberrant biology of an oncoprotein, providing opportunities for developing novel targeted therapy approaches.<\/jats:p>","DOI":"10.1371\/journal.pgen.1010463","type":"journal-article","created":{"date-parts":[[2022,10,26]],"date-time":"2022-10-26T18:29:44Z","timestamp":1666808984000},"page":"e1010463","update-policy":"https:\/\/doi.org\/10.1371\/journal.pgen.corrections_policy","source":"Crossref","is-referenced-by-count":11,"title":["Understanding a high-risk acute myeloid leukemia by analyzing the interactome of its major driver 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