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000294462 1001_ $$aBender, Alexander$$b0
000294462 245__ $$aRedistribution of PU.1 partner transcription factor RUNX1 binding secures cell survival during leukemogenesis.
000294462 260__ $$aHoboken, NJ [u.a.]$$bWiley$$c2024
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000294462 520__ $$aTranscription factors (TFs) orchestrating lineage-development often control genes required for cellular survival. However, it is not well understood how cells survive when such TFs are lost, for example in cancer. PU.1 is an essential TF for myeloid fate, and mice with downregulated PU.1 levels develop acute myeloid leukemia (AML). Combining a multi-omics approach with a functional genetic screen, we reveal that PU.1-downregulated cells fundamentally change their survival control from cytokine-driven pathways to overexpression of an autophagy-predominated stem cell gene program, for which we also find evidence in human AML. Control of this program involves redirected chromatin occupancy of the PU.1 partner TF Runx1 to a lineage-inappropriate binding site repertoire. Hence, genomic reallocation of TF binding upon loss of a partner TF can act as a pro-oncogenic failsafe mechanism by sustaining cell survival during leukemogenesis.
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000294462 650_7 $$2Other$$aMyeloid Development
000294462 650_7 $$2Other$$aMyeloid Leukemia
000294462 650_7 $$2Other$$aPU.1
000294462 650_7 $$2Other$$aRUNX1
000294462 7001_ $$aBoydere, Füsun$$b1
000294462 7001_ $$0P:(DE-He78)1546aa03aab6491ab3cf01f75ac2b6af$$aJayavelu, Ashok Kumar$$b2$$udkfz
000294462 7001_ $$aTibello, Alessia$$b3
000294462 7001_ $$aKönig, Thorsten$$b4
000294462 7001_ $$aAleth, Hanna$$b5
000294462 7001_ $$aMeyer Zu Hörste, Gerd$$b6
000294462 7001_ $$aVogl, Thomas$$b7
000294462 7001_ $$00000-0001-7977-9421$$aRosenbauer, Frank$$b8
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