BAF complexes facilitate decatenation of DNA by topoisomerase IIα

Emily C. Dykhuizen, Diana C. Hargreaves, Erik L. Miller, Kairong Cui, Andrey Korshunov, Marcel Kool, Stefan Pfister, Yoon-Jae Cho, Keji Zhao and Gerald R. Crabtree ()
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Emily C. Dykhuizen: Howard Hughes Medical Institute, Stanford University School of Medicine
Diana C. Hargreaves: Howard Hughes Medical Institute, Stanford University School of Medicine
Erik L. Miller: Howard Hughes Medical Institute, Stanford University School of Medicine
Kairong Cui: National Institutes of Health
Andrey Korshunov: CCU Neuropathology, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, Heidelberg 69120, Germany
Marcel Kool: German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, Heidelberg 69120, Germany
Stefan Pfister: German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, Heidelberg 69120, Germany
Yoon-Jae Cho: Stanford University Medical School
Keji Zhao: National Institutes of Health
Gerald R. Crabtree: Howard Hughes Medical Institute, Stanford University School of Medicine

Nature, 2013, vol. 497, issue 7451, 624-627

Abstract: Mutations in the subunits of BAF chromatin-remodelling complexes are frequently found in human cancer; here deletion of BAF subunits or expression of mutants of the ATPase subunit BRG1 attenuates genome-wide binding of topoisomerase IIα, resulting in tangled chromosomes, anaphase bridges and G2/M arrest.

Date: 2013
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DOI: 10.1038/nature12146

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