Cancer-associated ASXL1 mutations may act as gain-of-function mutations of the ASXL1–BAP1 complex

Abstract

ASXL1 is the obligate regulatory subunit of a deubiquitinase complex whose catalytic subunit is BAP1. Heterozygous mutations of ASXL1 that result in premature truncations are frequent in myeloid leukemias and Bohring-Opitz syndrome. Here we demonstrate that ASXL1 truncations confer enhanced activity on the ASXL1-BAP1 complex. Stable expression of truncated… (More)
DOI: 10.1038/ncomms8307

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