Cancer-associated ASXL1 mutations may act as gain-of-function mutations of the ASXL1–BAP1 complex
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...
| Main Authors: | , , , , , , , |
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| Format: | Online |
| Language: | English |
| Published: |
Nature Pub. Group
2015
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557297/ |