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...

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Detalles Bibliográficos
Autores principales: Balasubramani, Anand, Larjo, Antti, Bassein, Jed A., Chang, Xing, Hastie, Ryan B., Togher, Susan M., Lähdesmäki, Harri, Rao, Anjana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Pub. Group 2015
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557297/
https://www.ncbi.nlm.nih.gov/pubmed/26095772
http://dx.doi.org/10.1038/ncomms8307

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557297/
https://www.ncbi.nlm.nih.gov/pubmed/26095772
http://dx.doi.org/10.1038/ncomms8307

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