Wild-type U2AF1 antagonizes the splicing program characteristic of U2AF1-mutant tumors and is required for cell survival
Dennis Liang Fei, Hayley Motowski, Rakesh Chatrikhi, Sameer Prasad, Jovian Yu, Shaojian Gao, Clara Kielkopf, Robert K Bradley, Harold Varmus
The paper shows that wild-type U2AF1 counteracts the splicing changes caused by the S34F mutation in lung cancer and is essential for cell survival, while the mutant protein is not required for growth.
bioRxiv · Aug 24, 2016Cancer Biology