Integrative Profiling of Alternative Splicing Induced by <i>U2AF1</i> S34F Mutation in Lung Adenocarcinoma Reveals a Mechanistic Link to Mitotic Stress.
By altering levels of mutant or wild-type U2AF1 in this cell line and by analyzing published data on human lung adenocarcinomas, we show that S34F-associated changes in alternative splicing are proportional to the ratio of S34F:wild-type gene products and not to absolute levels of either the mutant or wild-type factor.