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- August 24, 2016.
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- Version 1 (April 13, 2016 - 21:57).
- Version 2 (April 16, 2016 - 16:55).
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- Version 4 (May 20, 2016 - 10:48).
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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
Author Information
- Dennis Liang Fei1,2,*,
- Hayley Motowski1,
- Rakesh Chatrikhi3,
- Sameer Prasad1,
- Jovian Yu1,
- Shaojian Gao4,
- Clara Kielkopf3,*,
- Robert K. Bradley5,6,* and
- Harold Varmus1,2,*
- 1Cancer Biology Section, Cancer Genetics Branch, National Human Genome Research Institute, Bethesda, MD 20892, United States
- 2Department of Medicine, Meyer Cancer Center, Weill Cornell Medicine, New York, NY 10065, United States
- 3Department of Biochemistry and Biophysics, Center for RNA Biology, University of Rochester Medical Center, Rochester, NY 14642, United States
- 4Genetics Branch, National Cancer Institute, Bethesda, Maryland, 20892, United States
- 5Computational Biology Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, United States
- 6Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, United States
- ↵*Correspondence: D.L.F. dlf2002{at}med.cornell.edu; C.L.K. clara_kielkopf{at}urmc.rochester.edu; R.K.B. rbradley{at}fredhutch.org; H.V. varmus{at}med.cornell.edu
Posted August 24, 2016.
Wild-type U2AF1 antagonizes the splicing program characteristic of U2AF1-mutant tumors and is required for cell survival
