The metabolic reprogramming and vulnerability of SF3B1 mutations
Author:
Affiliation:
1. Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD, USA
Publisher
Informa UK Limited
Subject
Cancer Research,Molecular Medicine
Link
https://www.tandfonline.com/doi/pdf/10.1080/23723556.2019.1697619
Reference10 articles.
1. Cancer-Associated SF3B1 Hotspot Mutations Induce Cryptic 3′ Splice Site Selection through Use of a Different Branch Point
2. Frequent pathway mutations of splicing machinery in myelodysplasia
3. Cancer-associated SF3B1 mutations affect alternative splicing by promoting alternative branchpoint usage
4. The transporter ABCB7 is a mediator of the phenotype of acquired refractory anemia with ring sideroblasts
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