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Molecular and Cellular Biology|July 1, 2015
SRSF2 Is Essential for Hematopoiesis, and Its Myelodysplastic Syndrome-Related Mutations Dysregulate Alternative Pre-mRNA SplicingYukiko Komeno, Yi-Jou Huang, Jinsong Qiu, et al.
Nature|May 17, 2011
Reprogramming transcription by distinct classes of enhancers functionally defined by eRNADong Wang, Ivan Garcia-Bassets, Chris Benner, et al.
RNA (New York, N.Y.)|August 6, 2016
Distinct splicing signatures affect converged pathways in myelodysplastic syndrome patients carrying mutations in different splicing regulatorsJinsong Qiu, Bing Zhou, Felicitas Thol, et al.
Nature Structural & Molecular Biology|October 20, 2014
Mechanisms for U2AF to define 3' splice sites and regulate alternative splicing in the human genomeChangwei Shao, Bo Yang, Tongbin Wu, et al.
The Journal of Clinical Investigation|December 1, 2015
RBFox1-mediated RNA splicing regulates cardiac hypertrophy and heart failureChen Gao, Shuxun Ren, Jae-Hyung Lee, et al.
Molecular Cell|February 4, 2018
The Augmented R-Loop Is a Unifying Mechanism for Myelodysplastic Syndromes Induced by High-Risk Splicing Factor MutationsLiang Chen, Jia-Yu Chen, Yi-Jou Huang, et al.
Nature Communications|January 28, 2015
ALS-causative mutations in FUS/TLS confer gain and loss of function by altered association with SMN and U1-snRNPShuying Sun, Shuo-Chien Ling, Jinsong Qiu, et al.
Molecular Cell|September 30, 2014
BS69/ZMYND11 reads and connects histone H3.3 lysine 36 trimethylation-decorated chromatin to regulated pre-mRNA processingRui Guo, Lijuan Zheng, Juw Won Park, et al.
The EMBO Journal|March 9, 2016
Toxic gain of function from mutant FUS protein is crucial to trigger cell autonomous motor neuron lossJelena Scekic-Zahirovic, Oliver Sendscheid, Hajer El Oussini, et al.
Proceedings of the National Academy of Sciences of the United States of America|October 31, 2013
Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degenerationClotilde Lagier-Tourenne, Michael Baughn, Frank Rigo, et al.
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