U2AF1 mutations induce oncogenic IRAK4 isoforms and activate innate immune pathways in myeloid malignancies

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Physiologic Expression of Sf3b1 K700E Causes Impaired Erythropoiesis, Aberrant Splicing, and Sensitivity to Therapeutic Spliceosome Modulation

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Ubiquitination of hnRNPA1 by TRAF6 links chronic innate immune signaling with myelodysplasia

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Wild-Type U2AF1 Antagonizes the Splicing Program Characteristic of U2AF1-Mutant Tumors and Is Required for Cell Survival

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Comprehensive RNAi-based screening of human and mouse TLR pathways identifies species-specific preferences in signaling protein use

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The N-terminal loop of IRAK-4 death domain regulates ordered assembly of the Myddosome signalling scaffold

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SRSF2 Mutations Contribute to Myelodysplasia by Mutant-Specific Effects on Exon Recognition

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Mutant U2AF1 Expression Alters Hematopoiesis and Pre-mRNA Splicing In Vivo

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Inhibition of IRAK1/4 sensitizes T cell acute lymphoblastic leukemia to chemotherapies

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Loss ofTifab, a del(5q) MDS gene, alters hematopoiesis through derepression of Toll-like receptor–TRAF6 signaling

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SRSF2 Is Essential for Hematopoiesis, and Its Myelodysplastic Syndrome-Related Mutations Dysregulate Alternative Pre-mRNA Splicing

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Disease-associated mutation inSRSF2misregulates splicing by altering RNA-binding affinities

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IRAK1 is a therapeutic target that drives breast cancer metastasis and resistance to paclitaxel

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Combining gene mutation with gene expression data improves outcome prediction in myelodysplastic syndromes

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Targeting IRAK1 in T-cell acute lymphoblastic leukemia

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U2AF1mutations alter splice site recognition in hematological malignancies

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U2AF1 mutations alter sequence specificity of pre-mRNA binding and splicing

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IRAK4 Dimerization and trans -Autophosphorylation Are Induced by Myddosome Assembly

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A Pan-Cancer Analysis of Transcriptome Changes Associated with Somatic Mutations in U2AF1 Reveals Commonly Altered Splicing Events

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Mnk2 Alternative Splicing Modulates the p38-MAPK Pathway and Impacts Ras-Induced Transformation

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Clinical and biological implications of driver mutations in myelodysplastic syndromes

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Targeting IRAK1 as a Therapeutic Approach for Myelodysplastic Syndrome

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Chronic Immune Stimulation Might Act As a Trigger for the Development of Acute Myeloid Leukemia or Myelodysplastic Syndromes

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Frequent pathway mutations of splicing machinery in myelodysplasia

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Recurrent mutations in the U2AF1 splicing factor in myelodysplastic syndromes

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A high-throughput screening strategy identifies cardiotonic steroids as alternative splicing modulators

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