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Interactions with Sm proteins can provide a way in which regulatory factors can modulate alternative splice site choices.

Genetic analyses and biochemical studies show that JMJD6 promotes MYC-mediated transformation and is required for neuroblastoma growth by complexing with pre-mRNA splicing factors.

The distinct protein-RNA interactomes of HIV-1 RNA splice forms are revealed using a powerful multiplex strategy for RNA capture and mass spectrometric analysis.

A dysregulated circular RNA in bladder cancer controls oncogenic pathways by tethering specific RNA-binding proteins, which in turn inhibits their normal functions.

SF3B1 mutation in myelodysplastic syndromes and acute myeloid leukemia lead to oncogenic long isoforms of IRAK4 that are therapeutically targetable.

A small RNA molecule called miR-124 controls pheromone production and sexual behaviour in Drosophila by regulating sex-specific gene expression in males.

A single missense mutation in an RNA recognition motif within a nucleolar protein disrupts ribosome assembly and contributes to human pathology.

The complete architecture of human spliceosomal U1 snRNP and its interaction with the 5′ splice site of pre-mRNA are described in atomic detail.

Viewing the dynamic interactions of individual spliceosomal subcomplexes with single pre-messenger RNA molecules reveals how nearby flanking splice sites accelerate pre-spliceosome assembly and the splicing of multi-intron pre-mRNAs.

SF3B1-K700E, a gene mutaiton found recurrently mutated in pancreatic cancer, increases malignancy in an autochthonous mouse model of pancreatic cancer and induces resistance against TGF-β-induced apoptosis in vitro by missplicing of MAP3K7.