Partial copy loss of spliceosome genes are common non-driver gene dependencies in cancer.

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.

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

Hinokiflavone is identified as a splicing modulator that blocks progression from spliceosome complex A to complex B and inhibits SUMO protease SENP1, causing hyper-SUMOylation affecting 6 U2 snRNP proteins.

The loss of genes that encode RNA splicing factors weakens cancer cells in a way that could be exploited by new approaches to treatment.

Alternative splicing and the endoplasmic reticulum (ER)-associated protein degradation (ERAD) system represent essential, fat depot-specific components of the adipogenesis that are altered in preadipocytes from obese individuals with metabolic disease.

Inhibiting PRMT1 enzymatic activity promotes megakaryocyte terminal differentiation via RBM15-mediated RNA metabolism, which is dysregulated in hematological malignancies.

A gene-centric functional screen uncovers biological mechanisms underlying genome-wide association study signals for human red blood cell traits.

A general framework captures the evolutionary routes leading to the formation and progression of tumors.