HNRNPM regulates exon inclusion and circularization events on transcripts of key homeostatic genes promoting cancer growth.

A single human cell makes 10-100 transcriptional errors per second; these errors affect splicing and may influence the evolution of coding sequences.

Interconnected RNA processing mechanisms ensure the fidelity of non-conventional mRNA splicing during the unfolded protein response.

Analysis of neo-splicetope-specific T cell responses strongly questions the idea that in vitro proteasome-catalyzed peptide splicing reaction simulates the in vivo situation with the same high fidelity as the in vitro generation of non-spliced epitopes.

Post-translational modification of histone H3K36 is not required to suppress cryptic transcription initiation or to include alternative exons in Drosophila; instead it promotes expression of active genes by stimulating polyadenylation.

During evolutionary progression of Alu-exons, repressive U-tracts buffer sudden gains in 3' splice site strength and prevent inclusion of cryptic exons.

High throughput sequencing of Arabidopsis mutants lacking the U6 snRNA methyltransferase FIONA1/METTL16 uncovers the role of U6 methylation in splicing signal preferences.

Genetic variants that modulate transcriptomic response to doxorubicin in human iPSC-derived cardiomyocytes are predictive of cardiac damage and in vivo sensitivity to anthracycline cardiotoxicity.

Ire1's RNase specificity and its cleavage sites coordination shape the evolutionary specialization of the unfolded protein response.

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