A cell-surface receptor called Gpr52 is able to lower the levels of the disease-causing protein mutant huntingtin and suppress its toxicity when knocked-down, making this receptor a promising drug target in Huntington's disease.

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.

Group II introns can target mRNA, causing inhibition of gene expression, as a potential driver for evolution to the spliceosome.

B cells regulate production of neutrophils by a novel mechanism by releasing ST6Gal-1, an active sialyltransferase, that suppresses granulopoiesis.

Genome-wide profiling of R-loops at near single-nucleotide resolution reveals distinct R-loop boundaries depending on the presence and location of the first exon-intron junction.

Removal of mitochondrial introns (Saccharomyces cerevisiae) from their host genes leads to detrimental increase in their transcript levels.

Prp43 binds to the pre-mRNA and contacts predominantly U2 proteins in the budding yeast spliceosome.

Building on previous work (Nagarkar-Jaiswal et al., 2015), we report an elegant genetic strategy for endogenous tagging of MiMIC containing genes.

Hundreds of cell growth and stress response genes are controlled by a rare small RNA component of an ancient splicing machinery, providing a raison d'être for its previously unexplained evolutionary conservation.

microRNAs can serve as a surveillance system to repress nonsense mRNAs by recognizing miRNA-responsive elements in the open reading frame region downstream of the premature termination codon.