Youzhong Wan

Abstract Nuclear actin filament is required for efficient repair of DNA double-strand breaks. While cancer-associated SF3B1 mutation leads to impaired DNA repair, the underlying mechanism remains elusive. Here, we found that SF3B1 mutation led to defective nuclear actin network during DNA repair. Mechanistically, SF3B1 mutation increased the expression of circATP9B, which interacted with and facilitated the degradation of MYH9.

Abstract Recent studies have identified glycosylated RNAs (glycoRNAs) as a novel class of biomolecules potentially involved in cancers and immunological diseases. However, their presence and functional roles in glioma remain unexplored. GlycoRNAs were extracted from glioma cells and detected using Ac4ManNAz labeling and Northern blot. Small RNA deep sequencing and qRT-PCR were employed to determine RNA types and content.