ARID1A stabilizes non-homologous end joining factors at DNA breaks induced by the G4 ligand pyridostatin

Puntos clave

• ARID1A stabilizes non-homologous end joining factors at DNA breaks, enhancing repair processes.
• Key evidence includes the interaction between ARID1A and repair factors at induced DNA breaks.
• The analysis employs targeted experimental approaches to study the effects of the G4 ligand pyridostatin.
• These findings highlight the critical role of ARID1A in maintaining genomic stability, which could lead to novel therapeutic strategies.