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Furthermore, G4C2 repeat RNA and its translation product, dipeptide repeat protein, have been reported to cause neurodegeneration by increasing DNA double-strand breaks, leading to a deficiency of ataxia telangiectasia mutated (ATM), which repairs DNA damage [67]

This chemistry sits directly at the genome interface: transient, targeted oxidation events modulate transcription factors and chromatin modifiers (e.g., redox-sensitive cysteines in DNA-binding proteins or histone-modifying enzymes), enabling physiological control of gene expression (Juan et al

Receptors involved in the extrinsic pathway form complexes with caspase 8, triggering apoptosis though the terminal pathway, which is also associated with the intrinsic apoptotic pathway (Medema et al., 1997