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Redox regulatory and anti-apoptotic functions of thioredoxin depend on S-nitrosylation at cysteine 69
These deficits, even when localized to higher frequencies, can induce compensatory plasticity within central auditory circuits extending beyond the original site of damage, producing percepts at dissociated frequencies 7,10,11
Furthermore, the in vitro results proposed that aberrant activation of both signalling pathways might support progression of DIE lesions by enhancing the survival in a fibrotic environment [65]
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