Publication List English

2019/10/15
C3orf70 Is Involved in Neural and Neurobehavioral Development

2019/09/22
Generation of a Triple-Transgenic Zebrafish Line for Assessment of Developmental Neurotoxicity during Neuronal Differentiation

2019/07/17
Aging-associated microstructural deterioration of vertebra in zebrafish

2019/03/18
Zebrafish yolk sac microinjection of thalidomide for assessment of developmental toxicology

2019/02/18
Toxicological Evaluation of SiO2 Nanoparticles by Zebrafish Embryo Toxicity Test

tS-nitrosylation regulates mitochondrial quality control via activation of parkin.

                     
2013/07/15

Parkin, a ubiquitin E3 ligase of the ring between ring fingers family, has been implicated in mitochondrial quality control. A series of recent reports have suggested that the recruitment of parkin is regulated by phosphorylation. However, the molecular mechanism that activates parkin to induce mitochondrial degradation is not well understood. Here, and in contrast to previous reports that S-nitrosylation of parkin is exclusively inhibitory, we identify a previously unrecognized site of S-nitrosylation in parkin (Cys323) that induces mitochondrial degradation. We demonstrate that endogenous S-nitrosylation of parkin is in fact responsible for activation of its E3 ligase activity to induce aggregation and degradation. We further demonstrate that mitochondrial uncoupling agents result in denitrosylation of parkin, and that prevention of denitrosylation restores mitochondrial degradation. Our data indicates that NO both positive effects on mitochondrial quality control, and suggest that targeted S-nitrosylation could provide a novel therapeutic strategy against Parkinson's disease.

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Scientific Reports

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S-nitrosylation regulates mitochondrial quality control via activation of parkin.