PARK2 loss promotes cancer progression via redox-mediated inactivation of PTEN

Cancer and Parkinson disease (PD) derive from distinct alterations in cellular processes, yet there are pathogenic mutations that are unequivocally linked to both diseases. Here we expand on our recent findings that loss of parkin RBR E3 ubiquitin protein ligase (PRKN, best known as PARK2)—which is...

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Detalles Bibliográficos
Autores principales: Gupta, Amit, Anjomani-Virmouni, Sara, Koundouros, Nikos, Poulogiannis, George
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2017
Materias:
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706935/
https://www.ncbi.nlm.nih.gov/pubmed/29209642
http://dx.doi.org/10.1080/23723556.2017.1329692
Descripción
Sumario:Cancer and Parkinson disease (PD) derive from distinct alterations in cellular processes, yet there are pathogenic mutations that are unequivocally linked to both diseases. Here we expand on our recent findings that loss of parkin RBR E3 ubiquitin protein ligase (PRKN, best known as PARK2)—which is genetically linked to PD—promotes cancer progression via redox-mediated inactivation of phosphatase and tensin homolog (PTEN) by S-nitrosylation.

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