PARK2 loss promotes cancer progression via redox-mediated inactivation of PTEN.
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Embargo End Date
ICR Authors
Authors
Gupta, A
Anjomani-Virmouni, S
Koundouros, N
Poulogiannis, G
Anjomani-Virmouni, S
Koundouros, N
Poulogiannis, G
Document Type
Journal Article
Date
2017-01-01
Date Accepted
2017-05-09
Abstract
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.
Citation
Molecular & cellular oncology, 2017, 4 (6), pp. e1329692 - ?
Source Title
Publisher
TAYLOR & FRANCIS INC
ISSN
2372-3556
eISSN
2372-3556
Collections
Research Team
Signalling & Cancer Metabolism