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Redox Biol2024;75103254.September 1, 2024Journal Article

NADPH oxidase 2 activity disrupts Calmodulin/CaMKIIα complex via redox modifications of CaMKIIα-contained Cys30 and Cys289: Implications in Parkinson's disease.

Filippo Pullara1, Madison C Forsmann2, Ignacio J General3, Joseph C Ayoob4, Emily Furbee4, Sandra L Castro2, Xiaoping Hu2, J Timothy Greenamyre2, Roberto Di Maio5
1PredxBio, Inc., Pittsburgh, PA, 15202, USA. Electronic address: filippo@predxbio.com.
2Department of Neurology, University of Pittsburgh, Pittsburgh, PA, 15213, USA; Pittsburgh Institute for Neurodegenerative Diseases, Pittsburgh, PA, 15213, USA.
3School of Science and Technology, Universidad Nacional de San Martin, San Martín, 1650, Buenos Aires, Argentina.
4Department of Computational and Systems Biology, University of Pittsburgh, Pittsburgh, PA, 15213, USA.
5Department of Neurology, University of Pittsburgh, Pittsburgh, PA, 15213, USA; Pittsburgh Institute for Neurodegenerative Diseases, Pittsburgh, PA, 15213, USA. Electronic address: rod16@pitt.edu.
PubMed PMC DOI PDF

Abstract

Ca2+/calmodulin-dependent protein kinase II α (CaMKIIα) signaling in the brain plays a critical role in regulating neuronal Ca2+ homeostasis. Its dysfunctional activity is associated with various neurological and neurodegenerative disorders, including Parkinson's disease (PD). Using computational modeling analysis, we predicted that, two essential cysteine residues contained in CaMKIIα, Cys30 and…

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