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| Content Provider | PubMed Central |
|---|---|
| Author | Caraveo, Gabriela Auluck, Pavan K. Whitesell, Luke Chung, Chee Yeun Baru, Valeriya Mosharov, Eugene V. Yan, Xiaohui Manu, Ben-johny Martin, Soste Paola, Picotti Kim, Hanna Caldwell, Kim A. Caldwell, Guy A. Sulzer, David Yue, David T. Lindquist, Susan |
| Abstract | Ca2+ homeostasis is indispensable for the well being of all living organisms. Ca2+ homeostasis is disrupted by α-synuclein (α-syn), whose misfolding plays a major role in neurodegenerative diseases termed synucleinopathies, such as Parkinson disease. We report that α-syn can induce sustained and highly elevated levels of cytoplasmic Ca2+, thereby activating a calcineurin (CN) cascade that results in toxicity. CN is a highly conserved Ca2+–calmodulin (CaM)-dependent phosphatase critical for sensing Ca2+ concentrations and transducing that information into cellular responses. Limiting, but not eliminating, the availability of CaM, CN and/or CN substrates directly with genetic or pharmacological tools shifts the α-syn–induced CN cascade to a protective mode. This has mechanistic implications for CN's activity and provides a therapeutic venue for the treatment of synucleinopathies. |
| Related Links | http://dx.doi.org/10.1073/pnas.1413201111 |
| Starting Page | 3544 |
| File Format | |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 34 |
| Volume Number | 111 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2014-08-26 |
| Access Restriction | Open |
| Rights Holder | National Academy of Sciences |
| Subject Keyword | General Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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