Abstract
Microtubule-associated protein tau in a hyperphosphorylated state is the major component of the filamentous lesions that define a number of neurodegenerative diseases commonly referred to as tauopathies. Hyperphosphorylation of tau at most sites appears to precede filament assembly. Many of the hyperphosphorylated sites are serine/threonine-proline sequences. Here we show that c-Jun N-terminal kinases JNK1, JNK2 and JNK3 phosphorylate tau at many serine/threonine-prolines, as assessed by the generation of the epitopes of phosphorylation-dependent anti-tau antibodies. Of the three protein kinases, JNK2 phosphorylated the most sites in tau, followed by JNK3 and JNK1. Phosphorylation by JNK isoforms resulted in a greatly reduced ability of tau to promote microtubule assembly. These findings extend the number of candidate protein kinases for the hyperphosphorylation of tau in Alzheimer's disease and other neurodegenerative disorders.
| Original language | English |
|---|---|
| Pages (from-to) | 352-358 |
| Number of pages | 7 |
| Journal | Journal of Neurochemistry |
| Volume | 90 |
| Issue number | 2 |
| DOIs | |
| State | Published - Jul 2004 |
| Externally published | Yes |
Keywords
- Stress-activated protein kinase
- Tau protein
- Tauopathy
- c-Jun N-terminal kinase