Abstract:
:Impaired functioning of the proteasome pathway is one of the molecular mechanism underlying neurodegenerative changes in Alzheimer's disease. In this study, we report that dysfunction of the proteasome pathway in astroglial cells leads to decreased survival and dysregulation of chemokines by differential regulation of the nuclear factor kappa B and c-jun N-terminal kinase (JNK) pathways. We further demonstrated that proteasome inhibition augmented interleukin-1 beta- and tumor necrosis factor-alpha-induced activation of the IkappaBalpha kinase and MKK4/JNK/c-Jun pathway along with TAK1 activation. These results suggest that impaired function of the proteasome pathway may potentiate the immuno-pathologic role of secondarily activated astrocytes in the brain.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Choi K,Lee J,Choi Cdoi
10.1016/j.febslet.2007.08.065subject
Has Abstractpub_date
2007-10-02 00:00:00pages
4691-6issue
24eissn
0014-5793issn
1873-3468pii
S0014-5793(07)00947-7journal_volume
581pub_type
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