Regulation of Proteasome Activity in Development, Aging and Disease

JOHANNES GUTENBERG-UNIVERSITÄT MAINZ D-55099 Mainz
EINL ADUNG Z UM VORTR AG
Am Montag, den 19. Dezember 2016 um 11:00 Uhr, hält
FB 09
Chemie, Pharmazie und
Geowissenschaften
Institut
für Pharmazie und Biochemi
Abteilung Biochemie
Prof. Dr.
Claudia Koch-Brandt
Herr Prof. Hermann Steller
Rockefeller University, New York (USA)
den Vortrag
Johannes GutenbergUniversität Mainz
Johann-Joachim-Becherweg 30
55128 Mainz
Tel. +49(0)6131-39 2 38 30
Fax +49(0)6131-39 2 51 38
[email protected]
Regulation of Proteasome Activity
in Development, Aging and Disease
Institut für Biochemie der
Johannes Gutenberg-Universität Mainz, Johann J. Becher-Weg 30,
Bibliothek, Raum 01-215 ( 1OG)
gez. Prof. Dr. Claudia Koch-Brandt
www.uni-mainz.de
www.bio.chemie.uni-mainz.de
02.08.2016
Sekretariat
Tel. +49(0)6131-39 2 58 39
Fax +49(0)6131-39 2 51 38
The long-term health of cells critically relies on selective protein
degradation since damaged or aggregated proteins cause proteotoxic
stress that can impair cell function and cause cell death. Many neurodegenerative diseases, including Alzheimer’s, Parkinson’s, Huntington’s
Disease, ALS and retinitis pigmentosa, are caused by the accumulation of
protein aggregates. We recently discovered a novel mechanism that
enables cells to avoid proteotoxic stress by stimulating the assembly of
proteasomes, the multi-protein protease complex responsible for the
regulated proteolysis of intracellular proteins. Significantly, this pathway is
sensitive to diet, mitochondrial function, and oxidative stress. Furthermore,
the activity of this pathway declines with age. Finally, polymorphisms in the
central factor in this pathway, PI31, are associated factor with Alzheimer’s
Disease and mutations in Fbxo7/PARK15, a critical activator of PI31, cause
early onset Parkinson’s Disease Our findings suggest that insufficient
availability of proteasomes contributes to the aging process and chronic
neuro-degenerative diseases.

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