31st Annual Meeting of the Japan Neuroscience Society (Neuro 2008)
開催地
和文:
東京
英文:
Tokyo
アブストラクト
Recent researches demonstrated that dysfunction in ubiquitin-proteasome system (UPS) can cause a kind of hereditary Parkinson’s disease (PD). In order to explore the effect of proteasomal inhibition on catecholamine-producing cells, we treated PC12D cells with MG-132, an inhibitor of 26S proteasome. We found that phosphorylated tyrosine hydroxylase (TH) proteins formed insoluble aggregates in PC12D cells after proteasomal inhibition. The aggregates were colocalized with
ubiquitin. We also found that Lewy bodies of PD patients were immunoreactive with anti-TH antibody. We suggest that aggregation of phosphorylated TH may be implicated in formation of Lewy bodies in monoaminergic neurons.
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