期刊
DEVELOPMENTAL CELL
卷 2, 期 6, 页码 831-837出版社
CELL PRESS
DOI: 10.1016/S1534-5807(02)00188-0
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资金
- NICHD NIH HHS [HD18655, P01 HD24926] Funding Source: Medline
- NINDS NIH HHS [R01 NS39074] Funding Source: Medline
In the search for neuroprotective factors in Huntington's disease, we found that insulin growth factor 1 via activation of the serine/threonine kinase Akt/PKB is able to inhibit neuronal death specifically induced by mutant huntingtin containing an expanded polyglutamine stretch. The IGF-1/Akt pathway has a dual effect on huntingtin-induced toxicity, since activation of this pathway also results in a decrease in the formation of intranuclear inclusions of mutant huntingtin. We demonstrate that huntingtin is a substrate of Akt and that phosphorylation of huntingtin by Akt is crucial to mediate the neuroprotective effects of IGF-1. Finally, we show that Akt is altered in Huntington's disease patients. Taken together, these results support a potential role of the Akt pathway in Huntington's disease.
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