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			PubMed Journals: Dev Cell

  Source:		PMID: 12062094


    		Dev Cell. 2002 Jun;2(6):831-7.
     
			The IGF-1/Akt pathway is neuroprotective
			in Huntington's disease and involves Huntingtin
			phosphorylation by Akt.

			Humbert S(1), Bryson EA, Cordelières FP,
			Connors NC, Datta SR, Finkbeiner S, Greenberg
			ME, Saudou F.

			Author Information
			(1) UMR 146 CNRS/Institut Curie, Centre Universitaire,
			91405 Orsay Cedex, France.

			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.

			PMID: 12062094 [Indexed for MEDLINE]

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