The IGF-1/Akt Pathway Is Neuroprotective in Huntington's Disease and Involves Huntingtin Phosphorylation by Akt-Reference-Cited by-同舟云学术

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The IGF-1/Akt Pathway Is Neuroprotective in Huntington's Disease and Involves Huntingtin Phosphorylation by Akt

Published:2002-06 Issue:6 Volume:2 Page:831-837
ISSN:1534-5807
Container-title:Developmental Cell
language:en
Short-container-title:Developmental Cell

Author:

Humbert Sandrine,Bryson Elzbieta A.,Cordelières Fabrice P.,Connors Nathan C.,Datta Sandeep R.,Finkbeiner Steven,Greenberg Michael E.,Saudou Frédéric

Publisher

Elsevier BV

Subject

Developmental Biology,Cell Biology,General Biochemistry, Genetics and Molecular Biology,Molecular Biology

Reference33 articles.

1. Molecular basis for the substrate specificity of protein kinase B; comparison with MAPKAP kinase-1 and p70 S6 kinase;Alessi;FEBS Lett.,1996

2. The IGF-I amino-terminal tripeptide glycine-proline-glutamate (GPE) is neuroprotective to striatum in the quinolinic acid lesion animal model of Huntington's disease;Alexi;Exp. Neurol.,1999

3. Creatine increases survival and delays motor symptoms in a transgenic animal model of Huntington's disease;Andreassen;Neurobiol. Dis.,2001

4. p53 inhibits α 6 β 4 integrin survival signaling by promoting the caspase 3-dependent cleavage of AKT/PKB;Bachelder;J. Cell Biol.,1999

5. Replicating Huntington's disease phenotype in experimental animals;Brouillet;Prog. Neurobiol.,1999

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