The IGF-1/Akt pathway is neuroprotective in Huntington's disease and involves Huntingtin phosphorylation by Akt.
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Fabrice P Cordelières | Steven Finkbeiner | Michael E Greenberg | S. R. Datta | M. Greenberg | S. Finkbeiner | S. Humbert | F. Saudou | F. Cordelières | Frédéric Saudou | Sandrine Humbert | Nathan C Connors | Elzbieta A Bryson | Sandeep R Datta | E. A. Bryson | Nathan C. Connors
[1] S. R. Datta,et al. Transcription-dependent and -independent control of neuronal survival by the PI3K–Akt signaling pathway , 2001, Current Opinion in Neurobiology.
[2] F. François,et al. Phosphorylation‐Dependent Akt Cleavage in Neural Cell In Vitro Reconstitution of Apoptosis , 1999, Journal of neurochemistry.
[3] He Li,et al. Amino-terminal fragments of mutant huntingtin show selective accumulation in striatal neurons and synaptic toxicity , 2000, Nature Genetics.
[4] S. R. Datta,et al. Akt Phosphorylation of BAD Couples Survival Signals to the Cell-Intrinsic Death Machinery , 1997, Cell.
[5] Françoise Condé,et al. Replicating Huntington's disease phenotype in experimental animals , 1999, Progress in Neurobiology.
[6] C. Widmann,et al. Caspase-dependent Cleavage of Signaling Proteins during Apoptosis , 1998, The Journal of Biological Chemistry.
[7] S. Hersch,et al. Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington disease , 2000, Nature Medicine.
[8] J. Cha,et al. Transcriptional dysregulation in Huntington’s disease , 2000, Trends in Neurosciences.
[9] T. Tsuruo,et al. Cleavage and inactivation of antiapoptotic Akt/PKB by caspases during apoptosis , 2000, Journal of cellular physiology.
[10] S. Snyder,et al. A huntingtin-associated protein enriched in brain with implications for pathology , 1995, Nature.
[11] O. Andreassen,et al. Creatine Increases Survival and Delays Motor Symptoms in a Transgenic Animal Model of Huntington's Disease , 2001, Neurobiology of Disease.
[12] Harry T Orr,et al. Ataxin-1 Nuclear Localization and Aggregation Role in Polyglutamine-Induced Disease in SCA1 Transgenic Mice , 1998, Cell.
[13] P. Gluckman,et al. 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 , 1999, Experimental Neurology.
[14] C. Ross,et al. Nuclear Targeting of Mutant Huntingtin Increases Toxicity , 1999, Molecular and Cellular Neuroscience.
[15] J. Woodgett,et al. Protein Kinase B/Akt Participates in GLUT4 Translocation by Insulin in L6 Myoblasts , 1999, Molecular and Cellular Biology.
[16] S. Humbert,et al. Neuronal Death in Huntington’s Disease: Multiple Pathways for One Issue? , 2001 .
[17] James F. Gusella,et al. Molecular genetics: Unmasking polyglutamine triggers in neurodegenerative disease , 2000, Nature Reviews Neuroscience.
[18] C. Portera-Cailliau,et al. Evidence for apoptotic cell death in Huntington disease and excitotoxic animal models , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.
[19] S. Yeh,et al. Akt suppresses androgen-induced apoptosis by phosphorylating and inhibiting androgen receptor , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[20] D. Housman,et al. Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila , 2001, Nature.
[21] S. W. Davies,et al. Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain. , 1997, Science.
[22] Steven Finkbeiner,et al. Huntingtin Acts in the Nucleus to Induce Apoptosis but Death Does Not Correlate with the Formation of Intranuclear Inclusions , 1998, Cell.
[23] X. Li,et al. Intranuclear huntingtin increases the expression of caspase-1 and induces apoptosis. , 2000, Human molecular genetics.
[24] Lisa Garrett,et al. Behavioural abnormalities and selective neuronal loss in HD transgenic mice expressing mutated full-length HD cDNA , 1998, Nature Genetics.
[25] Harry T Orr,et al. Mutation of the E6-AP Ubiquitin Ligase Reduces Nuclear Inclusion Frequency While Accelerating Polyglutamine-Induced Pathology in SCA1 Mice , 1999, Neuron.
[26] A. Hackam,et al. Huntingtin Interacting Protein 1 Induces Apoptosis via a Novel Caspase-dependent Death Effector Domain* , 2000, The Journal of Biological Chemistry.
[27] S. Doré,et al. Rediscovering good old friend IGF-I in the new millenium: possible usefulness in Alzheimer's disease and stroke. , 2000, Pharmaceutica acta Helvetiae.
[28] K. Fischbeck,et al. Androgen receptor mutation in Kennedy's disease. , 1999, Philosophical transactions of the Royal Society of London. Series B, Biological sciences.
[29] Y. Kawaoka,et al. Epidermal immunization by a needle-free powder delivery technology: Immunogenicity of influenza vaccine and protection in mice , 2000, Nature Medicine.
[30] N. Weigel,et al. Motoneuronal cell death is not correlated with aggregate formation of androgen receptors containing an elongated polyglutamine tract. , 2000, Human molecular genetics.
[31] E. Hirsch,et al. Cellular localization of the Huntington's disease protein and discrimination of the normal and mutated form , 1995, Nature Genetics.
[32] S. Soddu,et al. P53 Inhibits α6β4 Integrin Survival Signaling by Promoting the Caspase 3–Dependent Cleavage of Akt/PKB , 1999, The Journal of cell biology.
[33] Mark Turmaine,et al. Formation of Neuronal Intranuclear Inclusions Underlies the Neurological Dysfunction in Mice Transgenic for the HD Mutation , 1997, Cell.
[34] P. Cohen,et al. Molecular basis for the substrate specificity of protein kinase B; comparison with MAPKAP kinase‐1 and p70 S6 kinase , 1996, FEBS letters.