A Huntingtin-based peptide inhibitor of caspase-6 provides protection from mutant Huntingtin-induced motor and behavioral deficits
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Title
A Huntingtin-based peptide inhibitor of caspase-6 provides protection from mutant Huntingtin-induced motor and behavioral deficits
Authors
Keywords
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Journal
HUMAN MOLECULAR GENETICS
Volume 24, Issue 9, Pages 2604-2614
Publisher
Oxford University Press (OUP)
Online
2015-01-24
DOI
10.1093/hmg/ddv023
References
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Note: Only part of the references are listed.- p53 increases caspase-6 expression and activation in muscle tissue expressing mutant huntingtin
- (2013) Dagmar E. Ehrnhoefer et al. HUMAN MOLECULAR GENETICS
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- (2012) Valeria Uribe et al. HUMAN MOLECULAR GENETICS
- Marked differences in neurochemistry and aggregates despite similar behavioural and neuropathological features of Huntington disease in the full-length BACHD and YAC128 mice
- (2012) M. A. Pouladi et al. HUMAN MOLECULAR GENETICS
- Caspase-6 Activity in a BACHD Mouse Modulates Steady-State Levels of Mutant Huntingtin Protein But Is Not Necessary for Production of a 586 Amino Acid Proteolytic Fragment
- (2012) J. Gafni et al. JOURNAL OF NEUROSCIENCE
- Mutant Huntingtin Causes Metabolic Imbalance by Disruption of Hypothalamic Neurocircuits
- (2011) Sofia Hult et al. Cell Metabolism
- Transgenic mice expressing caspase-6-derived N-terminal fragments of mutant huntingtin develop neurologic abnormalities with predominant cytoplasmic inclusion pathology composed largely of a smaller proteolytic derivative
- (2011) Andrew T.N. Tebbenkamp et al. HUMAN MOLECULAR GENETICS
- Mice lacking caspase-2 are protected from behavioral changes, but not pathology, in the YAC128 model of Huntington disease
- (2011) Jeffrey B Carroll et al. Molecular Neurodegeneration
- A Quantitative Method for the Specific Assessment of Caspase-6 Activity in Cell Culture
- (2011) Dagmar E. Ehrnhoefer et al. PLoS One
- Nanoparticles enhance brain delivery of blood-brain barrier-impermeable probes for in vivo optical and magnetic resonance imaging
- (2011) R. M. Koffie et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Identification and Evaluation of Small Molecule Pan-Caspase Inhibitors in Huntington's Disease Models
- (2010) Melissa J. Leyva et al. CHEMISTRY & BIOLOGY
- Cleavage at the 586 Amino Acid Caspase-6 Site in Mutant huntingtin Influences Caspase-6 Activation In Vivo
- (2010) R. K. Graham et al. JOURNAL OF NEUROSCIENCE
- Huntington's disease: from molecular pathogenesis to clinical treatment
- (2010) Christopher A Ross et al. LANCET NEUROLOGY
- Prevention of depressive behaviour in the YAC128 mouse model of Huntington disease by mutation at residue 586 of huntingtin
- (2009) M. A. Pouladi et al. BRAIN
- APP binds DR6 to trigger axon pruning and neuron death via distinct caspases
- (2009) Anatoly Nikolaev et al. NATURE
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- Activated caspase-6 and caspase-6-cleaved fragments of huntingtin specifically colocalize in the nucleus
- (2008) Simon C. Warby et al. HUMAN MOLECULAR GENETICS
- Full-Length Human Mutant Huntingtin with a Stable Polyglutamine Repeat Can Elicit Progressive and Selective Neuropathogenesis in BACHD Mice
- (2008) M. Gray et al. JOURNAL OF NEUROSCIENCE
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