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

By Tebbenkamp Andrew T.N.   Green Cameron   Xu Guilian   Denovan-Wright Eileen M.   Rising Aaron C.   Fromholt Susan E.   Brown Hilda H.   Swing Debbie   Mandel Ronald J.   Tessarollo Lino   Borchelt David R.  

Human Molecular Genetics, Vol. 20, Iss. 14, 2011-07 ,pp. : 2770-2782

Oxford University Press

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Intranuclear inclusions and neuritic aggregates in transgenic mice expressing a mutant N-terminal fragment of huntingtin

By Jenkins N.A.  

Human Molecular Genetics, Vol. 8, Iss. 3, 1999-03 ,pp. : 397-407

Oxford University Press

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In vivo cell-autonomous transcriptional abnormalities revealed in mice expressing mutant huntingtin in striatal but not cortical neurons

By Thomas Elizabeth A.   Coppola Giovanni   Tang Bin   Kuhn Alexandre   Kim SoongHo   Geschwind Daniel H.   Brown Timothy B.   Luthi-Carter Ruth   Ehrlich Michelle E.  

Human Molecular Genetics, Vol. 20, Iss. 6, 2011-03 ,pp. : 1049-1060

Oxford University Press

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Nuclear-targeting of mutant huntingtin fragments produces Huntington's disease-like phenotypes in transgenic mice

By Schilling Gabriele  

Human Molecular Genetics, Vol. 13, Iss. 15, 2004-08 ,pp. : 1599-1610

Oxford University Press

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Raised intracellular glucose concentrations reduce aggregation and cell death caused by mutant huntingtin exon 1 by decreasing mTOR phosphorylation and inducing autophagy

By Ravikumar B.  

Human Molecular Genetics, Vol. 12, Iss. 9, 2003-05 ,pp. : 985-994

Oxford University Press

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