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Nature, ISSN 0028-0836, 05/2017, Volume 545, Issue 7652, pp. 108 - 111
Nine neurodegenerative diseases are caused by expanded polyglutamine (polyQ) tracts in different proteins, such as huntingtin in Huntington's disease and... 
PATHOGENESIS | CELLS | PROTEIN | MULTIDISCIPLINARY SCIENCES | MACHADO-JOSEPH-DISEASE | MUTANT HUNTINGTIN | ATAXIN-3 | INTRANUCLEAR INCLUSIONS | LC3 | MOUSE MODELS | AGGREGATION | Humans | Ubiquitin - metabolism | Male | Neurons - cytology | Autophagy | Brain - metabolism | Peptides - metabolism | Protein Domains | Ataxin-3 - chemistry | Female | Food Deprivation | Neurons - metabolism | Protein Stability | Ataxin-3 - metabolism | Disease Models, Animal | Binding, Competitive | Cell Line | Ataxin-3 - deficiency | Huntingtin Protein - metabolism | Mice, Inbred C57BL | Phagosomes - metabolism | Cells, Cultured | Mutant Proteins - genetics | Exons - genetics | Mutant Proteins - metabolism | Huntington Disease - metabolism | Huntingtin Protein - chemistry | Animals | Mutant Proteins - chemistry | Brain - pathology | Huntington Disease - genetics | Protein Binding | Mice | Huntingtin Protein - genetics | Mutation | Proteasome Endopeptidase Complex - metabolism | Beclin-1 - metabolism | Ataxin-3 - genetics | Physiological aspects | Autophagy (Cytology) | Neural circuitry | Observations | Huntingtons disease | Competition | Biotechnology | Huntingtin | Toxicity | Pathogenesis | Impairment | Biosynthesis | Kinases | Experiments | Degradation | Proteins | Scholarships & fellowships | Ataxin | Rodents | Spinocerebellar ataxia | Ataxia | Biocompatibility | Trinucleotide repeat diseases | Medical research | Starvation | Neurodegenerative diseases | Polyglutamine diseases | Huntington's disease | Neurological diseases | Machado-Joseph disease | Cell lines | Scientific imaging | Mass spectrometry | Phagocytosis | Index Medicus
Journal Article
Brain, ISSN 0006-8950, 2011, Volume 134, Issue 5, pp. 1400 - 1415
Journal Article
Brain, ISSN 0006-8950, 2013, Volume 136, Issue 7, pp. 2173 - 2188
Machado-Joseph disease or spinocerebellar ataxia type 3, the most common dominantly-inherited spinocerebellar ataxia, results from translation of the... 
ataxin-3 | autophagy | beclin-1, Machado-Joseph disease, spinocerebellar ataxia type 3 | AUTOPHAGY GENE | PROTEIN | spinocerebellar ataxia type 3 | PHOSPHATIDYLINOSITOL 3-KINASE | SPINOCEREBELLAR ATAXIA TYPE-3 | MUTANT HUNTINGTIN | NEURODEGENERATION | NEUROSCIENCES | beclin-1 | CLINICAL NEUROLOGY | Machado-Joseph disease | ACID RAT MODEL | ACCUMULATION | HUNTINGTONS-DISEASE | TRANSGENIC MICE | Age Factors | Ataxin-3 | Machado-Joseph Disease - metabolism | Humans | Peptides - genetics | Motor Activity - drug effects | Sensation Disorders - etiology | Male | Green Fluorescent Proteins - genetics | Membrane Proteins - therapeutic use | Psychomotor Performance - physiology | Machado-Joseph Disease - complications | Transfection | Nerve Degeneration - prevention & control | Apoptosis Regulatory Proteins - genetics | Female | Membrane Proteins - metabolism | Autophagy - genetics | Nuclear Proteins - genetics | Repressor Proteins - metabolism | Disease Models, Animal | Animals, Newborn | Beclin-1 | Gene Expression Regulation - genetics | Membrane Proteins - genetics | Mice, Inbred C57BL | Cells, Cultured | Repressor Proteins - genetics | Sensation Disorders - metabolism | Mice, Transgenic | Nuclear Proteins - metabolism | Postural Balance - genetics | Dopamine and cAMP-Regulated Phosphoprotein 32 - metabolism | Nerve Tissue Proteins - genetics | Apoptosis Regulatory Proteins - metabolism | Machado-Joseph Disease - drug therapy | Nerve Tissue Proteins - metabolism | Motor Activity - genetics | Animals | Analysis of Variance | Cerebellum - cytology | Mice | Sensation Disorders - genetics | Apoptosis Regulatory Proteins - therapeutic use | Nerve Degeneration - etiology | Machado-Joseph Disease - genetics | Animal models
Journal Article
PLoS ONE, ISSN 1932-6203, 01/2013, Volume 8, Issue 1, p. e52396
Machado-Joseph disease (MJD) or spinocerebellar ataxia type 3 (SCA3) is an autosomal dominantly-inherited neurodegenerative disorder caused by the... 
NUCLEAR-LOCALIZATION | EXPANDED POLYGLUTAMINE | CEREBELLAR DYSFUNCTION | SPINOCEREBELLAR ATAXIA | CAG REPEATS | MULTIDISCIPLINARY SCIENCES | POLYGLUTAMINE-INDUCED NEURODEGENERATION | MOUSE MODEL | INTRANUCLEAR INCLUSIONS | HUNTINGTONS-DISEASE | RAT MODEL | Locomotion - genetics | Ataxin-3 | Humans | Nerve Tissue Proteins - deficiency | Machado-Joseph Disease - complications | Repressor Proteins - deficiency | Nuclear Proteins - deficiency | Anxiety - complications | Nuclear Proteins - genetics | Machado-Joseph Disease - pathology | Exploratory Behavior | Mice, Inbred C57BL | Gene Silencing | Repressor Proteins - genetics | Mice, Transgenic | Nerve Tissue Proteins - genetics | Intranuclear Inclusion Bodies - pathology | Motor Activity - genetics | Animals | Alleles | Machado-Joseph Disease - physiopathology | Mice | Mutation | Purkinje Cells - pathology | Machado-Joseph Disease - genetics | Nervous system diseases | Genetic aspects | Genetic engineering | Viral genetics | Cerebellar ataxia | Analysis | Cerebellum | Huntingtons disease | Brain | Neurosciences | Calbindin | Gait | Neuropathology | Pathogenesis | Biology | Proteins | Ataxin | Neurodegeneration | Transgenic animals | Rodents | Inclusion bodies | Ataxia | Trinucleotide repeat diseases | Quantitative analysis | Polyglutamine | Neurodegenerative diseases | RNA-mediated interference | Exploratory behavior | Abnormalities | Medical treatment | Transgenic mice | Trinucleotide repeats | Ribonucleic acid--RNA | Activity patterns | Thickness | Gene silencing | Machado-Joseph disease | Brain research | Pharmacy | DARPP-32 protein | Immunoreactivity | RNA | Ribonucleic acid
Journal Article
Annual Review of Neuroscience, ISSN 0147-006X, 2007, Volume 30, Issue 1, pp. 575 - 621
The discovery that expansion of unstable repeats can cause a variety of neurological disorders has changed the landscape of disease-oriented research for... 
Unstable repeats | Polyglutamine | Ataxin | Frataxin | Myotonic dystrophy | Huntington disease | Ataxia | Fragile X syndrome | Mental retardation | Spinal bulbar muscular atrophy | SPINOCEREBELLAR ATAXIA TYPE-1 | UBIQUITIN-PROTEASOME SYSTEM | unstable repeats | fragile X syndrome | polyglutamine | NEUROSCIENCES | X MENTAL-RETARDATION | frataxin | myotonic dystrophy | mental retardation | HUNTINGTONS-DISEASE GENE | ataxia | spinal bulbar muscular atrophy | MACHADO-JOSEPH-DISEASE | ataxin | TRANSGENIC MOUSE MODEL | DENTATORUBRAL-PALLIDOLUYSIAN ATROPHY | DOMINANT CEREBELLAR-ATAXIA | BULBAR MUSCULAR-ATROPHY | FMR1 KNOCKOUT MICE | Fragile X Syndrome - genetics | Heredodegenerative Disorders, Nervous System - genetics | Genetic Predisposition to Disease - genetics | Cerebellar Ataxia - metabolism | Brain - physiopathology | Fragile X Syndrome - physiopathology | Humans | Peptides - genetics | Fragile X Syndrome - metabolism | Heredodegenerative Disorders, Nervous System - physiopathology | Mutation - genetics | Huntington Disease - metabolism | Brain - metabolism | Cerebellar Ataxia - physiopathology | Animals | Cerebellar Ataxia - genetics | Peptides - metabolism | Huntington Disease - genetics | Trinucleotide Repeat Expansion - genetics | Heredodegenerative Disorders, Nervous System - metabolism | Huntington Disease - physiopathology | Trinucleotide repeats | Care and treatment | Genetic aspects | Diagnosis
Journal Article
Journal Article