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Molecular Cell, ISSN 1097-2765, 07/2011, Volume 43, Issue 1, pp. 19 - 32
Journal Article
Acta Neuropathologica, ISSN 0001-6322, 11/2014, Volume 128, Issue 5, pp. 705 - 722
There is still no treatment for polyglutamine disorders, but clearance of mutant proteins might represent a potential therapeutic strategy. Autophagy, the... 
Pathology | Neurosciences | Medicine & Public Health | SCA7 knock-in mouse | Lysosome | Transcriptome | Ataxia | Autophagy | Patients | NEURODEGENERATIVE DISEASE | POLYGLUTAMINE | BECLIN 1 | ALZHEIMERS-DISEASE | AGGREGATE-PRONE PROTEINS | PATHOLOGY | NEUROSCIENCES | CLINICAL NEUROLOGY | MUTANT ATAXIN-7 | SPINOCEREBELLAR ATAXIAS | MACHADO-JOSEPH-DISEASE | GENETIC MOUSE MODELS | HUNTINGTONS-DISEASE | Leukocytes, Mononuclear - metabolism | TOR Serine-Threonine Kinases - metabolism | Humans | Ataxin-7 | Male | Autophagy - physiology | Trinucleotide Repeats - genetics | Case-Control Studies | Small Ubiquitin-Related Modifier Proteins - genetics | Lysosomes - metabolism | TOR Serine-Threonine Kinases - genetics | Apoptosis Regulatory Proteins - genetics | Female | Lysosomes - pathology | Membrane Proteins - metabolism | Microfilament Proteins - metabolism | Microfilament Proteins - genetics | Nerve Tissue Proteins - ultrastructure | Spinocerebellar Ataxias - genetics | Beclin-1 | Gene Expression Regulation - genetics | Membrane Proteins - genetics | Small Ubiquitin-Related Modifier Proteins - metabolism | Mice, Transgenic | Signal Transduction - genetics | Spinocerebellar Ataxias - pathology | Nerve Tissue Proteins - genetics | Apoptosis Regulatory Proteins - metabolism | Lysosomes - ultrastructure | Nerve Tissue Proteins - metabolism | Carrier Proteins - genetics | Leukocytes, Mononuclear - pathology | Animals | Carrier Proteins - metabolism | Brain - pathology | Mice | Cell Line, Transformed | Ubiquitin | Brain | Nervous system diseases | Health aspects | Analysis | Index Medicus
Journal Article
PLoS Genetics, ISSN 1553-7390, 02/2010, Volume 6, Issue 2, pp. e1000838 - e1000838
Expansion of a stretch of polyglutamine in huntingtin (htt), the protein product of the IT15 gene, causes Huntington's disease (HD). Previous investigations... 
LIFE-SPAN | OXIDATIVE STRESS | GENE HOMOLOG | MUTANT HUNTINGTIN | IN-VIVO | DISEASE | GENETICS & HEREDITY | AGGREGATE-PRONE PROTEINS | TOXICITY | DIETARY RESTRICTION | CELL-DEATH | Neurons - pathology | Neuropil - pathology | Microtubule-Associated Proteins - metabolism | Humans | Huntington Disease - pathology | Peptides - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Motor Activity | Autophagy | Behavior, Animal | Nerve Tissue Proteins - chemistry | Protein Structure, Quaternary | Neostriatum - metabolism | Nuclear Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Cell Line | Neostriatum - pathology | Signal Transduction | Phagosomes - metabolism | Nuclear Proteins - metabolism | Longevity | Nuclear Proteins - chemistry | Huntington Disease - metabolism | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Huntingtin Protein | Neuropil - metabolism | Animals | Autophagy-Related Protein 5 | Mice | TOR Serine-Threonine Kinases | Lipofuscin - metabolism | Sequence Deletion - genetics | Autophagy (Cytology) | Huntington's chorea | Neurons | Development and progression | Genetic aspects | Health aspects | Glutamine | Index Medicus | Proteins | Huntingtons disease | Disease | Pathogenesis | Rodents | Behavior | Evacuations & rescues
Journal Article
Journal Article
Journal of Cell Biology, ISSN 0021-9525, 09/2009, Volume 186, Issue 5, pp. 703 - 711
Target of rapamycin (TOR) signaling is a regulator of cell growth. TOR activity can also enhance cell death, and the TOR inhibitor rapamycin protects cells... 
RETINAL DEGENERATION | SURVIVAL | APOPTOSIS | POLYGLUTAMINE | TUBEROUS SCLEROSIS COMPLEX | GROWTH | AGGREGATE-PRONE PROTEINS | TOXICITY | SUPPRESSION | NF-KAPPA-B | CELL BIOLOGY | Drosophila melanogaster - physiology | Ras Homolog Enriched in Brain Protein | Autophagy - physiology | Phosphatidylinositol 3-Kinases - metabolism | Drosophila Proteins - metabolism | Photoreceptor Cells, Invertebrate - ultrastructure | Autophagy-Related Protein-1 Homolog | Neuropeptides - genetics | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | Neurodegenerative Diseases - pathology | Animals, Genetically Modified | Drosophila melanogaster - cytology | Protein-Serine-Threonine Kinases - genetics | Neuropeptides - metabolism | Monomeric GTP-Binding Proteins - genetics | Phosphatidylinositol 3-Kinases - genetics | Autophagy-Related Protein 7 | Animals | Neurodegenerative Diseases - physiopathology | Cell Death - physiology | Monomeric GTP-Binding Proteins - metabolism | Protein Kinases | Signal Transduction - physiology | TOR Serine-Threonine Kinases | Drosophila Proteins - genetics | Photoreceptor Cells, Invertebrate - metabolism | Cellular proteins | Physiological aspects | Nervous system | Cellular signal transduction | Degeneration | Genetic aspects | Research | Risk factors | Apoptosis | Cell growth | Insects | Cells | Neurological disorders | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2016, Volume 113, Issue 50, pp. 14342 - 14347
Journal Article
Experimental Cell Research, ISSN 0014-4827, 02/2013, Volume 319, Issue 3, pp. 122 - 133
Autophagy, or autophagocytosis, is a selective intracellular degradative process involving the cell's own lysosomal apparatus. An essential component in cell... 
Akt1 | UVRAG | LC3B | Autophagy | SUPPRESSOR | APOPTOSIS | AGGREGATE-PRONE PROTEINS | MACROAUTOPHAGY | MAMMALIAN-CELLS | CELL BIOLOGY | BECLIN-1 | GENE | ONCOLOGY | PATHWAY | TUMOR-CELL SURVIVAL | TUMORIGENESIS | Tumor Suppressor Proteins - antagonists & inhibitors | Autophagy - radiation effects | Humans | Autophagy - physiology | Down-Regulation - radiation effects | Autophagy - drug effects | Transfection | Ultraviolet Rays | Neoplasms - genetics | Protein Processing, Post-Translational - drug effects | Tumor Suppressor Proteins - genetics | Autophagy - genetics | Gene Expression Regulation, Neoplastic - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Tumor Suppressor Proteins - metabolism | RNA, Small Interfering - pharmacology | Cells, Cultured | Proto-Oncogene Proteins c-akt - physiology | Down-Regulation - drug effects | Down-Regulation - genetics | Cell Proliferation - drug effects | Gene Expression Regulation, Neoplastic - radiation effects | Protein Kinase Inhibitors - pharmacology | Neoplasms - pathology | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Cell Proliferation - radiation effects | Protein kinases | Genes | Proteins | Mutation | Cellular biology | Kinases | Gene expression | Cancer | Index Medicus | HOMEOSTASIS | MAMMARY GLANDS | NEOPLASMS | PHOSPHORYLATION | TRANSCRIPTION | 60 APPLIED LIFE SCIENCES | IRRADIATION | SERINE | GENES | BIOLOGICAL REPAIR | MUTATIONS | PROTEINS | THREONINE
Journal Article
The Cerebellum, ISSN 1473-4222, 12/2014, Volume 13, Issue 6, pp. 713 - 727
The accumulation of misfolded proteins in neurons, leading to the formation of cytoplasmic and nuclear aggregates, is a common theme in age-related... 
Neurology | Therapy | Triplet repeats | Neurosciences | Biomedicine | Polyglutamine | Spinocerebellar ataxia | Neurobiology | Lithium | Autophagy | NEUROTROPHIC FACTOR | ALZHEIMERS-DISEASE | SPINOCEREBELLAR ATAXIA TYPE-3 | GLYCOGEN-SYNTHASE KINASE-3 | AGGREGATE-PRONE PROTEINS | AMYOTROPHIC-LATERAL-SCLEROSIS | BIPOLAR DISORDER | NEUROSCIENCES | NEURODEGENERATIVE DISEASES | POLYGLUTAMINE-EXPANDED ATAXIN-3 | INTRANUCLEAR INCLUSIONS | Motor Activity - physiology | Ataxin-3 | Microtubule-Associated Proteins - metabolism | Humans | Motor Activity - drug effects | Male | Autophagy - physiology | Postural Balance - drug effects | Weight Loss - drug effects | Tremor - physiopathology | Autophagy - drug effects | Exploratory Behavior - physiology | Lithium Chloride - pharmacology | Exploratory Behavior - drug effects | Neuromuscular Agents - pharmacology | Tremor - drug therapy | Nuclear Proteins - genetics | Repressor Proteins - metabolism | Disease Models, Animal | Beclin-1 | Brain - physiopathology | Repressor Proteins - genetics | Mice, Transgenic | Nuclear Proteins - metabolism | Treatment Outcome | Nerve Tissue Proteins - genetics | Disease Progression | Apoptosis Regulatory Proteins - metabolism | Brain - drug effects | Machado-Joseph Disease - drug therapy | Nerve Tissue Proteins - metabolism | Autophagy-Related Protein 7 | Animals | Weight Loss - physiology | Machado-Joseph Disease - physiopathology | Postural Balance - physiology | Cellular proteins | Nervous system diseases | Tremor | Cerebellar ataxia | Analysis | Genetic engineering | Lithium compounds | Index Medicus
Journal Article