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Nature Neuroscience, ISSN 1097-6256, 05/2012, Volume 15, Issue 5, pp. 713 - 721
The Huntington's disease gene product, huntingtin, is indispensable for neural tube formation, but its role is obscure. We studied neurulation in htt-null... 
TARGETED DISRUPTION | ZEBRAFISH | LACKING HUNTINGTIN | EMBRYONIC STEM-CELLS | MUTANT HUNTINGTIN | ADAM10 | MICE | DISEASE GENE HOMOLOG | WILD-TYPE HUNTINGTIN | NEUROSCIENCES | N-CADHERIN CLEAVAGE | Body Patterning - drug effects | Guanylate Kinases - genetics | Amyloid Precursor Protein Secretases - genetics | RNA, Small Interfering - genetics | Wnt1 Protein - genetics | Brain - embryology | PAX2 Transcription Factor - metabolism | Cadherins - metabolism | Apoptosis - drug effects | Embryo, Mammalian | Hedgehog Proteins - metabolism | Apoptosis - genetics | Green Fluorescent Proteins - genetics | Brain - metabolism | NFI Transcription Factors - metabolism | Cadherins - genetics | Tissue Inhibitor of Metalloproteinase-1 - pharmacology | Discs Large Homolog 1 Protein | Membrane Proteins - genetics | Gene Expression Regulation, Developmental - drug effects | PAX2 Transcription Factor - genetics | Cell Adhesion - drug effects | Mutation - genetics | Biological Evolution | Brain - drug effects | Huntingtin Protein | ADAM Proteins - metabolism | Amyloid Precursor Protein Secretases - metabolism | Analysis of Variance | Membrane Proteins - antagonists & inhibitors | Cell Adhesion - physiology | Embryo, Nonmammalian | Guanylate Kinases - metabolism | Neuroepithelial Cells - physiology | Mice | Zebrafish Proteins - genetics | ADAM Proteins - genetics | Cerebral Ventricles - cytology | Drosophila melanogaster | Neuroepithelial Cells - drug effects | Embryonic Stem Cells - metabolism | Nestin | Immunoprecipitation | Gene Expression Regulation, Developmental - genetics | Wnt1 Protein - metabolism | Zebrafish - embryology | Cell Differentiation - genetics | Transfection | Hedgehog Proteins - genetics | Intermediate Filament Proteins - genetics | Neurons - physiology | Membrane Proteins - metabolism | Cerebral Ventricles - embryology | Neurons - drug effects | Nuclear Proteins - genetics | Hydroxamic Acids - pharmacology | Green Fluorescent Proteins - metabolism | Brain - cytology | ADAM Proteins - antagonists & inhibitors | Animals, Genetically Modified | Zebrafish Proteins - metabolism | Dipeptides - pharmacology | Cells, Cultured | ADAM10 Protein | Morpholines - pharmacology | Nuclear Proteins - metabolism | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Animals | Dictyostelium | Embryonic Stem Cells - drug effects | Cell Differentiation - drug effects | Amyloid Precursor Protein Secretases - antagonists & inhibitors | Body Patterning - genetics | Huntington's chorea | Physiological aspects | Cadherins | Genetic aspects | Research | Embryonic stem cells | Risk factors | Index Medicus
Journal Article
Journal Article
Nature Communications, ISSN 2041-1723, 04/2015, Volume 6, Issue 1, pp. 6768 - 6768
The brain has a limited capacity to self-protect against protein aggregate-associated pathology, and mounting evidence supports a role for phagocytic glia in... 
MOTOR-NEURONS | CELLS | IN-VITRO | ACTIVATION | ENGULFMENT | MULTIDISCIPLINARY SCIENCES | MUTANT HUNTINGTIN | DISEASE | TAU | PATHOLOGY | PROPAGATION | Protein Aggregates | Neurons - pathology | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Neuroglia - pathology | Humans | Huntington Disease - pathology | Drosophila Proteins - metabolism | Drosophila melanogaster - genetics | Brain - metabolism | Drosophila melanogaster - metabolism | Molecular Mimicry | Membrane Proteins - metabolism | Neurons - metabolism | Protein Aggregation, Pathological - genetics | Genes, Reporter | Disease Models, Animal | Neuroglia - chemistry | Prions - metabolism | Neurons - chemistry | Signal Transduction | Membrane Proteins - genetics | Bacterial Proteins - genetics | Gene Expression Regulation | Prions - chemistry | Huntington Disease - metabolism | Disease Progression | Huntingtin Protein | Animals | Brain - pathology | Huntington Disease - genetics | Bacterial Proteins - metabolism | Luminescent Proteins - genetics | Neuroglia - metabolism | Drosophila Proteins - genetics | Mutation | Phagocytosis | Protein Aggregation, Pathological - metabolism | Luminescent Proteins - metabolism | Draper protein | Neuroprotection | Brain | Huntingtin | Neurodegenerative diseases | Pathogenesis | Drosophila | Conversion | Neuronal-glial interactions | Proteins | Neurological diseases | Phagocytes | Signal transduction | Aggregates | Insects | Cytoplasm | Index Medicus
Journal Article
Nature Cell Biology, ISSN 1465-7392, 03/2015, Volume 17, Issue 3, pp. 262 - 275
Journal Article
Molecular Cell, ISSN 1097-2765, 07/2004, Volume 15, Issue 1, pp. 95 - 105
The expression of polyglutamine-expanded mutant proteins in Huntington's disease and other neurodegenerative disorders is associated with the formation of... 
NEURONAL INTRANUCLEAR INCLUSIONS | YEAST | EXPANDED POLYGLUTAMINE | SCA1 MICE | BIOCHEMISTRY & MOLECULAR BIOLOGY | DISEASE | BODY FORMATION | HUNTINGTIN | EXPRESSION | BINDING | AGGREGATION | CELL BIOLOGY | Molecular Chaperones - metabolism | Exons | Neurodegenerative Diseases - etiology | Peptides - genetics | TATA-Box Binding Protein - metabolism | Nerve Tissue Proteins - toxicity | Cell Nucleus - metabolism | Peptides - metabolism | TATA-Box Binding Protein - genetics | Trans-Activators - genetics | Nuclear Proteins - genetics | CREB-Binding Protein | Molecular Chaperones - genetics | HSP70 Heat-Shock Proteins - genetics | Neurodegenerative Diseases - genetics | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Neurodegenerative Diseases - metabolism | Transcription Factors - genetics | Mutation - genetics | Nerve Tissue Proteins - genetics | Nuclear Proteins - toxicity | Protein Folding | HSP70 Heat-Shock Proteins - metabolism | Macromolecular Substances | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Animals | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Trinucleotide Repeat Expansion - genetics | Protein Conformation | Trans-Activators - metabolism | Mice | TATA-Box Binding Protein - antagonists & inhibitors | Trans-Activators - antagonists & inhibitors | Saccharomyces cerevisiae | Oligomers | Nervous system diseases | DNA binding proteins | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2009, Volume 106, Issue 52, pp. 22480 - 22485
Huntington disease (HD) is an inherited neurological disorder caused by a polyglutamine expansion in the protein huntingtin and is characterized by selective... 
Proteins | Brain | Phenotypes | Neuroscience | Astrocytes | Transgenic animals | Neurons | Neuroglia | Huntington disease | Mice | Polyglutamine | Glia | Glutamate | Neurodegeneration | Excitotoxicity | NEURODEGENERATIVE DISEASE | CONTRIBUTE | MULTIDISCIPLINARY SCIENCES | neurodegeneration | polyglutamine | GLIAL-CELLS | glia | GLUTAMATE TRANSPORT | PATHOGENESIS | NEURONS | INTRANUCLEAR INCLUSIONS | ACCUMULATION | excitotoxicity | glutamate | TRANSGENIC MICE | Glial Fibrillary Acidic Protein - genetics | Humans | Huntington Disease - pathology | Sp1 Transcription Factor - metabolism | DNA Primers - genetics | Gliosis - pathology | Aging - genetics | Base Sequence | Excitatory Amino Acid Transporter 2 - genetics | Nuclear Proteins - genetics | Huntington Disease - physiopathology | Recombinant Proteins - metabolism | Promoter Regions, Genetic | Gene Expression | Gliosis - genetics | Nerve Tissue Proteins - physiology | Brain - physiopathology | Mice, Transgenic | Recombinant Proteins - genetics | Excitatory Amino Acid Transporter 2 - metabolism | Nerve Tissue Proteins - genetics | Aging - pathology | Huntingtin Protein | Astrocytes - physiology | Phenotype | Animals | Aging - physiology | Brain - pathology | Huntington Disease - genetics | Glutamic Acid - metabolism | Nuclear Proteins - physiology | Mutation | Huntington's chorea | Physiological aspects | Development and progression | Genetic aspects | Risk factors | Nerve proteins | Rodents | Neurological disorders | Cells | Index Medicus | Biological Sciences
Journal Article
Molecular Cell, ISSN 1097-2765, 09/2016, Volume 63, Issue 6, pp. 951 - 964
Huntington’s disease is one of several neurodegenerative disorders characterized by the aggregation of polyglutamine (polyQ)-expanded mutant protein. How polyQ... 
POLYGLUTAMINE | PROTEIN | FUS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MUTANT HUNTINGTIN | PHASE-TRANSITION | DISEASE | MUTATIONS | INCLUSION-BODY FORMATION | AGGREGATION | PROTEOSTASIS | CELL BIOLOGY | Protein Aggregates | Neurons - pathology | Humans | Protein Multimerization | Peptides - genetics | Green Fluorescent Proteins - genetics | Recombinant Fusion Proteins - metabolism | Ribosomal Proteins - metabolism | Peptides - metabolism | Neurons - metabolism | Gene Ontology | Green Fluorescent Proteins - metabolism | Gene Expression | HSP40 Heat-Shock Proteins - metabolism | HSP40 Heat-Shock Proteins - genetics | Peptides - chemistry | Ribosomal Proteins - genetics | Huntingtin Protein - metabolism | Molecular Sequence Annotation | Bacterial Proteins - genetics | Solubility | Spectrometry, Fluorescence | Single Molecule Imaging - methods | Protein Interaction Mapping | Animals | Cell Line, Tumor | Recombinant Fusion Proteins - genetics | Bacterial Proteins - metabolism | Luminescent Proteins - genetics | Mice | HeLa Cells | Huntingtin Protein - genetics | Mutation | Luminescent Proteins - metabolism | Ubiquitin | Fluorescence spectroscopy | Nervous system diseases | RNA | Heat shock proteins | Fluorescence | Biosynthesis | Genetic transcription | Oligomers | Analysis | Cellular signal transduction | Research institutes | Binding proteins | Protein binding | Index Medicus
Journal Article
PLoS Genetics, ISSN 1553-7390, 04/2018, Volume 14, Issue 4, pp. e1007363 - e1007363
The hereditary spastic paraplegias (HSP) are a clinically and genetically heterogeneous group of disorders characterized by progressive lower limb spasticity.... 
INTELLECTUAL DISABILITY | RECESSIVE LOSS | COMPLEX-4 AP-4 | HEREDITARY SPASTIC PARAPLEGIA | ALZHEIMERS-DISEASE | CORPUS-CALLOSUM | ADAPTER | GENETICS & HEREDITY | VICI SYNDROME | AMYLOID PRECURSOR PROTEIN | AUTOPHAGY | Receptors, Glutamate - metabolism | Spastic Paraplegia, Hereditary - genetics | Spinal Cord - metabolism | Vesicular Transport Proteins - metabolism | Humans | Adaptor Protein Complex 4 - chemistry | Male | Adaptor Protein Complex 4 - genetics | Spastic Paraplegia, Hereditary - metabolism | Brain - metabolism | trans-Golgi Network - metabolism | Protein Aggregates - genetics | Spinal Cord - pathology | Adaptor Protein Complex 4 - deficiency | Female | Membrane Proteins - metabolism | Neurons - metabolism | Spastic Paraplegia, Hereditary - pathology | Protein Aggregation, Pathological - genetics | Disease Models, Animal | Adaptor Protein Complex Subunits - deficiency | Huntingtin Protein - metabolism | Mice, Inbred C57BL | Axons - metabolism | Behavior, Animal - physiology | Adaptor Protein Complex Subunits - chemistry | Huntingtin Protein - chemistry | Mice, Knockout | Animals | Brain - pathology | Mice | Huntingtin Protein - genetics | Mutation | Autophagy-Related Proteins - metabolism | Adaptor Protein Complex Subunits - genetics | Protein Aggregation, Pathological - metabolism | Development and progression | Genetic aspects | Diagnosis | Paralysis, Spastic | Visualization | Spinal cord | Neurosciences | Huntingtin | Funding | Intellectual disabilities | Genes | Neurobiology | Childrens health | Biology | Microcephaly | Autophagy | Proteins | Fibroblasts | Paralysis | Seizures | Phenotypes | Language disorders | Neurons | Heat shock proteins | Spasticity | Corpus callosum | Golgi apparatus | Axons | Microencephaly | Skin | Dystrophy | Phagocytosis | Cytoplasm | Index Medicus
Journal Article
Human Molecular Genetics, ISSN 0964-6906, 05/2012, Volume 21, Issue 10, pp. 2245 - 2262
Journal Article
Neuron, ISSN 0896-6273, 12/2009, Volume 64, Issue 6, pp. 828 - 840
The N-terminal 17 amino acids of huntingtin (NT17) can be phosphorylated on serines 13 and 16; however, the significance of these modifications in Huntington's... 
humdisease | molneuro | NEURONAL INTRANUCLEAR INCLUSIONS | NUCLEAR | PHOSPHORYLATION | EXPANSION | NEURODEGENERATION | TOXICITY | PATHOLOGY | TRANSGENIC MOUSE MODEL | NEUROSCIENCES | AGGREGATION | TRINUCLEOTIDE REPEAT | Molecular Weight | Humans | Nerve Degeneration - physiopathology | Nerve Degeneration - genetics | Alanine - chemistry | Amino Acid Sequence - genetics | Nerve Degeneration - metabolism | Aspartic Acid - genetics | Nerve Tissue Proteins - chemistry | Alanine - genetics | Amyloid - metabolism | Nuclear Proteins - genetics | Huntington Disease - physiopathology | Disease Models, Animal | Amyloid - genetics | Genetic Predisposition to Disease - genetics | Gene Expression Regulation - genetics | Serine - genetics | Alanine - metabolism | Mice, Transgenic | Protein Structure, Tertiary - genetics | Mutation - genetics | Nuclear Proteins - chemistry | Serine - chemistry | Huntington Disease - metabolism | Nerve Tissue Proteins - genetics | Serine - metabolism | Huntingtin Protein | Phenotype | Animals | Huntington Disease - genetics | Trinucleotide Repeat Expansion - genetics | Amino Acid Substitution - genetics | Aspartic Acid - metabolism | Mice | Aspartic Acid - chemistry | Proteins | Medical colleges | Alanine | Nervous system diseases | Neurosciences | Huntington's chorea | Neurons | Physiological aspects | Aspartate | Huntingtons disease | Phosphorylation | Neurodegeneration | Pathogenesis | Neuropathology | Rodents | Mutation | Index Medicus
Journal Article