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The American Journal of Human Genetics, ISSN 0002-9297, 08/2009, Volume 85, Issue 2, pp. 155 - 167
We report the case of a congenital myasthenic syndrome due to a mutation in , the gene encoding agrin, an extracellular matrix molecule released by the nerve... 
MUTANT MICE | PROTEIN | DEFICIENT | GENETICS & HEREDITY | MUSCULAR-DYSTROPHY | SKELETAL-MUSCLE FIBERS | DIFFERENTIATION | NEUROMUSCULAR-JUNCTION | DYSTROGLYCAN | BINDING | ACETYLCHOLINE-RECEPTOR | Agrin - chemistry | Models, Chemical | Neuromuscular Junction - metabolism | Humans | Dystroglycans - metabolism | Male | Muscle, Skeletal - metabolism | Muscle Fibers, Skeletal - metabolism | Mutation, Missense | Agrin - metabolism | Muscle, Skeletal - surgery | Synapses - metabolism | DNA Mutational Analysis | Neuromuscular Junction - genetics | Adult | Female | Myasthenic Syndromes, Congenital - genetics | Protein Structure, Tertiary | Recombinant Proteins - metabolism | Agrin - genetics | Cell Line | Receptors, Cholinergic - metabolism | Muscle, Skeletal - ultrastructure | Rats | Recombinant Proteins - chemistry | Neuromuscular Junction - ultrastructure | Receptors, Cholinergic - physiology | Animals | Biopsy | Pedigree | Muscle Fibers, Skeletal - cytology | Muscle, Skeletal - pathology | Neuromuscular Junction - physiology | Receptors, Cholinergic - genetics | Myasthenia gravis | Gene mutations | Analysis | Physiological aspects | Genetic aspects | Research | Neuromuscular junction | Synapses | Cell culture | Glycoproteins | Genetic disorders | Mutation | Muscular system | Rodents | Index Medicus | Life Sciences | Genetics | Neurons and Cognition
Journal Article
Molecular and Cellular Biology, ISSN 0270-7306, 01/2013, Volume 33, Issue 2, pp. 194 - 212
Journal Article
Neuron, ISSN 0896-6273, 2008, Volume 60, Issue 2, pp. 285 - 297
Neuromuscular junction (NMJ) formation requires agrin, a factor released from motoneurons, and MuSK, a transmembrane tyrosine kinase that is activated by... 
CELLBIO | MOLNEURO | SIGNALING | ADULT-RAT BRAIN | POSTSYNAPTIC DIFFERENTIATION | TYROSINE PHOSPHORYLATION | ACETYLCHOLINE-RECEPTOR AGGREGATION | IN-VIVO | SYNAPSE FORMATION | NEUROMUSCULAR-JUNCTION | BETA-CATENIN | HIPPOCAMPAL-NEURONS | NEUROSCIENCES | MUSCLE-SPECIFIC KINASE | Phosphorylation | Synaptic Transmission - genetics | Neuromuscular Junction - metabolism | Humans | Muscle Fibers, Skeletal - metabolism | Presynaptic Terminals - ultrastructure | Agrin - metabolism | Motor Neurons - ultrastructure | Neuromuscular Junction - embryology | Receptor Aggregation - genetics | Muscle Fibers, Skeletal - ultrastructure | Neuromuscular Junction - genetics | Agrin - genetics | Cell Line | Receptors, LDL - genetics | Receptors, Cholinergic - metabolism | Receptors, LDL - metabolism | Signal Transduction - genetics | Receptor Protein-Tyrosine Kinases - metabolism | Synaptic Membranes - ultrastructure | Motor Neurons - metabolism | Tyrosine - metabolism | Animals | Receptor Protein-Tyrosine Kinases - genetics | Receptors, Cholinergic - ultrastructure | Presynaptic Terminals - metabolism | Mice | Synaptic Membranes - metabolism | Protein Binding - physiology | Receptors, Cholinergic - genetics | Synaptic Membranes - genetics | Tyrosine | Neurons | Autonomic drugs | Low density lipoproteins | Proteins | Software | Epidermal growth factor | Muscular system | Index Medicus
Journal Article
Human Molecular Genetics, ISSN 0964-6906, 8/2008, Volume 17, Issue 16, pp. 2552 - 2569
Journal Article
Journal Article
Neuron, ISSN 0896-6273, 11/2006, Volume 52, Issue 4, pp. 663 - 677
Homeostatic signaling systems are thought to interface with the mechanisms of neural plasticity to achieve stable yet flexible neural circuitry. However, the... 
MOLNEURO | SIGNALING | BUNGAROTOXIN-TREATED RATS | CALCIUM-CHANNEL FUNCTION | RETROGRADE SIGNAL | GENETIC-ANALYSIS | PRESYNAPTIC TRANSMITTER RELEASE | SENSITIVE PARALYTIC MUTANT | QUANTAL CONTENT | NEUROMUSCULAR-JUNCTION | ALPHA-1 SUBUNIT | NEUROSCIENCES | DENDRITIC PROTEIN-SYNTHESIS | Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors | Membrane Potentials - genetics | Synaptic Vesicles - metabolism | Calcium Channels - metabolism | Synaptic Transmission - genetics | Neuromuscular Junction - drug effects | Neuromuscular Junction - metabolism | Receptors, N-Methyl-D-Aspartate - metabolism | Calcium Channels, N-Type - metabolism | Drosophila Proteins - metabolism | Drosophila melanogaster - genetics | Excitatory Postsynaptic Potentials - drug effects | Receptors, N-Methyl-D-Aspartate - genetics | Drosophila melanogaster - metabolism | Excitatory Postsynaptic Potentials - physiology | Time Factors | Neuromuscular Junction - genetics | Synaptic Transmission - drug effects | Calcium Channels - genetics | Receptors, AMPA - genetics | Motor Neurons - drug effects | Receptors, AMPA - metabolism | Membrane Potentials - drug effects | Calcium Channels, N-Type - genetics | Mutation - genetics | Motor Neurons - metabolism | Synaptic Membranes - drug effects | Animals | Synaptic Vesicles - drug effects | Drosophila Proteins - genetics | Synaptic Membranes - metabolism | Homeostasis - genetics | Receptors, AMPA - antagonists & inhibitors | Synaptic Membranes - genetics | Homeostasis | Protein biosynthesis | Calcium channels | Neurosciences | Glutamate | Genotype & phenotype | Insects | Rodents | Compensation | Mutation | Muscular system | Experiments | Index Medicus | calcium channel | development | migraine | memory | Drosophila | plasticity | learning | synapse | CaV2.1 | excitability | ataxia | neuromuscular junction | glutamate receptor
Journal Article
Neuron, ISSN 0896-6273, 12/2015, Volume 88, Issue 5, pp. 892 - 901
Noncoding expansions of a hexanucleotide repeat (GGGGCC) in the gene are the most common cause of familial amyotrophic lateral sclerosis and frontotemporal... 
DEMENTIA | EXPANDED C9ORF72 | DIPEPTIDE-REPEAT PROTEINS | EXPANSIONS | AMYOTROPHIC-LATERAL-SCLEROSIS | FRONTOTEMPORAL LOBAR DEGENERATION | TRANSLATION | HEXANUCLEOTIDE REPEAT | NEUROSCIENCES | GGGGCC REPEAT | RNA FOCI | Muscle Strength - genetics | Spinal Cord - metabolism | Age Factors | Amyotrophic Lateral Sclerosis - physiopathology | DNA Repeat Expansion - genetics | Humans | Psychomotor Performance - physiology | Brain - metabolism | Chromosomes, Artificial, Bacterial - genetics | Spinal Cord - pathology | Chromosomes, Artificial, Bacterial - metabolism | Neuromuscular Junction - genetics | C9orf72 Protein | Neurons - drug effects | Neuromuscular Junction - pathology | Disease Models, Animal | Frontotemporal Dementia - pathology | Frontotemporal Dementia - genetics | Frontotemporal Dementia - physiopathology | Glutamic Acid - pharmacology | Amyotrophic Lateral Sclerosis - genetics | Cells, Cultured | Mice, Transgenic | Proteins - genetics | Motor Activity - genetics | Amyotrophic Lateral Sclerosis - pathology | Animals | Brain - pathology | Mice | Neurosciences | Genetic engineering | RNA | Dementia | Medical colleges | Peptides | Proteins | Brain research | Transgenic animals | Neurodegeneration | Laboratories | Rodents | Amyotrophic lateral sclerosis | Genomes | Artificial chromosomes | Alzheimers disease | Experiments | Patients | Index Medicus
Journal Article
Neuron, ISSN 0896-6273, 04/2013, Volume 78, Issue 1, pp. 65 - 80
Mutations in VCP cause multisystem degeneration impacting the nervous system, muscle, and/or bone. Patients may present with ALS, Parkinsonism, frontotemporal... 
PATHOGENESIS | PARKIN | VALOSIN-CONTAINING-PROTEIN | INCLUSION-BODY MYOPATHY | DROSOPHILA MODEL | FRONTOTEMPORAL DEMENTIA | PAGETS-DISEASE | BONE | NEUROSCIENCES | P97 | DEGENERATION | Embryo, Mammalian | Humans | Ganglia, Spinal - cytology | Drosophila Proteins - metabolism | HSP72 Heat-Shock Proteins - genetics | Protein Tyrosine Phosphatases - genetics | Neurons - ultrastructure | Time Factors | Carbonyl Cyanide m-Chlorophenyl Hydrazone - pharmacology | Neuromuscular Junction - genetics | Neurons - metabolism | Protein-Serine-Threonine Kinases - metabolism | Mitochondrial Membrane Transport Proteins - metabolism | Cell Cycle Proteins - metabolism | Enzyme Inhibitors - pharmacology | Ubiquitin-Protein Ligases - metabolism | Adenosine Triphosphatases - metabolism | Mutation - genetics | Leupeptins - pharmacology | GTP Phosphohydrolases - metabolism | Luminescent Proteins - genetics | Adenosine Triphosphatases - genetics | Ubiquitin-Protein Ligases - genetics | RNA, Small Interfering - metabolism | Immunoprecipitation | Neuromuscular Junction - metabolism | Valosin Containing Protein | Mitochondria - ultrastructure | Transfection | Mitochondria - genetics | Proton Ionophores - pharmacology | Cell Cycle Proteins - genetics | Microscopy, Electron, Transmission | Animals, Genetically Modified | Gene Expression Regulation - genetics | Drosophila | RNA, Small Interfering - pharmacology | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Nuclear Proteins - metabolism | Mitochondria - metabolism | Mitochondria - drug effects | Transcription Factors - genetics | Transcription Factors - metabolism | Animals | Proteins - metabolism | Drosophila Proteins - genetics | In Vitro Techniques | Ubiquitination - genetics | Luminescent Proteins - metabolism | Ubiquitin | Analysis | Genomics | Quality control | Amyotrophic lateral sclerosis | Genetic aspects | Mitochondrial DNA | Dementia | Neurons | Parkinsons disease | Biosynthesis | Digital cameras | Kinases | DNA repair | Proteins | Mitochondria | Brain research | Insects | Microscopy | Morphology | Mutation | Index Medicus
Journal Article
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 2019, Volume 294, Issue 5, pp. 1739 - 1752
Journal Article