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PLoS Genetics, ISSN 1553-7390, 05/2009, Volume 5, Issue 5, pp. e1000487 - e1000487
Journal Article
The American Journal of Human Genetics, ISSN 0002-9297, 12/2015, Volume 97, Issue 6, pp. 922 - 932
We describe an X-linked genetic syndrome associated with mutations in and manifesting with global developmental delay, intellectual disability (ID),... 
transcription | abnormal gait | dystonia | developmental delay | facial dysmorphology | neurologic features | intellectual disability | intergluteal crease | TAF1 | COMPLEX | CORNELIA | GENE | TRANSCRIPTION | GENETICS & HEREDITY | NEURON-SPECIFIC ISOFORM | PHENOTYPE | DE-LANGE-SYNDROME | MUTATIONS | EXPRESSION | BINDING | TATA-Binding Protein Associated Factors - metabolism | Developmental Disabilities - metabolism | Humans | Child, Preschool | Histone Acetyltransferases - genetics | Infant | Male | Developmental Disabilities - genetics | Transcription Factor TFIID - metabolism | Intellectual Disability - genetics | Intellectual Disability - metabolism | Inheritance Patterns | Transcription Factor TFIID - genetics | Young Adult | Developmental Disabilities - pathology | Histone Acetyltransferases - metabolism | Facies | Child | Disease Models, Animal | Neurodegenerative Diseases - pathology | Signal Transduction | Gene Expression Regulation | Intellectual Disability - pathology | Neurodegenerative Diseases - genetics | Zebrafish | Neurodegenerative Diseases - metabolism | TATA-Binding Protein Associated Factors - genetics | E-Box Elements | Phenotype | Animals | Pedigree | Adolescent | Family | Mutation | Causes of | Neurologic manifestations of general diseases | Genetic aspects | Genetic variation | Health aspects | Mental retardation | Report
Journal Article
PLoS Genetics, ISSN 1553-7390, 10/2017, Volume 13, Issue 10, pp. e1007051 - e1007051
LINE-1 (L1) retrotransposons can mobilize (retrotranspose) within the human genome, and mutagenic de novo L1 insertions can lead to human diseases, including... 
PROTEIN INTERACTIONS | MESSENGER-RNA | TRANSFER-RNA SYNTHETASE | HUMAN L1 RETROTRANSPOSITION | REVERSE TRANSCRIPTION | INITIATION-FACTOR | ANTISENSE PROMOTER | GENETICS & HEREDITY | SOMATIC RETROTRANSPOSITION | NONCANONICAL FUNCTION | TRANSLATIONAL CONTROL | Epithelial Cells - metabolism | Humans | Long Interspersed Nucleotide Elements - genetics | RNA, Messenger - genetics | Multiprotein Complexes - genetics | DNA-Binding Proteins - genetics | Retroelements - genetics | Interferon-Stimulated Gene Factor 3 - genetics | Cell Cycle Proteins - genetics | Protein Binding | Adenosine Triphosphatases - genetics | Interferon-gamma - genetics | Genome, Human | Nuclear Proteins - genetics | Protein Synthesis Inhibitors | Retrotransposons | Cellular proteins | Genetic aspects | Epithelial cells | Health aspects | Immunoprecipitation | Gait | Transcription | Glyceraldehyde | Genomes | Glyceraldehyde 3-phosphate | Kinases | Proteins | Cooperation | Proline-tRNA ligase | Research centers | Deoxyribonucleic acid--DNA | Medical research | Initiation complex | Translation | Myeloid cells | tRNA | RNA-protein interactions | Translation initiation | Inflammation | Retrotransposition | Gene expression | Ribonucleic acid--RNA | Condensin | Medicine | Somatic cells | γ-Interferon | Cell lines | Proteomics | Glyceraldehyde-3-phosphate dehydrogenase | Interferon | Mutation | Cancer | Index Medicus | RNA | Deoxyribonucleic acid | Ribonucleic acid | DNA
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 08/2012, Volume 32, Issue 32, pp. 10841 - 10853
Delineation of key molecules that act epigenetically to transduce diverse stressors into established patterns of disease would facilitate the advent of... 
OXIDATIVE STRESS | HEME OXYGENASE-1 EXPRESSION | PREPULSE INHIBITION | ALZHEIMERS-DISEASE | SPINAL CORD BARRIER | ALPHA-SYNUCLEIN EXPRESSION | IMMUNE ACTIVATION | INCREASE LOCOMOTOR-ACTIVITY | OVER-EXPRESSION | CEREBROSPINAL-FLUID | NEUROSCIENCES | Glial Fibrillary Acidic Protein - genetics | Heme Oxygenase-1 - metabolism | Protein Binding - genetics | Superoxide Dismutase - genetics | Embryo, Mammalian | Homeodomain Proteins - metabolism | Humans | MicroRNAs - metabolism | Gait Disorders, Neurologic - genetics | Schizophrenia - pathology | Nuclear Receptor Subfamily 4, Group A, Member 2 - genetics | Glial Fibrillary Acidic Protein - metabolism | RNA, Messenger - metabolism | Receptors, Dopamine D1 - metabolism | Schizophrenia - genetics | Dopamine Agents - pharmacokinetics | Protein Binding - drug effects | alpha-Synuclein - genetics | Disease Models, Animal | Inhibition (Psychology) | Animals, Newborn | Mice, Transgenic | Laser-Doppler Flowmetry | Astrocytes - ultrastructure | Tyrosine 3-Monooxygenase - genetics | Analysis of Variance | Brain - pathology | Mice | MicroRNAs - genetics | Biogenic Monoamines - metabolism | Gait Disorders, Neurologic - etiology | Tritium - pharmacokinetics | Astrocytes - metabolism | Tyrosine 3-Monooxygenase - metabolism | Age Factors | Benzamides - pharmacokinetics | Gene Expression Regulation, Developmental - genetics | Chromatography, High Pressure Liquid | Receptors, Dopamine D2 - metabolism | Heme Oxygenase-1 - genetics | Schizophrenia - physiopathology | Sensory Gating - genetics | Superoxide Dismutase - metabolism | Enzyme-Linked Immunosorbent Assay | Acoustic Stimulation | Transcription Factors - genetics | Benzazepines - pharmacokinetics | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Animals | Nuclear Receptor Subfamily 4, Group A, Member 2 - metabolism | alpha-Synuclein - metabolism
Journal Article
Clinical Genetics, ISSN 0009-9163, 03/2013, Volume 83, Issue 3, pp. 279 - 283
Journal Article
Brain, ISSN 0006-8950, 2012, Volume 135, Issue 6, pp. 1964 - 1980
Ambivalent effects of interleukin-6 on the pathogenesis of ischaemic stroke have been reported. However, to date, the long-term actions of interleukin-6 after... 
cerebral ischaemia | inflammation | regeneration | angiogenesis | interleukin-6 | FOCAL CEREBRAL-ISCHEMIA | NEUROSCIENCES | CLINICAL NEUROLOGY | ENDOTHELIAL PROGENITOR CELLS | IN-VITRO | BRAIN ISCHEMIA | NITRIC-OXIDE | GENE-EXPRESSION | PHYSICAL-ACTIVITY | RAT-BRAIN | GROWTH-FACTOR | INFLAMMATORY CYTOKINES | Angiogenic Proteins - genetics | Infarction, Middle Cerebral Artery - physiopathology | Oligonucleotide Array Sequence Analysis | Cytokine Receptor gp130 - genetics | Embryo, Mammalian | Gene Expression Profiling | Green Fluorescent Proteins - genetics | Receptor, trkB - genetics | Bone Marrow Transplantation - methods | Infarction, Middle Cerebral Artery - complications | Perfusion Imaging | Cytokines - genetics | Interleukin-6 - metabolism | STAT3 Transcription Factor - genetics | Disease Models, Animal | Cytokine Receptor gp130 - metabolism | Interleukin-6 - genetics | Endothelin-1 - genetics | Hypoxia - complications | Signal Transduction - genetics | Analysis of Variance | Brain - pathology | Mice | Neovascularization, Pathologic - metabolism | Endothelial Cells - pathology | Angiogenic Proteins - metabolism | Gait Disorders, Neurologic - etiology | Mice, Knockout - genetics | Cerebral Cortex - cytology | Neovascularization, Pathologic - etiology | Tetrazolium Salts | Thiazoles | Microfilament Proteins - metabolism | Neurons - drug effects | STAT3 Transcription Factor - metabolism | Calcium-Binding Proteins - metabolism | Green Fluorescent Proteins - metabolism | Cytokines - metabolism | Enzyme-Linked Immunosorbent Assay | Endothelin-1 - metabolism | Gene Expression Regulation - genetics | Cells, Cultured | Neuroglia - physiology | Infarction, Middle Cerebral Artery - pathology | Glucose - deficiency | Rotarod Performance Test | Animals | Infarction, Middle Cerebral Artery - surgery | Signal Transduction - physiology | Receptor, trkB - metabolism | Original
Journal Article
Journal of the Neurological Sciences, ISSN 0022-510X, 2010, Volume 296, Issue 1, pp. 22 - 29
Abstract An X-linked myopathy was recently associated with mutations in the four-and-a-half-LIM domains 1 ( FHL1 ) gene. We identified a family with late... 
Neurology | X-linked myopathy | Scapuloperoneal | Neurogenetics | Muscular dystrophy | FHL1 | Genetic diagnosis | ELECTROSTATIC ENERGIES | DOMINANT | BINDING PROTEIN | NEUROSCIENCES | CLINICAL NEUROLOGY | GENE | REDUCING BODY MYOPATHY | Immunohistochemistry | Homeodomain Proteins - metabolism | Humans | Middle Aged | Child, Preschool | Infant | Male | Muscle, Skeletal - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Mutation, Missense - genetics | Young Adult | Muscular Atrophy, Spinal - genetics | Mutation - physiology | Gait Disorders, Neurologic - physiopathology | Muscle Proteins - metabolism | Gait Disorders, Neurologic - pathology | Adult | Female | Genetic Diseases, X-Linked - genetics | Genetic Linkage - genetics | Child | Intracellular Signaling Peptides and Proteins - genetics | Muscular Atrophy, Spinal - physiopathology | Genetic Diseases, X-Linked - physiopathology | LIM Domain Proteins | Models, Molecular | Exons - genetics | Mutation - genetics | Reverse Transcriptase Polymerase Chain Reaction | Muscular Atrophy, Spinal - pathology | Homeodomain Proteins - genetics | Muscle Proteins - genetics | Phenotype | Pedigree | Adolescent | Genetic Diseases, X-Linked - pathology | Polymorphism, Single Nucleotide - genetics | LIM-Homeodomain Proteins | Protein Conformation | Aged | Transcription Factors | Ubiquitin | Family | Genetic aspects | Protein binding | muscular dystrophy | genetic diagnosis | neurogenetics | scapuloperoneal
Journal Article
Molecular Therapy, ISSN 1525-0016, 04/2017, Volume 25, Issue 4, pp. 839 - 854
X-linked myotubular myopathy (XLMTM) results from gene mutations and myotubularin deficiency. Most XLMTM patients develop severe muscle weakness leading to... 
myotubularin | centronuclear | neuromuscular | myotubular | myopathy | muscle | gene therapy | adeno-associated virus | canine | pediatric | NONHUMAN-PRIMATES | EFFICIENT TRANSDUCTION | MUSCLE PATHOLOGY | MEDICINE, RESEARCH & EXPERIMENTAL | CANINE MODEL | ADENOASSOCIATED VIRUS | MUSCULAR-DYSTROPHY | SKELETAL-MUSCLE | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | HEMOPHILIA-B | AAV | GENETICS & HEREDITY | RECEPTOR FOOTPRINT | Dependovirus - genetics | Gait | Genetic Vectors - administration & dosage | Genetic Vectors - adverse effects | Muscle, Skeletal - metabolism | Myopathies, Structural, Congenital - genetics | Recovery of Function | Tissue Distribution | Immunity, Humoral | Myopathies, Structural, Congenital - therapy | Protein Tyrosine Phosphatases, Non-Receptor - genetics | Muscle Strength | Disease Models, Animal | Reflex | Gene Expression | Transgenes - genetics | Kaplan-Meier Estimate | Muscle, Skeletal - ultrastructure | Treatment Outcome | Dependovirus - classification | Disease Progression | Genetic Vectors - genetics | Animals | Biopsy | Muscle, Skeletal - physiopathology | Dogs | Myopathies, Structural, Congenital - diagnosis | Myopathies, Structural, Congenital - mortality | Muscle, Skeletal - pathology | Respiratory Function Tests | Genetic Vectors - pharmacokinetics | Transgenes - immunology | Immunity, Cellular | Genetic Therapy - adverse effects | Genetic Therapy - methods | Animal models | Respiratory function | MTM1 gene | Animal euthanasia | Immune response | Disease | Clinical trials | Grants | Males | Desmin | Muscular dystrophy | Pathology | Genotype & phenotype | Musculoskeletal system | Walking | Ostomy | Life span | Trends | Mutation | Gene therapy | Age | Myopathy | Life Sciences | Original
Journal Article
Journal Article