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Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2011, Volume 108, Issue 25, pp. 10337 - 10342
Spinal muscular atrophy (SMA), caused by the deletion of the SMN1 gene, is the leading genetic cause of infant mortality. SMN protein is present at high levels... 
Axons | Motor neurons | Growth cones | Neuroscience | Messenger RNA | RNA | Neurons | Antibodies | Gene expression regulation | SMN complex proteins | Neuritin | Local protein synthesis | Embryonic lethal abnormal vision drosophila-like 4 (ELAV-L4) | LOCALIZATION | RIBONUCLEOPROTEIN | MULTIDISCIPLINARY SCIENCES | ACTIVITY-DEPENDENT EXPRESSION | IDENTIFICATION | neuritin | GROWTH CONES | TRANSPORT | DETERMINING GENE-PRODUCT | SPINAL MUSCULAR-ATROPHY | IN-VIVO | ASSOCIATION | embryonic lethal abnormal vision Drosophila-like 4 (ELAV-L4) | local protein synthesis | ELAV-Like Protein 4 | Humans | RNA, Messenger - metabolism | Zebrafish - embryology | Recombinant Fusion Proteins - metabolism | Embryo, Mammalian - anatomy & histology | Motor Neurons - cytology | Survival of Motor Neuron 1 Protein - genetics | Neuropeptides - genetics | Animals, Genetically Modified | RNA, Messenger - genetics | Cells, Cultured | ELAV Proteins - metabolism | Axons - metabolism | Neuropeptides - metabolism | Survival of Motor Neuron 1 Protein - metabolism | Nerve Tissue Proteins - genetics | GPI-Linked Proteins - metabolism | Motor Neurons - metabolism | Nerve Tissue Proteins - metabolism | Embryo, Mammalian - physiology | Animals | Axons - pathology | Recombinant Fusion Proteins - genetics | Zebrafish - physiology | Mice | ELAV Proteins - genetics | GPI-Linked Proteins - genetics | Gene mutations | Physiological aspects | Genetic aspects | Research | Health aspects | Risk factors | Spinal muscular atrophy | Proteins | Genotype & phenotype | Neuromuscular diseases | Zebrafish | Infant mortality | Ribonucleic acid--RNA | Index Medicus | Spinal cord | Translation | Cell survival | Mental disorders | Axonogenesis | Mortality | SMN protein | survival | Mass spectroscopy | Infants | Gene deletion | infant mortality | HuD protein | Pathology | RNA-binding protein | Actin | Neuromuscular junctions | spinal muscular atrophy | Axon guidance | Mass spectrometry | Biological Sciences
Journal Article
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 11/2017, Volume 377, Issue 18, pp. 1713 - 1722
Journal Article
Nature, ISSN 0028-0836, 10/2011, Volume 478, Issue 7367, pp. 123 - 126
Spinal muscular atrophy (SMA) is a motor neuron disease and the leading genetic cause of infant mortality; it results from loss-of-function mutations in the... 
SURVIVAL | IGF-I | DISEASES | MULTIDISCIPLINARY SCIENCES | GROWTH | PHENOTYPE | MICE | CARDIAC DEFECTS | DELIVERY | Spinal Cord - metabolism | Longevity - drug effects | Humans | Glycoproteins - metabolism | RNA, Messenger - analysis | Survival of Motor Neuron 2 Protein - metabolism | Motor Neurons - pathology | Muscular Atrophy, Spinal - genetics | Spinal Cord - pathology | Survival of Motor Neuron 2 Protein - genetics | Survival of Motor Neuron 1 Protein - genetics | RNA Isoforms - analysis | Glycoproteins - deficiency | Spinal Cord - cytology | Transgenes | Muscular Atrophy, Spinal - physiopathology | Motor Neurons - drug effects | Disease Models, Animal | Animals, Newborn | Muscular Atrophy, Spinal - metabolism | Oligonucleotides, Antisense - pharmacology | RNA Isoforms - genetics | Growth Hormone - metabolism | Alternative Splicing - genetics | Liver - metabolism | RNA, Messenger - genetics | Kaplan-Meier Estimate | Insulin-Like Growth Factor I - deficiency | Mice, Transgenic | Muscular Atrophy, Spinal - pathology | Motor Neurons - metabolism | Rotarod Performance Test | Alternative Splicing - drug effects | Animals | Carrier Proteins - metabolism | Oligonucleotides, Antisense - genetics | Oligonucleotides, Antisense - administration & dosage | Mice | Insulin-Like Growth Factor I - metabolism | Complications and side effects | Care and treatment | Gene mutations | Patient outcomes | Genetic aspects | Infants | Research | Diagnosis | Risk factors | Spinal muscular atrophy | Gene expression | Medical research | Rodents | Index Medicus
Journal Article
Nature Biotechnology, ISSN 1087-0156, 03/2010, Volume 28, Issue 3, pp. 271 - 274
Journal Article
Nucleic Acids Research, ISSN 0305-1048, 2017, Volume 45, Issue 1, pp. 395 - 416
Journal Article
The American Journal of Human Genetics, ISSN 0002-9297, 02/2017, Volume 100, Issue 2, pp. 297 - 315
Homozygous loss causes spinal muscular atrophy (SMA), the most common lethal genetic childhood motor neuron disease. encodes SMN, a ubiquitous housekeeping... 
incomplete penetrance | spinal muscular dystrophy | SMA | asymptomatic | SMN2 | endocytosis | PLS3 | SMN1 | genetic modifier | NCALD | neuronal sensor protein | SURVIVAL | MOTOR-NEURON GENE | NERVE-TERMINALS | MESSENGER-RNA | SMA PHENOTYPE | MOUSE MODEL | GENETICS & HEREDITY | LINKAGE ANALYSIS | PLASTIN 3 | PROTEINS | NEUROMUSCULAR-JUNCTIONS | Humans | Transcriptome | Male | Genetic Loci | Survival of Motor Neuron 2 Protein - metabolism | PC12 Cells | Motor Neurons - pathology | Muscular Atrophy, Spinal - genetics | Survival of Motor Neuron 2 Protein - genetics | Cloning, Molecular | Survival of Motor Neuron 1 Protein - genetics | Female | Endocytosis - genetics | Neurocalcin - genetics | Disease Models, Animal | Cell Line | Genome-Wide Association Study | Caenorhabditis elegans - genetics | Mice, Inbred C57BL | Gene Expression Regulation | Rats | Survival of Motor Neuron 1 Protein - metabolism | Zebrafish - genetics | Homozygote | Animals | Pedigree | Muscular Atrophy, Spinal - therapy | Neurocalcin - metabolism | Mice | Prevention | Endocytosis | Genetic aspects | Gene expression | Health aspects | Atrophy, Muscular | Physiological aspects | Research | Gene mutations | Risk factors | Spinal muscular atrophy | Musculoskeletal diseases | Genotype & phenotype | Protein expression | Genetic disorders | Neurons | Index Medicus
Journal Article
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2016, Volume 113, Issue 30, pp. E4377 - E4386
Journal Article