Neuromuscular effects of G93A-SOD1 expression in zebrafish

[1]  J. Dowling,et al.  Neuromuscular effects of G93A-SOD1 expression in zebrafish , 2012, Molecular Neurodegeneration.

[2]  Bruce L. Miller,et al.  Expanded GGGGCC Hexanucleotide Repeat in Noncoding Region of C9ORF72 Causes Chromosome 9p-Linked FTD and ALS , 2011, Neuron.

[3]  David Heckerman,et al.  A Hexanucleotide Repeat Expansion in C9ORF72 Is the Cause of Chromosome 9p21-Linked ALS-FTD , 2011, Neuron.

[4]  Xavier Navarro,et al.  Evolution of gait abnormalities in SOD1G93A transgenic mice , 2011, Brain Research.

[5]  J. Haines,et al.  Mutations in UBQLN2 cause dominant X-linked juvenile and adult onset ALS and ALS/dementia , 2011, Nature.

[6]  E. Brustein,et al.  FUS and TARDBP but Not SOD1 Interact in Genetic Models of Amyotrophic Lateral Sclerosis , 2011, PLoS genetics.

[7]  A. Acevedo-Arozena,et al.  SOD1 and TDP-43 animal models of amyotrophic lateral sclerosis: recent advances in understanding disease toward the development of clinical treatments , 2011, Mammalian Genome.

[8]  L. Hao,et al.  Generation and Characterization of a genetic zebrafish model of SMA carrying the human SMN2 gene , 2011, Molecular Neurodegeneration.

[9]  E. Brustein,et al.  Zebrafish models for the functional genomics of neurogenetic disorders. , 2011, Biochimica et biophysica acta.

[10]  E. Melamed,et al.  The “Dying-Back” Phenomenon of Motor Neurons in ALS , 2011, Journal of Molecular Neuroscience.

[11]  A. Echaniz-Laguna,et al.  Skeletal muscle in motor neuron diseases: therapeutic target and delivery route for potential treatments. , 2010, Current drug targets.

[12]  C. Beattie,et al.  A genetic model of amyotrophic lateral sclerosis in zebrafish displays phenotypic hallmarks of motoneuron disease , 2010, Disease Models & Mechanisms.

[13]  E. Brustein,et al.  In the swim of things: recent insights to neurogenetic disorders from zebrafish. , 2010, Trends in genetics : TIG.

[14]  C. Bendotti,et al.  Unraveling the complexity of amyotrophic lateral sclerosis: recent advances from the transgenic mutant SOD1 mice. , 2010, CNS & neurological disorders drug targets.

[15]  L. Martin,et al.  Skeletal muscle-restricted expression of human SOD1 causes motor neuron degeneration in transgenic mice. , 2010, Human molecular genetics.

[16]  Takeo Kato,et al.  Mutations of optineurin in amyotrophic lateral sclerosis , 2010, Nature.

[17]  F. Muller,et al.  Increased superoxide in vivo accelerates age‐associated muscle atrophy through mitochondrial dysfunction and neuromuscular junction degeneration , 2010, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[18]  G. Rouleau,et al.  Gain and loss of function of ALS-related mutations of TARDBP (TDP-43) cause motor deficits in vivo. , 2010, Human molecular genetics.

[19]  H. Yoon,et al.  Dose-dependent efficacy of ALS-human mesenchymal stem cells transplantation into cisterna magna in SOD1-G93A ALS mice , 2010, Neuroscience Letters.

[20]  D. Cleveland,et al.  Non–cell autonomous toxicity in neurodegenerative disorders: ALS and beyond , 2009, The Journal of cell biology.

[21]  E. Feldman,et al.  Vascular endothelial growth factor prevents G93A‐SOD1‐induced motor neuron degeneration , 2009, Developmental neurobiology.

[22]  C. Moens,et al.  Zebrafish survival motor neuron mutants exhibit presynaptic neuromuscular junction defects. , 2009, Human molecular genetics.

[23]  E. Feldman,et al.  Neuroprotection using gene therapy to induce vascular endothelial growth factor-A expression , 2009, Gene Therapy.

[24]  J. Loeffler,et al.  Neuromuscular junction destruction during amyotrophic lateral sclerosis: insights from transgenic models. , 2009, Current opinion in pharmacology.

[25]  D. Cleveland,et al.  Rethinking ALS: The FUS about TDP-43 , 2009, Cell.

[26]  J L Haines,et al.  Supporting Online Material Materials and Methods Figs. S1 to S7 Tables S1 to S4 References Mutations in the Fus/tls Gene on Chromosome 16 Cause Familial Amyotrophic Lateral Sclerosis , 2022 .

[27]  Andrew P. Vreede,et al.  Loss of Myotubularin Function Results in T-Tubule Disorganization in Zebrafish and Human Myotubular Myopathy , 2009, PLoS genetics.

[28]  A. Schuyler,et al.  Insulin-like growth factor-I for the treatment of amyotrophic lateral sclerosis , 2009, Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases.

[29]  Claire L. Simpson,et al.  Variants of the elongator protein 3 (ELP3) gene are associated with motor neuron degeneration , 2008, Human molecular genetics.

[30]  J. Julien,et al.  Als2 mRNA splicing variants detected in KO mice rescue severe motor dysfunction phenotype in Als2 knock-down zebrafish. , 2008, Human molecular genetics.

[31]  Cheol‐Hee Kim,et al.  Real-time imaging of mitochondria in transgenic zebrafish expressing mitochondrially targeted GFP. , 2008, BioTechniques.

[32]  T. Becker,et al.  Motor Neuron Regeneration in Adult Zebrafish , 2008, The Journal of Neuroscience.

[33]  J. Dowling,et al.  Membrane Traffic and Muscle: Lessons from Human Disease , 2008, Traffic.

[34]  J. Golden,et al.  Kindlin-2 Is an Essential Component of Intercalated Discs and Is Required for Vertebrate Cardiac Structure and Function , 2008, Circulation research.

[35]  Hiromi Hirata,et al.  The zebrafish ennui behavioral mutation disrupts acetylcholine receptor localization and motor axon stability , 2008, Developmental neurobiology.

[36]  Melissa Hardy,et al.  The Tol2kit: A multisite gateway‐based construction kit for Tol2 transposon transgenesis constructs , 2007, Developmental dynamics : an official publication of the American Association of Anatomists.

[37]  P. Carmeliet,et al.  Overexpression of mutant superoxide dismutase 1 causes a motor axonopathy in the zebrafish. , 2007, Human molecular genetics.

[38]  J. Glass,et al.  Axonal Degeneration in Motor Neuron Disease , 2007, Neurodegenerative Diseases.

[39]  Hiromi Hirata,et al.  Zebrafish relatively relaxed mutants have a ryanodine receptor defect, show slow swimming and provide a model of multi-minicore disease , 2007, Development.

[40]  A. Echaniz-Laguna,et al.  Sodium Valproate Exerts Neuroprotective Effects In Vivo through CREB-Binding Protein-Dependent Mechanisms But Does Not Improve Survival in an Amyotrophic Lateral Sclerosis Mouse Model , 2007, The Journal of Neuroscience.

[41]  C. Franzini-armstrong,et al.  Differential requirement for MuSK and dystroglycan in generating patterns of neuromuscular innervation , 2007, Proceedings of the National Academy of Sciences.

[42]  D. Cleveland,et al.  ALS: A Disease of Motor Neurons and Their Nonneuronal Neighbors , 2006, Neuron.

[43]  R. Oppenheim,et al.  Complete Dissociation of Motor Neuron Death from Motor Dysfunction by Bax Deletion in a Mouse Model of ALS , 2006, The Journal of Neuroscience.

[44]  S. Ennis,et al.  ANG mutations segregate with familial and 'sporadic' amyotrophic lateral sclerosis , 2006, Nature Genetics.

[45]  R. Balice-Gordon,et al.  In Vivo Imaging of Preferential Motor Axon Outgrowth to and Synaptogenesis at Prepatterned Acetylcholine Receptor Clusters in Embryonic Zebrafish Skeletal Muscle , 2006, The Journal of Neuroscience.

[46]  J. Sanes,et al.  Neuromuscular synapses can form in vivo by incorporation of initially aneural postsynaptic specializations , 2005, Development.

[47]  R. Balice-Gordon,et al.  Neuromuscular synaptogenesis in wild-type and mutant zebrafish. , 2005, Developmental biology.

[48]  T. Gillingwater,et al.  A mutation in the vesicle-trafficking protein VAPB causes late-onset spinal muscular atrophy and amyotrophic lateral sclerosis. , 2004, American journal of human genetics.

[49]  A. Ludolph,et al.  Point mutations of the p150 subunit of dynactin (DCTN1) gene in ALS , 2004, Neurology.

[50]  K. Kawakami,et al.  A transposon-mediated gene trap approach identifies developmentally regulated genes in zebrafish. , 2004, Developmental cell.

[51]  John W Griffin,et al.  DNA/RNA helicase gene mutations in a form of juvenile amyotrophic lateral sclerosis (ALS4). , 2004, American journal of human genetics.

[52]  J. Glass,et al.  Amyotrophic lateral sclerosis is a distal axonopathy: evidence in mice and man , 2004, Experimental Neurology.

[53]  U. Monani,et al.  Molecular, Cellular and Developmental Biology Program – Specialization 2018/2019 , 2017 .

[54]  E. Feldman,et al.  Delivery of an Adenoviral Vector to the Crushed Recurrent Laryngeal Nerve , 2003, The Laryngoscope.

[55]  Shin J. Oh,et al.  Mutant dynactin in motor neuron disease , 2003, Nature Genetics.

[56]  T. Maures,et al.  Structural, biochemical, and expression analysis of two distinct insulin-like growth factor I receptors and their ligands in zebrafish. , 2002, Endocrinology.

[57]  M. Imperiale,et al.  Neuronal survival following remote adenovirus gene delivery. , 2002, Journal of neurosurgery.

[58]  M. Pericak-Vance,et al.  Erratum: The gene encoding alsin, a protein with three guanine-nucleotide exchange factor domains, is mutated in a form of recessive amyotrophic lateral sclerosis (Nature Genetics (2001) 29 (160-165)) , 2001 .

[59]  E. Feldman,et al.  Remote Delivery of rAAV‐GFP to the Rat Brainstem Through the Recurrent Laryngeal Nerve , 2001, The Laryngoscope.

[60]  M. Pericak-Vance,et al.  The gene encoding alsin, a protein with three guanine-nucleotide exchange factor domains, is mutated in a form of recessive amyotrophic lateral sclerosis , 2001, Nature Genetics.

[61]  S. Scherer,et al.  A gene encoding a putative GTPase regulator is mutated in familial amyotrophic lateral sclerosis 2 , 2001, Nature Genetics.

[62]  P. Stieg,et al.  Functional role of caspase-1 and caspase-3 in an ALS transgenic mouse model. , 2000, Science.

[63]  P. Caroni,et al.  Early and Selective Loss of Neuromuscular Synapse Subtypes with Low Sprouting Competence in Motoneuron Diseases , 2000, The Journal of Neuroscience.

[64]  H Okamoto,et al.  High-frequency generation of transgenic zebrafish which reliably express GFP in whole muscles or the whole body by using promoters of zebrafish origin. , 1997, Developmental biology.

[65]  M. Farrell,et al.  Promoter analysis in living zebrafish embryos identifies a cis-acting motif required for neuronal expression of GATA-2. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[66]  M. Dubois‐Dauphin,et al.  Bcl-2 overexpression prevents motoneuron cell body loss but not axonal degeneration in a mouse model of a neurodegenerative disease , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[67]  M. Gurney,et al.  Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation. , 1994, Science.

[68]  J. Haines,et al.  Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis , 1993, Nature.

[69]  S. Hadano,et al.  A gene encoding a putative GTPase regulator is mutated in familial amyotrophic lateral sclerosis 2 , 2001, Nature Genetics.

[70]  M. Westerfield The zebrafish book : a guide for the laboratory use of zebrafish (Danio rerio) , 1995 .