Glen B Banks

Summary

Affiliation: University of Washington
Country: USA

Publications

  1. ncbi request reprint Elucidating the molecular mechanisms that underlie the target control of motoneuron death
    Glen B Banks
    Department of Physiology Pharmacology, School of Biomedical Sciences, and SRC Bioinformatics and Applied Genomics, University of Queensland, Australia
    Int J Dev Biol 46:551-8. 2002
  2. pmc Truncated dystrophins can influence neuromuscular synapse structure
    Glen B Banks
    Department of Neurology, Senator Paul D Wellstone Muscular Dystrophy Cooperative Research Center, University of Washington, Seattle, Washington 98195, USA
    Mol Cell Neurosci 40:433-41. 2009
  3. ncbi request reprint Relevance of motoneuron specification and programmed cell death in embryos to therapy of ALS
    Glen B Banks
    Department of Neurology, University of Washington, Seattle, Washington 98195, USA
    Birth Defects Res C Embryo Today 75:294-304. 2005
  4. pmc Molecular and cellular adaptations to chronic myotendinous strain injury in mdx mice expressing a truncated dystrophin
    Glen B Banks
    Department of Neurology, Senator Paul D Wellstone Muscular Dystrophy Cooperative Research Center, University of Washington, Seattle, WA 98195, USA
    Hum Mol Genet 17:3975-86. 2008
  5. doi request reprint The value of mammalian models for duchenne muscular dystrophy in developing therapeutic strategies
    Glen B Banks
    Department of Neurology, University of Washington, Seattle, Washington, USA
    Curr Top Dev Biol 84:431-53. 2008
  6. ncbi request reprint rAAV6-microdystrophin rescues aberrant Golgi complex organization in mdx skeletal muscles
    Justin M Percival
    Department of Physiology and Biophysics, University of Washington, Box 357290, 1959 NE Pacific Street, Seattle, WA 98195, USA
    Traffic 8:1424-39. 2007
  7. pmc Expression of the dystrophin isoform Dp116 preserves functional muscle mass and extends lifespan without preventing dystrophy in severely dystrophic mice
    Luke M Judge
    Department of Neurology, University of Washington, 1959 NE Pacific St, Seattle, WA 98195 7720, USA
    Hum Mol Genet 20:4978-90. 2011
  8. pmc Successful regional delivery and long-term expression of a dystrophin gene in canine muscular dystrophy: a preclinical model for human therapies
    Zejing Wang
    Program in Transplantation Biology, Division of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA, USA
    Mol Ther 20:1501-7. 2012
  9. pmc Sequencing protocols to genotype mdx, mdx(4cv), and mdx(5cv) mice
    Glen B Banks
    Department of Neurology, University of Washington, Mail Stop 357720, 1959 NE Pacific St, Seattle, Washington 98195, USA
    Muscle Nerve 42:268-70. 2010
  10. doi request reprint Preclinical studies for gene therapy of Duchenne muscular dystrophy
    Guy L Odom
    Department of Neurology, University of Washington School of Medicine, Seattle, Washington 98195 7720, USA
    J Child Neurol 25:1149-57. 2010

Collaborators

Detail Information

Publications17

  1. ncbi request reprint Elucidating the molecular mechanisms that underlie the target control of motoneuron death
    Glen B Banks
    Department of Physiology Pharmacology, School of Biomedical Sciences, and SRC Bioinformatics and Applied Genomics, University of Queensland, Australia
    Int J Dev Biol 46:551-8. 2002
    ..Such interactions, along with intact synaptic basal lamina, may help to regulate the supply and presentation of trophic factors to motoneurons...
  2. pmc Truncated dystrophins can influence neuromuscular synapse structure
    Glen B Banks
    Department of Neurology, Senator Paul D Wellstone Muscular Dystrophy Cooperative Research Center, University of Washington, Seattle, Washington 98195, USA
    Mol Cell Neurosci 40:433-41. 2009
    ....
  3. ncbi request reprint Relevance of motoneuron specification and programmed cell death in embryos to therapy of ALS
    Glen B Banks
    Department of Neurology, University of Washington, Seattle, Washington 98195, USA
    Birth Defects Res C Embryo Today 75:294-304. 2005
    ..Here we review the clinical relevance of studying motoneuron specification and death during embryonic development...
  4. pmc Molecular and cellular adaptations to chronic myotendinous strain injury in mdx mice expressing a truncated dystrophin
    Glen B Banks
    Department of Neurology, Senator Paul D Wellstone Muscular Dystrophy Cooperative Research Center, University of Washington, Seattle, WA 98195, USA
    Hum Mol Genet 17:3975-86. 2008
    ..We suggest that changes in protein expression and the formation of rings are adaptations to myotendinous strain injury that help to prevent muscle necrosis and retain the function of necessary muscles during injury, ageing and disease...
  5. doi request reprint The value of mammalian models for duchenne muscular dystrophy in developing therapeutic strategies
    Glen B Banks
    Department of Neurology, University of Washington, Seattle, Washington, USA
    Curr Top Dev Biol 84:431-53. 2008
    ..Although each mammalian model has its limitations, together they have been essential for the development of several treatment strategies for DMD that target dystrophin replacement, disease progression, and muscle regeneration...
  6. ncbi request reprint rAAV6-microdystrophin rescues aberrant Golgi complex organization in mdx skeletal muscles
    Justin M Percival
    Department of Physiology and Biophysics, University of Washington, Box 357290, 1959 NE Pacific Street, Seattle, WA 98195, USA
    Traffic 8:1424-39. 2007
    ..In summary, GC distribution abnormalities are a novel component of mdx skeletal muscle pathology rescued by microdystrophin expression...
  7. pmc Expression of the dystrophin isoform Dp116 preserves functional muscle mass and extends lifespan without preventing dystrophy in severely dystrophic mice
    Luke M Judge
    Department of Neurology, University of Washington, 1959 NE Pacific St, Seattle, WA 98195 7720, USA
    Hum Mol Genet 20:4978-90. 2011
    ..We conclude that both mechanical and non-mechanical functions of dystrophin are important for its role in skeletal muscle...
  8. pmc Successful regional delivery and long-term expression of a dystrophin gene in canine muscular dystrophy: a preclinical model for human therapies
    Zejing Wang
    Program in Transplantation Biology, Division of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA, USA
    Mol Ther 20:1501-7. 2012
    ....
  9. pmc Sequencing protocols to genotype mdx, mdx(4cv), and mdx(5cv) mice
    Glen B Banks
    Department of Neurology, University of Washington, Mail Stop 357720, 1959 NE Pacific St, Seattle, Washington 98195, USA
    Muscle Nerve 42:268-70. 2010
    ..This method clearly distinguishes between wildtype, heterozygous, and mutant transcripts, and thereby time and money can be saved by avoiding false positives...
  10. doi request reprint Preclinical studies for gene therapy of Duchenne muscular dystrophy
    Guy L Odom
    Department of Neurology, University of Washington School of Medicine, Seattle, Washington 98195 7720, USA
    J Child Neurol 25:1149-57. 2010
    ..It is hoped that variations on these methods might be applicable for most, if not all, of the different types of muscular dystrophy...
  11. ncbi request reprint Functional capacity of dystrophins carrying deletions in the N-terminal actin-binding domain
    Glen B Banks
    Department of Neurology, Senator Paul D Wellstone Muscular Dystrophy Cooperative Research Center, University of Washington, Seattle, WA 98195, USA
    Hum Mol Genet 16:2105-13. 2007
    ..We conclude that an intact ABD1 is required to support normal contractile properties of skeletal muscle and to protect against myofiber necrosis...
  12. pmc The polyproline site in hinge 2 influences the functional capacity of truncated dystrophins
    Glen B Banks
    Department of Neurology, Senator Paul D Wellstone Muscular Dystrophy Cooperative Research Center, University of Washington, Seattle, Washington, United States of America
    PLoS Genet 6:e1000958. 2010
    ..We conclude that the rigid alpha-helical structure of the polyproline site significantly impairs the functional capacity of truncated dystrophins to maintain appropriate connections between the cytoskeleton and extracellular matrix...
  13. doi request reprint Animal models of muscular dystrophy
    Rainer Ng
    Division of Medical Genetics, Department of Neurology, University of Washington, Seattle, Washington, USA
    Prog Mol Biol Transl Sci 105:83-111. 2012
    ....
  14. ncbi request reprint The postsynaptic submembrane machinery at the neuromuscular junction: requirement for rapsyn and the utrophin/dystrophin-associated complex
    Glen B Banks
    Department of Physiology and Biophysics, University of Washington, Seattle, WA 98195 7290, USA
    J Neurocytol 32:709-26. 2003
    ..In addition we briefly review how these studies of the neuromuscular junction relate to GABAergic and glycinergic synapses in the CNS...
  15. ncbi request reprint Neuromuscular synapses mediate motor axon branching and motoneuron survival during the embryonic period of programmed cell death
    Glen B Banks
    School of Biomedical Sciences, Department of Physiology and Pharmacology and SRC for Bio informatics and Applied Genomics, University of Queensland, 4072, St Lucia, Queensland, Australia
    Dev Biol 257:71-84. 2003
    ..Thus, agrin-induced synaptic specializations are required for skeletal muscle to effectively control motoneuron numbers during embryonic development...
  16. ncbi request reprint Glycinergic and GABAergic synaptic activity differentially regulate motoneuron survival and skeletal muscle innervation
    Glen B Banks
    School of Biomedical Sciences, University of Queensland, St Lucia, 4072 Queensland, Australia
    J Neurosci 25:1249-59. 2005
    ....
  17. ncbi request reprint Genetic disruption of the growth hormone receptor does not influence motoneuron survival in the developing mouse
    Sean A Parsons
    School of Biomedical Sciences, SRC for Bioinformatics and Applied Genomics, University of Queensland, St Lucia, Australia
    Int J Dev Biol 47:41-9. 2003
    ..This may be a result of compensation by the signalling of other neurotrophic cytokines...