Hiromi Hirata

Summary

Affiliation: University of Michigan
Country: USA

Publications

  1. ncbi request reprint [Locomotion research with zebrafish]
    Hiromi Hirata
    Division of Biological Science, Graduate School of Science, Nagoya University, Furo cho, Chikusa ku, Nagoya, 464 8602 Japan
    Nihon Shinkei Seishin Yakurigaku Zasshi 27:127-34. 2007
  2. pmc Zebrafish bandoneon mutants display behavioral defects due to a mutation in the glycine receptor beta-subunit
    Hiromi Hirata
    Department of Molecular, Cellular, and Developmental Biology, University of Michigan, Ann Arbor, MI 48109 1048, USA
    Proc Natl Acad Sci U S A 102:8345-50. 2005
  3. ncbi request reprint The zebrafish ennui behavioral mutation disrupts acetylcholine receptor localization and motor axon stability
    Louis Saint-Amant
    Department of Molecular, Cellular and Developmental Biology, University of Michigan, MI, USA
    Dev Neurobiol 68:45-61. 2008
  4. pmc Na(v)1.6a is required for normal activation of motor circuits normally excited by tactile stimulation
    Sean E Low
    Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48109 1048, USA
    Dev Neurobiol 70:508-22. 2010
  5. pmc Stac3 is a component of the excitation-contraction coupling machinery and mutated in Native American myopathy
    Eric J Horstick
    Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109, USA
    Nat Commun 4:1952. 2013
  6. ncbi request reprint The zebrafish shocked gene encodes a glycine transporter and is essential for the function of early neural circuits in the CNS
    Wilson W Cui
    University of Michigan, Ann Arbor, Michigan 48109, USA
    J Neurosci 25:6610-20. 2005
  7. pmc TRPM7 is required within zebrafish sensory neurons for the activation of touch-evoked escape behaviors
    Sean E Low
    Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, Michigan, 48109 1048, USA
    J Neurosci 31:11633-44. 2011
  8. ncbi request reprint accordion, a zebrafish behavioral mutant, has a muscle relaxation defect due to a mutation in the ATPase Ca2+ pump SERCA1
    Hiromi Hirata
    Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109 0720, USA
    Development 131:5457-68. 2004
  9. ncbi request reprint Non-sense mutations in the dihydropyridine receptor beta1 gene, CACNB1, paralyze zebrafish relaxed mutants
    Weibin Zhou
    Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, 48109 1048, USA
    Cell Calcium 39:227-36. 2006
  10. ncbi request reprint Identification and expression of voltage-gated calcium channel beta subunits in Zebrafish
    Weibin Zhou
    Department of Molecular Biology, University of Michigan, Ann Arbor, Michigan 48109 1048, USA
    Dev Dyn 237:3842-52. 2008

Collaborators

Detail Information

Publications14

  1. ncbi request reprint [Locomotion research with zebrafish]
    Hiromi Hirata
    Division of Biological Science, Graduate School of Science, Nagoya University, Furo cho, Chikusa ku, Nagoya, 464 8602 Japan
    Nihon Shinkei Seishin Yakurigaku Zasshi 27:127-34. 2007
    ..Interestingly, both of these mutants exhibited similar simultaneous bilateral muscle contraction and shortening of the tail in response to touch...
  2. pmc Zebrafish bandoneon mutants display behavioral defects due to a mutation in the glycine receptor beta-subunit
    Hiromi Hirata
    Department of Molecular, Cellular, and Developmental Biology, University of Michigan, Ann Arbor, MI 48109 1048, USA
    Proc Natl Acad Sci U S A 102:8345-50. 2005
    ..Because GlyR mutations in humans lead to hyperekplexia, a motor disorder characterized by startle responses, the zebrafish beo mutant should be a useful animal model for this condition...
  3. ncbi request reprint The zebrafish ennui behavioral mutation disrupts acetylcholine receptor localization and motor axon stability
    Louis Saint-Amant
    Department of Molecular, Cellular and Developmental Biology, University of Michigan, MI, USA
    Dev Neurobiol 68:45-61. 2008
    ..These results suggest that ennui is important for nerve-dependent AChR clustering and the stability of axon growth...
  4. pmc Na(v)1.6a is required for normal activation of motor circuits normally excited by tactile stimulation
    Sean E Low
    Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48109 1048, USA
    Dev Neurobiol 70:508-22. 2010
    ..Interestingly fictive swimming could be initiated pharmacologically suggesting that a swim circuit was present in mutants. These results suggested that Na(V)1.6a was required for touch-induced activation of the swim locomotor network...
  5. pmc Stac3 is a component of the excitation-contraction coupling machinery and mutated in Native American myopathy
    Eric J Horstick
    Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109, USA
    Nat Commun 4:1952. 2013
    ..Analysis of NAM stac3 in zebrafish shows that the NAM mutation decreases excitation-contraction coupling. These findings enhance our understanding of both excitation-contraction coupling and the pathology of myopathies...
  6. ncbi request reprint The zebrafish shocked gene encodes a glycine transporter and is essential for the function of early neural circuits in the CNS
    Wilson W Cui
    University of Michigan, Ann Arbor, Michigan 48109, USA
    J Neurosci 25:6610-20. 2005
    ..Furthermore, physiological analysis after manipulation of glycinergic activity in wild-type and sho embryos suggests that the mutant phenotype is attributable to elevated extracellular glycine within the CNS...
  7. pmc TRPM7 is required within zebrafish sensory neurons for the activation of touch-evoked escape behaviors
    Sean E Low
    Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, Michigan, 48109 1048, USA
    J Neurosci 31:11633-44. 2011
    ..Collectively, these findings are consistent with a role for zebrafish TRPM7 within sensory neurons in the modulation of neurotransmitter release at central synapses, similar to that proposed for mammalian TRPM7 at peripheral synapses...
  8. ncbi request reprint accordion, a zebrafish behavioral mutant, has a muscle relaxation defect due to a mutation in the ATPase Ca2+ pump SERCA1
    Hiromi Hirata
    Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109 0720, USA
    Development 131:5457-68. 2004
    ..As SERCA1 mutations in humans lead to Brody disease, an exercise-induced muscle relaxation disorder, zebrafish accordion mutants could be a useful animal model for this condition...
  9. ncbi request reprint Non-sense mutations in the dihydropyridine receptor beta1 gene, CACNB1, paralyze zebrafish relaxed mutants
    Weibin Zhou
    Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, 48109 1048, USA
    Cell Calcium 39:227-36. 2006
    ..The structural and functional homology of CACNB1 in zebrafish and mammals, suggests that zebrafish can be useful for studying EC coupling and potential neuronal function of CACNB1...
  10. ncbi request reprint Identification and expression of voltage-gated calcium channel beta subunits in Zebrafish
    Weibin Zhou
    Department of Molecular Biology, University of Michigan, Ann Arbor, Michigan 48109 1048, USA
    Dev Dyn 237:3842-52. 2008
    ..Sequence homology, genomic synteny and expression patterns suggest that there are three pairs of duplicate genes for beta2, beta3, and beta4 in zebrafish with distinct expression patterns during embryonic development...
  11. ncbi request reprint Zebrafish relatively relaxed mutants have a ryanodine receptor defect, show slow swimming and provide a model of multi-minicore disease
    Hiromi Hirata
    Graduate School of Science, Nagoya University, Nagoya 464 8602, Japan
    Development 134:2771-81. 2007
    ..These findings suggest that zebrafish relatively relaxed mutants may be useful for understanding the development and physiology of MmD...
  12. ncbi request reprint Impaired fatty acid utilization in thioredoxin binding protein-2 (TBP-2)-deficient mice: a unique animal model of Reye syndrome
    Shin ichi Oka
    Cell Dynamics Research Group, Research Institute for Cell Engineering, National Institute of Advanced Industrial Science and Technology AIST, Midorigaoka, Ikeda, Osaka, Japan
    FASEB J 20:121-3. 2006
    ..Because the fatal impairment of fatty acid utilization is a characteristically metabolic feature of Reye (-like) syndrome, TBP-2-/- mouse may represent a novel model for investigating the pathophysiology of these disorders...
  13. ncbi request reprint The basic helix-loop-helix genes Hesr1/Hey1 and Hesr2/Hey2 regulate maintenance of neural precursor cells in the brain
    Masami Sakamoto
    Institute for Virus Research, Kyoto University, Kyoto 606 8507, Japan
    J Biol Chem 278:44808-15. 2003
    ..These results indicate that Hesr1 and Hesr2 negatively regulate neuronal bHLH genes, promote maintenance of neural precursor cells, and increase late-born cell types in the developing brain...
  14. pmc Periodic repression by the bHLH factor Hes7 is an essential mechanism for the somite segmentation clock
    Yasumasa Bessho
    Institute for Virus Research, Kyoto University, Kyoto 606 8507, Japan
    Genes Dev 17:1451-6. 2003
    ..Thus, periodic repression by Hes7 protein is critical for the cyclic transcription of Hes7 and Lfng, and this negative feedback represents a molecular basis for the segmentation clock...