Research Topics
Genomes and GenesSpecies | Hiromi HirataSummaryAffiliation: University of Michigan Country: USA Publications
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Detail Information
Publications
[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...
Zebrafish bandoneon mutants display behavioral defects due to a mutation in the glycine receptor beta-subunitHiromi 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...- Na(v)1.6a is required for normal activation of motor circuits normally excited by tactile stimulationSean 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... - The zebrafish ennui behavioral mutation disrupts acetylcholine receptor localization and motor axon stabilityLouis 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... - The zebrafish shocked gene encodes a glycine transporter and is essential for the function of early neural circuits in the CNSWilson 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... - TRPM7 is required within zebrafish sensory neurons for the activation of touch-evoked escape behaviorsSean 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... - Non-sense mutations in the dihydropyridine receptor beta1 gene, CACNB1, paralyze zebrafish relaxed mutantsWeibin 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... - accordion, a zebrafish behavioral mutant, has a muscle relaxation defect due to a mutation in the ATPase Ca2+ pump SERCA1Hiromi 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... 
Identification and expression of voltage-gated calcium channel beta subunits in ZebrafishWeibin 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...- Impaired fatty acid utilization in thioredoxin binding protein-2 (TBP-2)-deficient mice: a unique animal model of Reye syndromeShin 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... - Zebrafish relatively relaxed mutants have a ryanodine receptor defect, show slow swimming and provide a model of multi-minicore diseaseHiromi 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... - The basic helix-loop-helix genes Hesr1/Hey1 and Hesr2/Hey2 regulate maintenance of neural precursor cells in the brainMasami 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... - Periodic repression by the bHLH factor Hes7 is an essential mechanism for the somite segmentation clockYasumasa 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...