Hideki Enomoto

Summary

Affiliation: RIKEN Brain Science Institute
Country: Japan

Publications

  1. ncbi GFRalpha1 expression in cells lacking RET is dispensable for organogenesis and nerve regeneration
    Hideki Enomoto
    Department of Pathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neuron 44:623-36. 2004
  2. ncbi Regulation of neural development by glial cell line-derived neurotrophic factor family ligands
    Hideki Enomoto
    RIKEN Center for Developmental Biology, Kobe, Hyogo, Japan
    Anat Sci Int 80:42-52. 2005
  3. ncbi Death comes early: apoptosis observed in ENS precursors
    H Enomoto
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe, Japan
    Neurogastroenterol Motil 21:684-7. 2009
  4. pmc Autonomic neurocristopathy-associated mutations in PHOX2B dysregulate Sox10 expression
    Mayumi Nagashimada
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe, Japan
    J Clin Invest 122:3145-58. 2012
  5. doi Neural precursor death is central to the pathogenesis of intestinal aganglionosis in Ret hypomorphic mice
    Toshihiro Uesaka
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe 650 0047, Japan
    J Neurosci 30:5211-8. 2010
  6. doi GDNF signaling levels control migration and neuronal differentiation of enteric ganglion precursors
    Toshihiro Uesaka
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe 650 0047, Japan, Department of Development and Regeneration, Graduate School of Medicine, Osaka University, Osaka 565 0871, Japan, and Division of Neural Differentiation and Regeneration, Department of Physiology and Cell Biology, Graduate School of Medicine, Kobe University, Kobe 650 0017, Japan
    J Neurosci 33:16372-82. 2013
  7. pmc Diminished Ret expression compromises neuronal survival in the colon and causes intestinal aganglionosis in mice
    Toshihiro Uesaka
    Laboratory for Neuronal Differentiation and Regeneration and Laboratory for Cellular Morphogenesis, RIKEN Center for Developmental Biology, Kobe, Japan
    J Clin Invest 118:1890-8. 2008
  8. ncbi The neurotrophic effects of glial cell line-derived neurotrophic factor on spinal motoneurons are restricted to fusimotor subtypes
    Thomas W Gould
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe 650 0047, Japan
    J Neurosci 28:2131-46. 2008
  9. ncbi Conditional ablation of GFRalpha1 in postmigratory enteric neurons triggers unconventional neuronal death in the colon and causes a Hirschsprung's disease phenotype
    Toshihiro Uesaka
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe 650 0047, Japan
    Development 134:2171-81. 2007
  10. ncbi Trans-mesenteric neural crest cells are the principal source of the colonic enteric nervous system
    Chihiro Nishiyama
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe, Japan
    Nat Neurosci 15:1211-8. 2012

Collaborators

Detail Information

Publications15

  1. ncbi GFRalpha1 expression in cells lacking RET is dispensable for organogenesis and nerve regeneration
    Hideki Enomoto
    Department of Pathology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neuron 44:623-36. 2004
    ..Thus RET-independent GFRalpha1 is dispensable for organogenesis and nerve regeneration in vivo, indicating that trans-signaling and GFRalpha-dependent NCAM signaling play a minor role physiologically...
  2. ncbi Regulation of neural development by glial cell line-derived neurotrophic factor family ligands
    Hideki Enomoto
    RIKEN Center for Developmental Biology, Kobe, Hyogo, Japan
    Anat Sci Int 80:42-52. 2005
    ..The deciphering of GDNF family ligand signaling in neural cells promises to provide vital new insights into the development and pathology of the nervous system...
  3. ncbi Death comes early: apoptosis observed in ENS precursors
    H Enomoto
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe, Japan
    Neurogastroenterol Motil 21:684-7. 2009
    ..Thus, unlike the neurons themselves, ENS precursors do undergo apoptosis, which may, by regulating the size of the ENS precursor pool, be a crucial factor in determining the final cell number in the ENS...
  4. pmc Autonomic neurocristopathy-associated mutations in PHOX2B dysregulate Sox10 expression
    Mayumi Nagashimada
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe, Japan
    J Clin Invest 122:3145-58. 2012
    ..Our results also demonstrate that Sox10 regulation by PHOX2B is pivotal for the development and pathogenesis of the autonomic ganglia...
  5. doi Neural precursor death is central to the pathogenesis of intestinal aganglionosis in Ret hypomorphic mice
    Toshihiro Uesaka
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe 650 0047, Japan
    J Neurosci 30:5211-8. 2010
    ..These results indicate that ENCC death is a principal cause of intestinal aganglionosis in a Ret hypomorphic state, and suggest that the inhibition of cell death is a route to the prevention of HSCR...
  6. doi GDNF signaling levels control migration and neuronal differentiation of enteric ganglion precursors
    Toshihiro Uesaka
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe 650 0047, Japan, Department of Development and Regeneration, Graduate School of Medicine, Osaka University, Osaka 565 0871, Japan, and Division of Neural Differentiation and Regeneration, Department of Physiology and Cell Biology, Graduate School of Medicine, Kobe University, Kobe 650 0017, Japan
    J Neurosci 33:16372-82. 2013
    ....
  7. pmc Diminished Ret expression compromises neuronal survival in the colon and causes intestinal aganglionosis in mice
    Toshihiro Uesaka
    Laboratory for Neuronal Differentiation and Regeneration and Laboratory for Cellular Morphogenesis, RIKEN Center for Developmental Biology, Kobe, Japan
    J Clin Invest 118:1890-8. 2008
    ..Thus, enteric neuron survival is sensitive to RET dosage, and cell death is potentially involved in the etiology of HSCR...
  8. ncbi The neurotrophic effects of glial cell line-derived neurotrophic factor on spinal motoneurons are restricted to fusimotor subtypes
    Thomas W Gould
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe 650 0047, Japan
    J Neurosci 28:2131-46. 2008
    ..Therefore, although GDNF influences several aspects of MN development, the survival-promoting effects of GDNF during programmed cell death are mostly confined to spindle-innervating MNs...
  9. ncbi Conditional ablation of GFRalpha1 in postmigratory enteric neurons triggers unconventional neuronal death in the colon and causes a Hirschsprung's disease phenotype
    Toshihiro Uesaka
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe 650 0047, Japan
    Development 134:2171-81. 2007
    ..This study reveals an essential role for GFRalpha1 in the survival of enteric neurons and suggests that caspase-independent death can be triggered by abolition of neurotrophic signals...
  10. ncbi Trans-mesenteric neural crest cells are the principal source of the colonic enteric nervous system
    Chihiro Nishiyama
    Laboratory for Neuronal Differentiation and Regeneration, RIKEN Center for Developmental Biology, Kobe, Japan
    Nat Neurosci 15:1211-8. 2012
    ..The discovery of this trans-mesenteric ENCC population provides a basis for improving our understanding of ENS development and pathogenesis...
  11. pmc RET signaling is required for survival and normal function of nonpeptidergic nociceptors
    Judith P Golden
    Washington University Pain Center, Department of Anesthesiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 30:3983-94. 2010
    ..8 CKO mice. The results of this study identify the physiological role of endogenous Ret signaling in the survival and function of nociceptors...
  12. ncbi GDNF availability determines enteric neuron number by controlling precursor proliferation
    Scott Gianino
    Department of Pediatrics, Washington University School of Medicine, St Louis, MO 63110, USA
    Development 130:2187-98. 2003
    ..All of these heterozygous mice, however, have striking problems with intestinal contractility and neurotransmitter release, demonstrating that Ret signaling is critical for both ENS structure and function...
  13. pmc Differential gene expression and functional analysis implicate novel mechanisms in enteric nervous system precursor migration and neuritogenesis
    Bhupinder P S Vohra
    Department of Pediatrics, Washington University School of Medicine, St Louis, MO 63110, USA
    Dev Biol 298:259-71. 2006
    ..These results provide an extensive set of ENS biomarkers, demonstrate a role for SNARE proteins in ENS development and highlight additional candidate genes that could modify Hirschsprung's disease penetrance...
  14. ncbi Dok-6, a Novel p62 Dok family member, promotes Ret-mediated neurite outgrowth
    Robert J Crowder
    Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Biol Chem 279:42072-81. 2004
    ..Taken together, these data identify Dok-6 as a novel Dok-4/5-related adaptor molecule that may function in vivo to transduce signals that regulate Ret-mediated processes such as axonal projection...
  15. ncbi Neural cells in the esophagus respond to glial cell line-derived neurotrophic factor and neurturin, and are RET-dependent
    Hui Yan
    Department of Anatomy and Cell Biology, University of Melbourne, Parkville, 3010 Victoria, Australia
    Dev Biol 272:118-33. 2004
    ..Moreover, like intestinal neurons, the development of esophageal neurons is largely Ret-dependent...