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NeuroD is required for differentiation of the granule cells in the cerebellum and hippocampus.

NeuroD, a bHLH transcription factor, is implicated in differentiation of neurons and pancreatic beta cells. NeuroD-null mice die shortly after birth due to severe neonatal diabetes. To examine if there is postnatal neuronal phenotype in these mice, we rescued them from neonatal lethality by introducing a transgene encoding the mouse neuroD gene under the insulin promoter. These mice survive to adulthood but display severe neurological phenotype due to neuronal deficit in the granule layers of the cerebellum and hippocampus. We show here that NeuroD is required for these postnatally generated microneurons to undergo proper differentiation, the absence of which results in cell death.

Pubmed ID: 10398678


  • Miyata T
  • Maeda T
  • Lee JE


Genes & development

Publication Data

July 1, 1999

Associated Grants

  • Agency: NINDS NIH HHS, Id: R01NS35118

Mesh Terms

  • Animals
  • Apoptosis
  • Basic Helix-Loop-Helix Transcription Factors
  • Cell Count
  • Cell Differentiation
  • Cerebellum
  • Genetic Therapy
  • Hippocampus
  • In Situ Nick-End Labeling
  • Insulin
  • Mice
  • Mice, Knockout
  • Mice, Neurologic Mutants
  • Mice, Transgenic
  • Nerve Tissue Proteins
  • Neurons
  • Phenotype
  • Promoter Regions, Genetic
  • Recombinant Fusion Proteins
  • Transgenes