[De novo mutations in SYNGAP1 associated with non-syndromic mental retardation]

Med Sci (Paris). 2010 Feb;26(2):133-5. doi: 10.1051/medsci/2010262133.
[Article in French]
No abstract available

Publication types

  • News

MeSH terms

  • Animals
  • Child
  • Cognition Disorders / genetics
  • GTPase-Activating Proteins / genetics*
  • Humans
  • Intellectual Disability / genetics*
  • Learning Disabilities / genetics
  • Memory Disorders / genetics
  • Mice
  • Mice, Knockout
  • Models, Neurological
  • Neuronal Plasticity / genetics
  • Point Mutation*
  • Receptors, N-Methyl-D-Aspartate / physiology
  • Signal Transduction / genetics
  • Signal Transduction / physiology
  • Synaptic Transmission / genetics
  • Synaptic Transmission / physiology
  • ras GTPase-Activating Proteins / deficiency
  • ras GTPase-Activating Proteins / genetics

Substances

  • GTPase-Activating Proteins
  • Receptors, N-Methyl-D-Aspartate
  • SYNGAP1 protein, human
  • Syngap1 protein, mouse
  • ras GTPase-Activating Proteins