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Wnt pathway anomalies in developing amygdalae of Turner syndrome-like mice
Journal of Molecular Neuroscience (2007)
  • A. S. Raefski
  • Benjamin Carone, Rowan University
  • A. Kaur
  • W. Krueger
  • M. J. O'Neill
Certain neurobehavioral deficiencies associated with Turner Syndrome have been attributed to brain volumetric abnormalities, particularly of the amygdala. Haplo-insufficiency of a non-dosage compensated gene or genes on the X chromosome has been hypothesized to be the cause of the neuroanatomical defect. We examined gene expression levels of 6,628 genes in developing amygdalae of late-stage embryos of a mouse model for Turner Syndrome. In total, 161 genes show significant differences in expression level between TS and normal female amygdala. In silico pathway analysis of both X-linked and autosomal mis-regulated genes suggests that modulation of Wnt signaling is a critical factor in the normal growth and development of the amygdala.
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A. S. Raefski, Benjamin Carone, A. Kaur, W. Krueger, et al.. "Wnt pathway anomalies in developing amygdalae of Turner syndrome-like mice" Journal of Molecular Neuroscience Vol. 32 Iss. 2 (2007) p. 111 - 119
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