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Publication : Wnt pathway anomalies in developing amygdalae of Turner syndrome-like mice.

First Author  Raefski AS Year  2007
Journal  J Mol Neurosci Volume  32
Issue  2 Pages  111-9
PubMed ID  17873295 Mgi Jnum  J:128588
Mgi Id  MGI:3767520 Doi  10.1007/s12031-007-0022-7
Citation  Raefski AS, et al. (2007) Wnt pathway anomalies in developing amygdalae of Turner syndrome-like mice. J Mol Neurosci 32(2):111-9
abstractText  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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