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. |