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- W893812942 abstract "Altered activity of glycogen synthase kinase-3 (GSK-3) is associated with psychiatric diseases and neurodegenerative diseases. GSK-3 is a key regulator in multiple aspects of neuronal differentiation in the brain. However, little is known about the role of GSK-3 in astrocyte development. To examine the role of GSK-3 in astrocytes, we generated a conditional knockout mouse using a glial fibrillary acidic protein (GFAP)-cre driver, in which the GSK-3 alpha and beta genes are deleted in astrocytes. We found that GFAP-cre-mediated GSK-3 deletion led to a larger brain. The number and size of astrocytes were increased in GSK-3 mutant brains. The levels of GFAP and phospho-STAT3, indicators of astrogenesis, were elevated in GSK-3 mutants. Furthermore, we found upregulation of astrocyte regulatory molecules such as phospho-AKT, phospho-S6, and cyclin D in GSK-3 mutant brains. Finally, GSK-3 mutant mice exhibited aberrant anxiety and social behavior. Our results suggest that GSK-3 plays a significant role in astrocyte development and behavioral control in mice." @default.
- W893812942 created "2016-06-24" @default.
- W893812942 creator A5032792166 @default.
- W893812942 creator A5043489973 @default.
- W893812942 creator A5089512011 @default.
- W893812942 date "2015-07-17" @default.
- W893812942 modified "2023-09-25" @default.
- W893812942 title "Loss of GSK-3 Causes Abnormal Astrogenesis and Behavior in Mice" @default.
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- W893812942 doi "https://doi.org/10.1007/s12035-015-9326-8" @default.
- W893812942 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4716001" @default.
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