Loss of GSK-3 Causes Abnormal Astrogenesis and Behavior in Mice.
Omaha, United States. In Mol Neurobiol, Aug 2015
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.
Molecular mechanisms of thrombopoietin signaling.
San Diego, United States. In J Thromb Haemost, 2009
Additional signals activated by these secondary mediators include mammalian target of rapamycin, beta-catenin, hypoxia-inducible factor 1alpha and the homeobox proteins HOXB4 and HOXA9, and a number that are reduced, including glycogen synthase kinase 3alpha and the FOXO3 family of forkhead proteins.