Glycogen synthase kinase-3 beta,(GSK-3 beta), is anenzyme that in humans is encoded by theGSK3Bgene.[5][6] In mice, the enzyme is encoded by the Gsk3b gene.[7] Abnormal regulation and expression of GSK-3 beta is associated with an increased susceptibility towardsbipolar disorder.[8]
Glycogen synthase kinase-3 (GSK-3) is a proline-directedserine-threonine kinase that was initially identified as aphosphorylating and an inactivating agent ofglycogen synthase. Two isoforms, alpha (GSK3A) and beta, show a high degree of amino acid homology.[5] GSK3B is involved in energy metabolism, neuronal cell development, and body pattern formation.[9][10] It might be a new therapeutic target for ischemic stroke.
Homozygous disruption of the Gsk3b locus in mice results in embryonic lethality during mid-gestation.[7] This lethality phenotype could be rescued by inhibition oftumor necrosis factor.[7]
Two SNPs at this gene, rs334558 (-50T/C) and rs3755557 (-1727A/T), are associated with efficacy oflithium treatment inbipolar disorder.[11]
Pharmacological inhibition ofERK1/2 restores GSK-3 beta activity and protein synthesis levels in a model oftuberous sclerosis.[12]
GSK3B has been shown tointeract with:
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