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GSK-3Glycogen Synthase Kinase-3
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GSK-3 was originally demonstrated to play an important role in regulating glycogen synthesis, as one of the molecular events involved in insulin signaling.
GSK-3 can be phosphorylated and inhibited by cyclic AMP- (cAMP-) dependent protein kinase/protein kinase A (PKA) in the presence of high cAMP levels, following glucagon or adrenaline stimulus.
In fact, when GSK-3 phosphorylates cyclin D1 at threonine 286 and c-myc at threonine 58 they undergo ubiquitylation and proteolytic degradation.
Lucas, "Neuronal apoptosis and motor deficits in mice with genetic inhibition of GSK-3 are Fas-dependent," PLoS ONE, vol.
Alonso, "Glycogen synthase kinase 3 (GSK-3) inhibitors as new promising drugs for diabetes, neurodegeneration, cancer, and inflammation," Medicinal Research Reviews, vol.
All of the above evidences imply that GSK-3 may be linked to both A[beta] production and tau hyperphosphorylation during the course of diabetes.
Phospho-GS peptide, a specific GSK-3 substrate, was obtained from Upstate Biotechnology Inc.
A[beta] deposition is an important mechanism in both AD and diabetes, and GSK-3 plays an important role in regulation of A[beta] production.
Portanto a inibicao da GSK-3 mantem eIF2B ativo, estimulando sintese proteica.
Portanto a inibicao da GSK-3 impede a degradacao da [beta]-catenina que mantem sua atividade transcricional (Hinoi e colaboradores, 2000; Peifer e colaboradores, 1994).
"I don't believe anyone would have imagined that deleting GSK-3 would have such dramatic effects on neural stem cells," Nature quoted senior study author Dr William D.
During the study, the researchers genetically engineered mice to lack both forms of the GSK-3 gene, designated alpha and beta.