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Interaction IDMol ATypeSpeciesVerbNatureMol BTypeSpecies
104733Phosphoinositide-3-kinaseMulti subunitHomo sapiens-eInhibits activityindirectGSK3BProteinHomo sapiens-e
Here, we report that inhibition of ERK1/2 increased the basal activity of GSK3beta in cortical neurons and that both ERK1/2 and PI3K were required for brain-derived neurotrophic factor (BDNF) suppression of GSK3beta activity. / Interestingly, PI3K (but not ERK1/2) induced the inhibitory phosphorylation of GSK3beta at Ser-9.
Structure
Regulator
104736BDNFProteinHomo sapiens-eInhibits activityindirectGSK3BProteinHomo sapiens-e
Here, we report that inhibition of ERK1/2 increased the basal activity of GSK3beta in cortical neurons and that both ERK1/2 and PI3K were required for brain-derived neurotrophic factor (BDNF) suppression of GSK3beta activity.
143778GSK3BProteinHomo sapiens-ePhosphorylatedirectMAPTProteinHomo sapiens
The phosphorylation of the longest isoform of recombinant human brain tau, tau(441), at various sites was detected by Western blots and by radioimmuno-dot-blot assay with phosphorylation-dependent and site-specific tau antibodies. We found that cdk5 phosphorylated tau(441) at Thr-181, Ser-199, Ser-202, Thr-205, Thr-212, Ser-214, Thr-217, Thr-231, Ser-235, Ser-396, and Ser-404, but not at Ser-262, Ser-400, Thr-403, Ser-409, Ser-413, or Ser-422. GSK-3beta phosphorylated all the cdk5-catalyzed sites above except Ser-235. Deglycosylation by glycosidases depressed the subsequent phosphorylation of AD-tau (i) with cdk5 at Thr-181, Ser-199, Ser-202, Thr-205, and Ser-404, but not at Thr-212; and (ii) with GSK-3beta at Thr-181, Ser-202, Thr-205, Ser-217, and Ser-404, but not at Ser-199, Thr-212, Thr-231, or Ser-396. These data suggest that aberrant glycosylation of tau in AD might be involved in neurofibrillary degeneration by promoting abnormal hyperphosphorylation by cdk5 and GSK-3beta.
Structure
Disease
Regulator
153055GSK3BProteinHomo sapiens-eDecreases expressionindirectAPPProteinHomo sapiens-e
Here we report that GSK3 and CDK5 are involved in APP processing in a divergent manner. Specific inhibition of cellular GSK3 by lithium or GSK3beta antisense elicits a reduction in Abeta. / Moreover, oral administration of lithium significantly reduces Abeta production whereas direct ICV administration of roscovitine augmented Abeta production in the brains of PDAPP (APP(V717F)) mice. Our data support a function for both GSK3 and CDK5 in APP processing, further implicating these two kinases in the pathogenesis of Alzheimer's disease.
Disease
440503AKTProteinHomo sapiensDecreases activityindirectGSK3BProteinHomo sapiens
In the present studies, we examined the relationship between Akt and T212/S214 in primary cultures of human neurons and astrocytes, and evaluated the contribution of two other kinases. / In comparison, okadaic acid treatment severely depleted the content of GSK3beta and downregulated the remaining GSK3beta activity by Akt-dependent inhibition, consistent with minimal changes in phospho-T212.

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