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Interaction IDMol ATypeSpeciesVerbNatureMol BTypeSpecies
21555BDNFProteinHomo sapiens-eIncreases activityindirectAKTFamilyHomo sapiens-e
BDNF and NMDA increased Akt phosphorylation within 5 minutes but maximal activation by NMDA was observed at 3 hours.
Regulator
439996Phosphoinositide-3-kinaseProteinRattus norvegicusIncreases activityindirectAKTProteinRattus norvegicus
Neuroprotective effects of the synthetic cannabinoid HU-210 in primary cortical neurons are mediated by phosphatidylinositol 3-kinase/AKT signaling. / The neurotoxin S-AMPA induced significant death of rat primary cortical neurons, which was inhibited by the CB agonist HU-210. / HU-210 triggered activation of AKT, but not activation of the ERK1/2, JNK or p38 signaling pathways. The phosphatidylinositol 3-kinase (PI 3-K) inhibitors LY294002 and wortmannin prevented phosphorylation of AKT in response to HU-210, and reversed the neuroprotective effect of HU-210 on S-AMPA-induced excitotoxicity.
Regulator
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.