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Interaction IDMol ATypeSpeciesVerbNatureMol BTypeSpecies
2160BDNFProteinHomo sapiens-eIncreases expressionindirectSYPProteinHomo sapiens-e
BDNF also increased the levels of the vesicle proteins synaptophysin, synaptobrevin, and synaptotagmin, without affecting the presynaptic membrane proteins syntaxin and SNAP-25, or the vesicle-binding protein synapsin-I.
3819BDNFProteinHomo sapiens-eIncreases activitydirectNTRK2ProteinHomo sapiens-e
This signal has been shown to promote the granule cell survival through BDNF-mediated TrkB activation, leading to Purkinje cell differentiation by increasing the granule-Purkinje cell interaction.
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
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.
120146BDNFProteinHomo sapiens-eIncreases activityindirectPhosphoinositide-3-kinaseMulti subunitHomo sapiens-e
These results indicate that the activation of TrkB by BDNF induces the activation of PI3-K via IRS-1 and -2 rather than by a direct interaction of TrkB with PI3-K in cultured cortical neurons.
Regulator
185794BDNFProteinHomo sapiens-eDecreases activityindirectCasp3ProteinRattus norvegicus
We measured the neurotoxicity of two antipsychotic drug treatments, haloperidol and risperidone, in primary cultured rat cortical neurons. / Treatment with haloperidol also led the reduction of phosphorylation levels of Akt, and activated caspase-3. / Moreover, brain-derived neurotrophic factor (BDNF) reduced the caspase-3 activity and protected neurons from haloperidol-induced apoptosis. BDNF also reversed the reduced levels of phosphorylation of Akt caused by treatment with haloperidol.