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BDNF — GRIA1
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Xiong et al., Neuropharmacology 2002
(MAP Kinase Signaling System) :
Additionally, the mitogen activated protein ( MAP ) kinase inhibitor PD98059 enhances
BDNF induced
glutamate receptor-1 (GluR1) protein expression, but a phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 strongly reduces BDNF induced GluR1 protein expression
Wu et al., Brain Res Mol Brain Res 2004
:
Brain derived neurotrophic factor acutely
enhances tyrosine phosphorylation of the AMPA receptor subunit
GluR1 via NMDA receptor dependent mechanisms ... Activation of trkB receptors was critical as k252-a, an inhibitor of trk receptor tyrosine kinase, blocked the
BDNF activated
GluR1 phosphorylation ... Our findings suggest that
BDNF mediated
GluR1 tyrosine phosphorylation potentially regulates synaptic plasticity postsynaptically through NR2B subunits of the NMDA receptor
Caldeira et al., J Biol Chem 2007
:
Under the same conditions,
BDNF induced
GluR1 phosphorylation on Ser-831 through activation of protein kinase C and Ca ( 2+ ) -calmodulin dependent protein kinase II
Slipczuk et al., PloS one 2009
:
IN CONCLUSION, OUR FINDINGS DEMONSTRATE THAT : 1 ) mTOR mediated mRNA translation is required for memory consolidation during at least two restricted time windows ; 2 ) this kinase acts downstream
BDNF in the hippocampus and ; 3 ) it
controls the increase of synaptic
GluR1 necessary for memory consolidation
Fortin et al., J Neurosci 2012
:
GluA1 surface expression
induced by
BDNF , as assessed by immunocytochemistry using an extracellular N-terminal GluA1 antibody or by surface biotinylation, was impaired following knockdown of CaMKK or treatment with STO-609 ... Activation of CaMKK by BDNF requires transient receptor potential canonical ( TRPC ) channels as SKF-96365, but not the NMDA receptor antagonist d-APV, prevented
BDNF induced
GluA1 surface expression as well as phosphorylation of CaMKI, AKT ( T308 ), and mTOR