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BDNF — CAMK1

Text-mined interactions from Literome

Suzuki et al., J Neurosci 2005 : Consequently, when calcineurin was inhibited by its inhibitor FK506 under the depolarizing condition, the CaMK mediated increase in BDNF became a stimulatory signal, and the endogenous BDNF autocrine system was capable of upregulating NR2C mRNA via the common TrkB-ERK cascade
Fortin et al., J Neurosci 2012 : 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
Blanquet et al., J Biol Chem 1997 : In addition, we find that : ( i ) the time course of BDNF action is not accompanied by a change in the spectrum of either alpha- and beta-subunits of CaMK2 detected by immunoblotting ; ( ii ) both treatment of solubilized CaMK2 with alkaline phosphatase and treatment of immunoprecipitated CaMK2 with protein phosphatase 1 reverse phosphorylation and activation of the kinase ; ( iii ) phospholipase C inhibitor D609 and intracellular Ca2+ chelation by 1,2-bis- ( o-aminophenoxy ) ethane-N, N,N '', N ', -tetracetic acid tetra ( acetoxymethyl ) ester or 8- ( diethylamino ) octyl-3,4,5-trimethoxybenzoate but not omission of Ca2+ or Ca2+ chelation by EGTA, abolish the stimulatory effect of BDNF on phosphorylation and activation of CaMK2