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BDNF activates phosphorylated ERK. 32 / 32
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"When ERK1/2 phosphorylation was analyzed we found that BDNF treatment induced a robust and similar activation (~ 140%) of p-ERK1/2 in GFP and GFP-p75 STHdh 7/7Q cells (XREF_FIG)."

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"BDNF stimulation at the RGC soma increased both p-ERK5 and p-ERK1/2 (P = 0.035 and P = 0.032, respectively; n = 6; at 48 hours)."

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"BDNF robustly activated p-ERK and p-Akt within 0.5-2 hr and p-CREB within 0.5-6 hr of infusion into the dmPFC."

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"The pERK signal increase induced by BDNF or bFGF remained quantitatively similar in betaII-spectrin knockdown neurons as compared to wild type neurons (XREF_SUPPLEMENTARY, XREF_SUPPLEMENTARY and XREF_SUPPLEMENTARY), suggesting that the MPS does not act downstream of these RTKs, but likely affects their transactivation by CB1 and NCAM1."

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"Of note, we also observed that BDNF treatment strongly increased the intensity of nuclear p-ERK1/2 signal, an effect that was potentiated in cells overexpressing PLD1-GFP (XREF_FIG)."

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"In the next set of experiments we analyzed whether exogenous BDNF application increases pERK and pCREB in the nucleus of hippocampal primary neurons of Jacob and Nsmf ko mice."

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"Eph forward signaling induces ERK activation within the neurites while impairs BDNF induced p-ERK activation and its subsequent nuclear translocation."

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"A two-way ANOVA found that the i.v. drug (cocaine vs saline; F (1,25) = 4.61, p < 0.05) and the intracranial infusion (BDNF vs PBS; F (1,25) = 14.61, p < 0.001) had significant main effects on pERK (XREF_FIG) but there was no interaction between drug and infusion (F (1,25) = 1.01, p = 0.32) because BDNF increased pERK in the presence or absence of cocaine."

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"BDNF induced pERK is a downstream signaling component directly associated with TrkB activation that is enhanced through TrkB-SKF mediated co-activation of synaptic NMDA receptors."

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"Eph forward signaling induces ERK activation within the neurites while impairs BDNF induced p-ERK activation and its subsequent nuclear translocation."

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"We further found that phospho-ERK was increased by BDNF treatment in wild-type cultures, but not in EndophilinA TKO cultures, indicating specific BDNF-TrkB dependent signaling deficits in EndophilinA TKOs."

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"XREF_BIBR Most strikingly, the BDNF induced nuclear import of pERK, which likely acts upstream of CREB, was clearly reduced in Jacob deficient neurons."

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"Confirmation that 0.05 and 0.005 mug/0.5 mul of TCN-201 or 0.2 and 2 mug/0.5 mul of Ro-25-6981 infused 20 min before BDNF (0.75 mug/0.5 mul and side) prevented the ability of BDNF to increase phospho-[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"A marked increase of phosphorylated Erk 1/2 is observed when WT TrkB HEK293 cells are treated with BDNF and DeltaIgTrkB HEK293 cells (XREF_FIG) albeit at significantly lower levels when compared to the BDNF stimulated WT TrkB (XREF_FIG)."

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"Additionally, BDNF signaling through TrkB has been shown to activate pERK and lead to an increase in the clock genes BMAL1, CLOCK, and PER1, as well as Per1 mRNA in spinal neurons after spinal cord injury."

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"TCN-201 infusion into the prelimbic cortex inhibited the BDNF mediated increase in pERK and pGluN2A whereas Ro-25-6981 infusion into the prelimbic cortex blocked BDNF induced elevation of pERK and pGluN2B, indicating that both GluN2A- and GluN2B containing NMDA receptors underlie BDNF induced ERK activation."

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"Further, there was no significant difference in active lever pressing between rats infused with vehicle and PBS, TCN-201 and PBS, or Ro-25-6981 and PBS (p> 0.05), further confirming that the doses of [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Consistently, BDNF-induced p-ERK activation was also blocked by U0126 ( xref )."

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"This was not associated with phosphorylation of ERK in GnRH-immunoreactive cells, though BDNF treatment did stimulate pERK in neighbouring non GnRH cells."

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"Further, a single BDNF infusion into dmPFC abrogated the decrease of p-ERK and p-CREB in the dmPFC and normalized a disturbance in glutamate transmission in the nucleus accumbens that resulted in long-term inhibition of cocaine seeking behaviors."

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"Compared with the control group, expression of TrkB, Erk1/2, and phosphorylated Erk1/2 were markedly increased in cells treated with BDNF, particularly in the ACR + BDNF group."

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"BAPTA-AM suppresses p-Akt, but not p-ERK in BDNF stimulated neurons; KCl leads to p-Akt dephosphorylation and ERK phosphorylation; co-application of KCl with BDNF causes Akt dephosphorylation without affecting BDNF stimulated p-ERK."

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"In Experiment 2, drug-naive rats with bilateral intra-dmPFC cannulae received an intracranial infusion of BDNF or PBS and were euthanized by rapid decapitation 0.5 hr, 2 hrs, or 6 hrs post-infusion in order to demonstrate the time course over which intradmPFC BDNF would increase p-ERK, p-CREB, and p-Akt in vivo in the dmPFC (XREF_FIG)."

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"Finally, we found that rapamycin did not block BDNF induced up-regulation of p-ERK or p-Akt (XREF_FIG), despite the fact that rapamycin blocks BDNF induced phosphorylation at both Thr389 and Thr421 and Ser424 (XREF_FIG)."

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"Peripheral BDNF increases pERK and/or pCREB in the adult hippocampus and ventral striatum."

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"Confirmation that 0.05 and 0.005 mug/0.5 mul of TCN-201 or 0.2 and 2 mug/0.5 mul of Ro-25-6981 infused 20 min before BDNF (0.75 mug/0.5 mul and side) prevented the ability of BDNF to increase phospho-ERK expression in a dose dependent manner two hr later is presented in XREF_SUPPLEMENTARY and XREF_SUPPLEMENTARY."

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"Wahlin et al. found that injections of CNTF, BDNF, or FGF2 activated detectable signal transduction (pCREB, pERK, and cFOS) only in cells of the mature rodent INL [XREF_BIBR]."

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"In addition to attenuating reinstatement to cocaine seeking, BDNF infusion into the dorsomedial PFC elevates BDNF and phospho-ERK expression in the NAc."

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"Although BDNF (at 10 ng/ml) induced up-regulation of p-CREB and p-ERK1/2 at all developmental stages, DIV 7 neurons showed the most dynamic changes (5.8-fold induction for p-CREB; 14.1-fold induction for p-ERK1/2) (XREF_FIG)."

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"BDNF causes an early increase in pERK after addition to the medium which returns to baseline by 30 minutes after treatment."

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"In cultured RGCs, KLF9 requires expression of Dusp14 to suppress RGC axon growth, and knockdown of Dusp14 activity in vivo using adeno-associated virus 2 short hairpin ribonucleic acid (AAV2-anti-Dusp14-shRNA) increased BDNF-induced pERK signaling, RGC survival and the number and length of regenerating axons after optic nerve crush ."

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"We further found that Dusp14 shRNA significantly increased the number of BDNF induced pERK positive cells (XREF_FIG C, XREF_FIG D) and increased BDNF dependent pERK signaling (XREF_FIG E, XREF_FIG F)."