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AKT1 — NGF
Text-mined interactions from Literome
Fletcher et al., J Cell Biol 2000
:
Despite prolonged
Akt and ERK signaling
induced by
NGF after BAF treatment has prevented death, the neurons fail to increase protein synthesis, recover ATP levels, or grow
Burry et al., J Neurosci Res 2001
(MAP Kinase Signaling System) :
However,
NGF stimulated phosphorylation of ERK, p38, and
Akt in PC12-N09rasWT cells is similar in duration to that in PC12-N09 cells, indicating that the p21(ras) signaling through ERK, p38, and Akt was not involved in the restoration of normal neurite elongation in PC12-N09 cells
Egea et al., J Cell Biol 2001
:
We have found that reduction of intracellular Ca2+ concentration or functional blockade of CaM abolished
NGF induced activation of
PKB in PC12 cells
Bui et al., J Neurochem 2002
(Pheochromocytoma) :
Treatment with the blocking anti-p75 antibody also inhibited
NGF induced activation of the survival kinase
Akt
Yanai et al., Invest Ophthalmol Vis Sci 2002
:
Basic fibroblast growth factor, keratinocyte growth factor,
nerve growth factor , and hepatocyte growth factor stimulated cell proliferation but did not
induce Akt activation or protect the cells from SNP induced apoptosis
Mills et al., J Neurosci 2003
:
NGF mediated stimulation of phosphorylation of both
AKT and the Tau kinase glycogen synthase kinase-3 ( GSK-3 ) was inhibited in the presence of KP-392 and after overexpression of ILK-DN
Ito et al., J Neurosci Res 2003
:
Furthermore, anti-p75 neutralizing antibody reduced
NGF induced phosphorylation of
Akt in PC12 cells under the serum-free condition
Salvarezza et al., J Neurochem 2003
:
NGF activated
AKT and ERKs in single embryonic P-neurons, as assayed by immunofluorescence of phosphorylated proteins
Borgatti et al., J Cell Physiol 2003
:
NGF increased rapidly and transiently the enzymatic activity of immunoprecipitable nuclear
Akt and after 45 min the values returned to a level close to the basal one
Chang et al., J Biol Chem 2003
:
NGF regulated both extracellular regulated kinases 1/2 and
Akt activity in the differentiated PC12 cells via sustained TrkA activity
Wang et al., J Biol Chem 2004
:
PC12 cells stably overexpressing SH2-Bbeta, which exhibit enhanced NGF induced neuronal differentiation compared with control cells, showed enhanced and prolonged
NGF induced phosphorylation of Akt on Ser473 and
Akt enzymatic activity ... Surprisingly,
NGF induced phosphorylation of
Akt on Ser473 and Akt activity were not altered in cells overexpressing SH2-Bbeta ( R555E ) with a defective SH2 domain, despite the ability of the overexpressed SH2-Bbeta ( R555E ) to block NGF induced differentiation
Steinle et al., Auton Neurosci 2003
:
NGF stimulation
resulted in activation of ERK1/2,
Akt , and Src in choroidal endothelial cells, while little phosphorylation was noted following NGF treatment in retinal endothelial cells
Zhuang et al., J Neurosci 2004
(Hyperalgesia...) :
Capsaicin and
NGF induce phosphorylation of the PI3K downstream target
AKT ( protein kinase B ), which is blocked by the PI3K inhibitors LY294002 and wortmannin, indicative of the activation of PI3K by both agents
Ahn et al., EMBO J 2004
:
PI ( 3,4,5 ) P3 alone mimics the antiapoptotic activity of
NGF , for which nuclear
Akt is
required
Kim et al., Mol Cells 2004
:
The PI3-K inhibitors wortmannin and LY294002 blocked
NGF induced
Akt phosphorylation as well as neurite outgrowth
Wu et al., Cell Signal 2005
:
Here, we investigated the possible involvement of G ( i/o ) proteins in
nerve growth factor (NGF) induced pro-survival phosphatidylinositol-3-kinase
(PI3K)/Akt signaling in rat pheochromocytoma PC12 cells ... The
NGF dependent
Akt activation was partially attenuated by PTX or overexpression of regulators of G protein signaling Z1 ( RGSZ1 ) and Galpha interacting protein (GAIP) ), indicating the participation of G ( i/o ) proteins ... Expression of PTX-resistant mutants of Galpha ( i1 ), Galpha ( i3 ), Galpha ( oA ), and Galpha ( oB ), but not Galpha ( i2 ), abolished the inhibitory effect of PTX on
NGF induced
Akt activation ... This is the first study that demonstrates the involvement of G ( i/o ) proteins in
NGF induced
Akt signaling
Dixon et al., Biochim Biophys Acta 2006
:
While FRS3 over-expression in PC12 cells neither increases
NGF induced neuritogenesis nor activation of Map
kinase/AKT , comparable to previous reports on FRS2, over-expression of a chimeric adapter containing the PH/PTB domains of the insulin receptor substrate (IRS) 2, in place of the PTB domain of FRS3 ( IRS2-FRS3 ) supports insulin dependent Map kinase activation and neurite outgrowth in PC12 cells
Wang et al., J Neurochem 2006
:
Suppression of NEAP by RNA interference enhanced
NGF induced neurite outgrowth and
Akt activation
Perez-Pinera et al., Mol Cell Biochem 2007
(Adenocarcinoma...) :
Interestingly, inhibition of neurotrophin receptor signaling using K252a prevents
Akt activation in
response to
NGF or BDNF, induces apoptotic cell death, and diminishes the ability of A549 cells to growth in soft agar
Park et al., J Biol Chem 2007
:
Specifically,
NGF enhanced TrkA phosphorylation, PI3K activity, and
Akt phosphorylation
Tucker et al., Cell Signal 2008
:
Inhibition of either Src or FAK activity attenuated both laminin and/or
NGF induced PI
3-K/Akt and MEK/MAPK signalling pathways, as well as neurite growth
de Melo Reis et al., Brain Res 2008
:
Murine Müller glial conditioned medium ( MMG ) was concentrated and at 1 : 1 dilution supported 100 % survival of chick or rat sympathetic neurons after 48 h compared to < 5 % in controls. Partial purification of the MMG using centriprep concentrators showed that trophic activity is from molecules above 10 kDa. MMG stimulated
AKT , ERK and pStat3 in sympathetic neurons. Sympathetic or DRG neuronal survival induced by MMG was
blocked by anti-human
NGF , but not by anti-human CNTF ( sympathetic ) or by anti-BDNF ( DRGs ) neutralizing antibodies. MMG also induced neurite outgrowth in P4 mice retinal explants and on isolated RGC. RGCs plated on top of Müller glia cells had a much better survival rate ( > 80 %, 96 h ) compared to laminin+poly-L-lysine substrates
Koch et al., Oncogene 2008
(Cell Transformation, Neoplastic...) :
Knockdown of expression of Bcr-Abl using small interfering RNA technique also enhanced
NGF mediated
Akt phosphorylation, indicating that Bcr-Abl kinase modifies NGF signaling directly
Mantuano et al., J Biol Chem 2008
:
FP3 blocked activation of
Akt and ERK/MAP kinase in
response to
nerve growth factor-beta (NGF-beta) but not FP6
Good et al., J Biol Chem 2008
(MAP Kinase Signaling System) :
NGF induced a 2-fold increase in phosphorylation of
Akt , a PI3K target linked to mTOR activation, and a 2.2-fold increase in the activity of p70 S6 kinase, a downstream effector of mTOR
Yamada et al., J Pharmacol Sci 2008
:
We describe here our finding that the
NGF induced phosphorylation of both ERK and
Akt are accelerated by MCC-257
Mérot et al., Endocrinology 2009
:
Importantly, 17betaE2 has no impact on
NGF induced activity of MAPK and
Akt signaling pathways
Kawashima et al., J Nutr Biochem 2010
:
Phosphorylated-Akt expression was significantly increased in EPA treated cells, and
nerve growth factor withdrawal
induced increases in cell death and caspase-3 activity were suppressed by EPA treatment
Maures et al., Mol Endocrinol 2009
:
We show that depleting endogenous SH2B1 using short hairpin RNA against SH2B1 inhibits
NGF dependent neurite outgrowth, but not NGF mediated phosphorylation of
Akt or ERKs 1/2
Chung et al., J Biol Chem 2010
(Cystitis...) :
Suppression of endogenous
NGF level with neutralizing NGF antibody significantly
blocked the increased activity of
Akt , JNK, and ERK1/2 in the inflamed bladder during cystitis ... These results indicate that endogenous
NGF plays an important role in the activation of
Akt and MAPK in the urinary bladder and in bladder hypertrophy during cystitis
Kim et al., Neurochem Int 2010
:
Additionally, NPPB and SITS, another chloride channel blocker, suppressed
NGF induced TrkA phosphorylation and subsequent
PI3K/Akt phosphorylation and Rac1 activation in PC12 cells
Niewiadomska et al., Behav Brain Res 2011
(Alzheimer Disease) :
NGF released from target cells activates TrkA on axon terminals and
triggers activation of
PI3K/Akt , MEK/ERK, and PLC? ( phospholipase C ) signaling pathways
Jeon et al., Neurochem Int 2010
:
Inhibition of PI3K and Rac1 abolished the
NGF induced
Akt activation , indicating that Akt is at the downstream of PI3K and Rac1
Lu et al., Brain Pathol 2010
(Disease Models, Animal) :
On one hand,
NGF/TrkA induced activation of
Akt and ERK1/2, which led to neuronal survival ; on the other hand, NGF/TrkA mediated CaMKII and CREB phosphorylation and increased PSD95 expression, which improved cognitive performance
Rao et al., Mol Cancer Ther 2010
(Leukemia, Myeloid, Acute) :
Exposure to 17-DMAG inhibited
NGF induced p-TrkA,
p-AKT , and p-ERK1/2 levels, as well as induced apoptosis of K562, 32D cells with ectopic expression of wild-type TrkA or the constitutively active mutant Delta TrkA, and of primary myeloid leukemia cells
Ho et al., Cancer Lett 2011
(Neuroblastoma) :
Exogenous
NGF induced greater phosphorylation of TrkA and
AKT
Liu et al., Exp Mol Med 2013
:
Similar to the changes in neurite outgrowth, the
PI3K/Akt activation by
NGF was potentiated by PIP5Ka KD, but was attenuated by the reintroduction of PIP5Ka ... Moreover, exogenously applied PIP2 to PIP5Ka KD cells also suppressed
Akt activation by
NGF
Wuhanqimuge et al., FEBS open bio 2013
:
Lysophosphatidylcholine enhances
NGF induced MAPK and
Akt signals through the extracellular domain of TrkA in PC12 cells
Andjelković et al., Eur J Biochem 1998
:
We therefore asked whether stimulation of neuronal cells with
nerve growth factor (NGF) , on which certain types of neurons are dependent for survival,
causes activation of
PKB ... Stimulation of serum starved PC12 rat pheochromocytoma cells with
NGF caused an increase of up to 14-fold in
PKB activity