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AKT3 — NTF3

Text-mined interactions from Literome

Roux et al., J Biol Chem 2001 : The p75 neurotrophin receptor activates Akt ( protein kinase B ) through a phosphatidylinositol 3-kinase dependent pathway
Mograbi et al., J Biol Chem 2001 : Glial cell line derived neurotrophic factor stimulated phosphatidylinositol 3-kinase and Akt activities exert opposing effects on the ERK pathway : importance for the rescue of neuroectodermic cells
Ness et al., Mol Cell Neurosci 2002 : IGF-I or NT-3, but not CNTF, prevented apoptosis of pro-OLs by 24 h via a PI3-kinase dependent pathway ; however, only IGF-I protected pro-OLs from glutamate toxicity through 48 h. Long-term protection of pro-OLs by IGF-I was correlated with sustained activation of Akt while NT-3 activation of Akt was transient
Ness et al., Dev Neurosci 2002 : In addition, we also present data showing that IGF-I and NT-3 differentially activate their receptors and Akt depending on the maturational stage of the oligodendrocyte
Liot et al., Exp Neurol 2004 (MAP Kinase Signaling System) : Neurotrophin-3 induced PI-3 kinase/Akt signaling rescues cortical neurons from apoptosis ... First, we showed that, in cultured cortical neurons, NT-3 could promote extracellular signal regulated protein kinase/mitogen activated protein kinase ( ERK/MAPK ) and phosphatidylinositol-3' (PI-3) kinase/Akt phosphorylation
Leeds et al., Neurochem Int 2005 : BDNF, but not NT-3 , treatment of immature CGC caused a marked, but transient activation of Akt through phosphatidylinositol (PI) 3-kinase
Je et al., J Neurosci 2005 : Using neuromuscular junction ( NMJ ) as a model system, we identified three characteristic features required for long-term, but not acute, forms of synaptic modulation by neurotrophin-3 (NT-3) : endocytosis of NT-3-receptor complex, activation of the PI3 kinase substrate Akt , and new protein synthesis
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
Lim et al., Biochem Biophys Res Commun 2007 (MAP Kinase Signaling System) : However, the mechanisms by which neurotrophin-3 promotes prolonged Akt/MAPK signaling at an early stage are not well understood
Wang et al., Neurosci Lett 2008 : The hypothesis that neurotrophic factor dependent activation of Akt would regulate hexokinase association with the mitochondria was tested and quantitative Western blotting showed no effect of blockade of the phosphoinositide 3-kinase ( PI 3-kinase ) /Akt pathway using the inhibitor LY294002, indicating this interaction of hexokinase with mitochondria was not neurotrophic factor or Akt dependent
Li et al., Int J Dev Neurosci 2008 : Moreover, Akt phosphorylation was enhanced and 6-OHDA induced chromatin condensation was suppressed by NT-3
Chuenkova et al., Science signaling 2009 : Here, we show that in the cytosol, parasite derived neurotrophic factor ( PDNF ), a trans-sialidase that is located on the surface of T. cruzi, is both a substrate and an activator of the serine-threonine kinase Akt , an antiapoptotic molecule
Ceni et al., J Cell Sci 2010 : Neurons and PC12 cells lacking p75NTR display defects in neurotrophin dependent Akt activation
Je et al., Molecular brain 2011 (Synaptic Transmission) : Previously, we demonstrated that the long-term synaptic modulation requires the endocytosis of neurotrophin-receptor complex, the activation of PI3K and Akt , and mTOR mediated protein synthesis
Kommaddi et al., FASEB J 2011 : We show that Trk induced ADAM17 phosphorylation and generation of the p75NTR ( ICD ) is required for neurotrophin induced Erk and Akt activation and for neurotrophin dependent survival signaling
Hwang et al., J Agric Food Chem 2011 : Hesperetin also stimulated the activation of Akt , ERK, and CREB as well as induced brain derived neurotrophic factor , PPAR? coactivator 1a ( PGC-1a ), and seladin-1 ( selective Alzheimer 's disease indicator-1 ) via both ER and TrkA in the cells
Meuchel et al., Cardiovasc Res 2011 : Both BDNF and NT3 increased phosphorylation of Akt and endothelial NO synthase (eNOS)
Ivanov et al., Oncogene 2013 (Carcinoma, Adenoid Cystic...) : NT-3 stimulation of U2OS cells with ectopic TrkC expression triggered TrkC phosphorylation and resulted in Ras, Erk 1/2 and Akt activation, as well as VEGFR1 phosphorylation