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EPHB2 — NTRK1

Text-mined interactions from Literome

Fukumoto et al., J Biol Chem 2000 : In these transfectant cells, a continuous phosphorylation of TrkA and the activation of ERK1/2 without NGF treatment were observed
Jiang et al., J Mol Neurosci 2001 : A double cysteine trkA mutant exhibiting reduced NGF binding and delayed Erk signaling
Dey et al., Exp Cell Res 2005 : These data suggest a distinct requirement for CSK in the regulation of NGF/TrkA activation of RAS, RAC, ERK , and AKT via the differential control of SFKs in the orchestration of neuronal differentiation
Personett et al., Curr Neurovasc Res 2007 (Neuroblastoma) : Clones from the BF expressed high levels of the tyrosine kinase type A (TrkA) receptor expression and activation of the mitogen activated kinase ERK2 upon treatment with nerve growth factor
Akpan et al., Brain Res 2008 (Chagas Disease) : It also requires TrkA dependent PI3K and MAPK/Erk signaling pathways because PDNF stimulation of cholinergic transcripts is abolished by specific pharmacological inhibitors
Yamada et al., J Pharmacol Sci 2008 : Analysis of the common features of the augmented pathways suggests that TrkA is most likely to be the primary target of MCC-257 and that both ERK and Akt may be involved in the cellular effects of this compound
Eisinger et al., FEBS Lett 2008 (Glioma...) : Because inhibition of TrkA activation by AG879 completely blocked DOR- and integrin mediated ERK1/2 signaling, the present results indicate that in NG108-15 cells DOR stimulated ERK1/2 activation is mediated by integrin induced transactivation of TrkA
Clewes et al., J Neurochem 2008 : Surprisingly, binding of the pro region alone to TrkA , at a site other than that of NGF, caused TrkA and ERK1/2 phosphorylation
Wu et al., Growth Factors 2008 : These results demonstrated that CTGF induces production of fractalkine, MCP-1 and RANTES via ERK1/2 and PI3-K/PKB/NF-kappaB dependent signal pathway mediated by cell surface heparin sulfate proteoglycans and the tyrosine kinase receptor TrkA in human mesangial cells
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
Alsina et al., PloS one 2012 (MAP Kinase Signaling System) : At molecular level, our findings indicate that ectopic expression of a mutated form of Spry4 ( Y53A ), in which a conserved tyrosine residue was replaced, fail to block both TrkA mediated Erk/MAPK activation and neurite outgrowth induced by NGF, suggesting that an intact tyrosine 53 site is required for the inhibitory effect of Spry4 on NGF signaling
Tam et al., Blood 1997 : NGF stimulation of HMC-1 cells induced tyrosine phosphorylation of TrkA protein, increased expression of the early response genes c-fos and NGF1-A, and activation of ERK-mitogen activated protein ( MAP ) kinase, results which indicate that TrkA receptors in HMC-1 cells are fully functional