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NGF — SRC

Text-mined interactions from Literome

Wooten et al., Mol Cell Biol 2000 : Expression of dominant negative mutants of either Src ( DN2 ) or Ras ( Asn-17 ) impaired activation of PKC-iota by NGF
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
Obara et al., J Cell Sci 2004 : The activation of Rap1 by both cAMP and NGF was blocked by PP2, an inhibitor of Src family kinases, and by a Src mutant incapable of being phosphorylated by PKA ( SrcS17A ), consistent with the requirement of PKA phosphorylation of Src at S17 in these actions ... These results strongly indicate that PKA phosphorylation of Src at S17 is essential for cAMP and NGF signaling in PC12 cells and identify PKA as an important downstream target of NGF
Qiu et al., Dev Growth Differ 2004 : These results are consistent with the recent experimental evidence that persistent tyrosine receptor kinase A (TrkA) activity is necessary to maintain transcription in the differentiating PC12 cells ( Chang et al. 2003 ) and a sustained Src kinase activity is detected in response to NGF stimulation ( Gatti 2003 )
Kremer et al., J Cell Biol 1991 : These data demonstrate the involvement of both pp60c-src and p21c-ras proteins in NGF and FGF actions in PC12 cells, and establish a physiological role for the pp60c-src tyrosine kinase in signal transduction pathways initiated by receptor tyrosine kinases in these cells