Gene interactions and pathways from curated databases and text-mining

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FGFR3 — IGF1

Pathways - manually collected, often from reviews:

  • WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway: EFNA1/FGF1/FGF11/FGF10/EFNA2/EGF/FGF12/CSF1/ANGPT4/ANGPT2/ANGPT1/VEGFA/EFNA3/EFNA4/EFNA5/FGF14/FGF19/FGF17/FGF18/FGF2/FGF3/FGF4/FGF6/FGF7/FGF8/FGF9/FIGF/HGF/IGF1/INS/INS/KITLG/VEGFC/VEGFB/PDGFB/PGF/PDGFA/NGF/PDGFC/FGF21/FGF22/PDGFD/FGF20/FGF16 → FGFR2/KDR/INSR/FGFR3/IGF1R/KIT/FGFR1/EPHA2/EGFR/CSF1R/FGFR4/FLT1/FLT4/NGFR/MET/PDGFRA/PDGFRB/TEK (activation)

Text-mined interactions from Literome

Seto et al., Neuroscience 2002 (Synaptic Transmission) : The effects of IGF-I on hippocampal ACh release was sensitive to the Na ( + ) channel blocker tetrodotoxin, suggesting that IGF-I might act indirectly via the release of other transmitters/modulators ... In the present study, we have characterized the possible involvement of GABA in IGF-I mediated inhibition of ACh release and measured the effects of this growth factor on choline acetyltransferase (ChAT) activity and high-affinity choline uptake in the hippocampus of the adult rat brain ... IGF-I ( 10 nM ) inhibited K ( + ) - as well as veratridine evoked ACh release from rat hippocampal slices and the effect is possibly mediated via the activation of a typical IGF-I receptor and the subsequent phosphorylation of the insulin receptor substrate-1 (IRS-1) ... The inhibitory effects of IGF-I on hippocampal ACh release were not additive to those of either muscimol or baclofen, but were attenuated by GABA antagonists, bicuculline and phaclofen ... Furthermore, the evidence that effects of IGF-I could be modulated, at least in part, by GABA antagonists suggest that the release of GABA and the activation of its receptors may possibly be involved in mediating the inhibitory effects of IGF-I on hippocampal ACh release
Nilsson et al., Neurosci Lett 1988 : Insulin ( 1.8 x 10 ( -8 ) to 5.3 x 10 ( -8 ) M ), similarly, did not have any influence on the release of [ 3H ] ACh, demonstrating that the facilitatory effect of IGF-1 on [ 3H ] ACh release is not mediated via insulin receptors
Nilsson-HÃ¥kansson et al., Neuroreport 1993 : The effects of intact IGF-1 , truncated IGF-1 and Gly-Pro-Glu ( GPE ), the aminoterminal tripeptide of IGF-1, on the potassium ( 35 mM K+ ) stimulated release of acetylcholine (ACh) from rat cortical slices were investigated ... GPE significantly increased the release of ACh in the dose range of 10 ( -10 ) -10 ( -6 ) M, while IGF-1 significantly enhanced the release of ACh only at 4 x 10 ( -8 ) M