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FGFR3 — MAPK3
Pathways - manually collected, often from reviews:
-
Reactome Reaction:
MAPK3
→
FGFR3
(reaction)
Lax et al., Mol Cell 2002, Wu et al., Biol Chem 2003, Gotoh et al., Cancer Sci 2008, Zhou et al., Cell Res 2009
-
Reactome Reaction:
FGFR3
→
MAPK3
(reaction)
Lax et al., Mol Cell 2002, Wu et al., Biol Chem 2003, Gotoh et al., Cancer Sci 2008, Zhou et al., Cell Res 2009
Text-mined interactions from Literome
Hart et al., Oncogene 2000
(Cell Transformation, Neoplastic) :
Phosphorylation of Shp2, PLC-gamma, and
MAPK was also
stimulated by all three ` TDII-like '
FGFR derivatives
Cao et al., Am J Physiol Gastrointest Liver Physiol 2003
(MAP Kinase Signaling System...) :
ACh increased
MAPK activity and phosphorylation of MAPK and of p38 MAPK
Koziczak et al., Oncogene 2004
(Breast Neoplasms) :
The repression of
FGFR activity
caused downregulation of
MAPK in MDA-MB-415 and MDA-MB-453 cells
Lievens et al., J Mol Biol 2006
(Achondroplasia...) :
K644E/M
FGFR3 mutants
activate Erk1/2 from the endoplasmic reticulum through FRS2 alpha and PLC gamma independent pathways
Easton et al., J Neurochem 2006
(Neuroblastoma) :
In addition to Shc,
fibroblast growth factor receptor substrate 2 (FRS2) is
required for the BDNF induced activation of
MAPK
Kuslak et al., Differentiation 2007
(MAP Kinase Signaling System) :
Blocking FGFR activation with PD173074 showed that activation of
extracellular signal regulated kinase 1/2 ( ERK1/2 ) in the UGS is
dependent on
FGFR signaling
Lamont et al., Br J Cancer 2011
(Carcinoma, Transitional Cell...) :
All inhibitors prevented activation of
FGFR3 , and
inhibited downstream
MAPK pathway signalling
Jeong et al., J Pharm Pharmacol 2011
(MAP Kinase Signaling System) :
ACh and MIGB
induced phosphorylation of
ERK 1/2 and p38 MAPKs in ileal longitudinal muscles, and they also phosphorylated the caldesmon and 20-kDa regulatory light chain of myosin ( MLC(20) )
Makhnovskiĭ et al., Zh Vyssh Nerv Deiat Im I P Pavlova 2011
:
The reversible depression of sensitivity to ACh of command Helix neurons of defensive behavior in the cellular correlate of habituation depends on the decrease in the number of membrane connected
ACh receptors as a
result of activation of several serine/threonine protein kinases : A, G, CaMKII, p38
MAPK ( without the participation of PKC ), and tyrosine protein kinases including the family of Src-kinases
Jin et al., Hum Mol Genet 2012
(Disease Models, Animal...) :
P3 inhibited tyrosine kinase activity of
FGFR3 and its typical downstream molecules, extracellular signal
regulated kinase/mitogen activated protein kinase
Mavila et al., PloS one 2012
(Liver Neoplasms) :
FGF Receptor ( R ) activation
resulted in the downstream activation of
MAPK , PI3K-AKT, and ß-catenin pathways, as well as cellular proliferation
Kan et al., Mol Pharmacol 1996
:
ACh also
caused phosphorylation of p42
MAPK and cPLA2, which was inhibited by AG126 ( [ alpha-cyano- ( 3-hydroxy-4-nitro ) cinnamonitrile ] ), a tyrosine kinase inhibitor known to decrease MAPK activity