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F2R — MAPK3

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: MAPK3 → F2R (increases)
  Evidence: Pretreatment of HT29 cells with increasing concentrations of PD98059 (a specific inhibitor of ERK 1/2) resulted in a dose-dependent decrease in the cell number induced by thrombin (10 nM/L), suggesting that cell proliferation induced by thrombin or AP1 involves the phosphorylation of ERKs in these cells.
• Reactome Reaction: MAPK3 → F2R (reaction) Kuo et al., Cell Signal 2006, Luttrell et al., Science 1999*
• Reactome Reaction: MAPK3 → F2R (indirect_complex) Kuo et al., Cell Signal 2006, Luttrell et al., Science 1999*

Text-mined interactions from Literome

Cichowski et al., Biochim Biophys Acta 1999 : ( 3 ) Despite the failure to bind soluble fibrinogen, activation of PAR1 in CHRF-288 cells caused phosphoinositide hydrolysis, arachidonate mobilization and the phosphorylation of p42MAPK , phospholipase A2 and the Rac exchange protein, Vav, all of which occur in platelets
Sabri et al., Circ Res 2002 : Activation of PAR-1 leads to an increase in Src, Fyn, and epidermal growth factor receptor (EGFR) phosphorylation, with EGFR receptor transactivation by Src family kinases the major mechanism for PAR-1 dependent activation of extracellular signal regulated kinase, p38-mitogen activated protein kinase , and protein kinase B
Syeda et al., J Biol Chem 2006 : PAR-1 and PAR-2 stimulation rapidly activated both ERK1/2 and p38MAPK , and pharmacological blockade of MEK with either PD98059 or U0126 or of p38MAPK by SB203580 or SB202190 strongly inhibited thrombin- and SLIGKV induced COX-2 expression and 6-keto-PGF1alpha formation
Sekiguchi et al., Biochem Pharmacol 2007 : PAR1-AP caused persistent ( 6h or more ) and transient ( 5min ) phosphorylation of ERK and p38 MAPK , respectively, followed by delayed reinforcement at 18h
Arora et al., Oncogene 2008 (Breast Neoplasms...) : PAR1 stimulated EGFR and ErbB2 transactivation leads to prolonged extracellular signal regulated kinase-1 and -2 signaling and promotes breast carcinoma cell invasion
Bae et al., Thromb Res 2010 : The EPCR dependent cleavage of PAR-1 by both APC and thrombin increased the phosphorylation of ERK 1/2
Vouret-Craviari et al., Biochem J 1993 : Differential activation of p44mapk ( ERK1 ) by alpha-thrombin and thrombin-receptor peptide agonist
Jiang et al., Circ Res 1996 : These results support the notion that the thrombin receptor activates MAPK through PKC dependent pathways and that the incremental activation of MAPK by TRAP over that induced by thrombin is the consequence of enhanced activation through the PKC limb of the phosphoinositide lipid pathway
Trejo et al., J Biol Chem 1996 : The cloned thrombin receptor is necessary and sufficient for activation of mitogen activated protein kinase and mitogenesis in mouse lung fibroblasts ... This study focuses on the role of the thrombin receptor in thrombin induced mitogenesis and mitogen activated protein ( MAP ) kinase activation in mesenchymal cells