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MAPK14 — PLG
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Jingjing et al., Angiogenesis 2001
:
CM from 293-VEGF183 cells treated with heparin or
plasmin induced about a twofold increase in cell numbers and
stimulated MAPK phosphorylation in HUVECs as compared with CM from untreated 293-VEGF183 cells or from heparin- or plasmin treated 293 cells containing the vector alone
Simkhovich et al., Cardiovasc Pathol 2003
(Myocardial Ischemia) :
Protective genes included
mitogen activated protein kinase activated protein kinase 3 ( MAPKAPK 3 ), heat shock proteins 70, 27, 22, B-crystalline, vascular endothelial growth factor, inducible nitric oxide synthase and
plasminogen activator inhibitors 1 and 2
Ulfhammer et al., Journal of thrombosis and haemostasis : JTH 2006
(Cardiovascular Diseases...) :
TNF-alpha mediated suppression of tissue type
plasminogen activator expression in vascular endothelial cells is NF-kappaB- and p38
MAPK dependent
Zhang et al., J Immunol 2007
:
Interaction of
plasmin with annexin A2
resulted in the stimulation of ERK1/2 and p38
MAPK , cyclooxygenase-2, and PGE ( 2 ), leading to increased MMP-1 production
Zare et al., J Leukoc Biol 2008
:
In contrast,
Plg production did not require NF-kappaB, was only partly
down-regulated by p38
MAPK inhibitor, and was efficiently inhibited by insulin, indicating a different mechanism for its induction
Tang et al., J Biol Chem 1998
:
The urokinase-type
plasminogen activator receptor
mediates tyrosine phosphorylation of focal adhesion proteins and activation of
mitogen activated protein kinase in cultured endothelial cells