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HSPG2 — MAPK4

Text-mined interactions from Literome

Dajani et al., J Cell Physiol 1999 : The PKC inhibitor GF109203X did not diminish the effect of EGF on MAPK or DNA synthesis, but strongly inhibited the effects of norepinephrine, vasopressin, angiotensin II, TPA and B. cereus PC-PLC on MAPK and almost abolished the enhancement by these agents of EGF stimulated DNA synthesis
Saeed et al., Acta Pharmacol Sin 2003 : To examine the down-stream signalling pathways, we found that such an interaction was inhibited by calcium channel blockers ( diltiazem ; IC ( 50 ) =3 micromol/L and verapamil ; IC ( 50 ) =5 micromol/L ), phospholipase C (PLC) inhibitor ( U73122 ; IC50=4 micromol/L ), cyclooxygenase inhibitor, ( indomethacin ; IC ( 50 ) =0.2 micromol/L ) and mitogen activated protein ( MAP ) kinase inhibitor ( PD98059 ; IC ( 50 ) =3 micromol/L )
Lee et al., Am J Physiol Lung Cell Mol Physiol 2004 : These results suggest that in HTSMCs, LTA stimulated p42/p44 MAPK phosphorylation is mediated through a TLR2 receptor and involves tyrosine kinase, PLC , PKC, Ca ( 2+ ), MEK, and PI 3-kinase
Heo et al., Am J Physiol Cell Physiol 2006 (MAP Kinase Signaling System) : In addition, we observed that p44/42 MAPK phosphorylation by EGF and inhibition of EGFR tyrosine kinase, PLC , PKC, or Ca2+ channels blocked EGF induced phosphorylation of p44/42 MAPKs
Matsumoto et al., Mol Cell Neurosci 2006 : PLC-gamma inhibitor attenuated BDNF stimulated long lasting MAPK activation
Bourguignon et al., J Biol Chem 2006 (Carcinoma, Squamous Cell...) : Overexpression of the LARG-PDZ domain also functions as a dominant negative mutant ( similar to the PLC/Ca2+-calmodulin dependent kinase II ( CaMKII ) and EGFR/MAPK inhibitor effects ) to block HA/CD44 mediated signaling events ( e.g. EGFR kinase activation, Ras/RhoA co-activation, Raf-ERK signaling, PLC epsilon mediated inositol 1,4,5-triphosphate production, intracellular Ca2+ mobilization, CaMKII activity, filamin phosphorylation, and filamin-actin binding ) and to abrogate tumor cell growth/migration
van Dijk et al., Biochem J 1997 : However, unlike platelet derived growth factor ( PDGF ) or epidermal growth factor (EGF), PC-PLC fails to activate Ras and to induce DNA synthesis, and activates MAPK only transiently ( < 45 min ) ... Down-regulation of protein kinase C (PKC) -alpha, -delta and -epsilon isotypes has little or no effect on MAPK activation by either PC-PLC or growth factors ... However, Ro 31-8220, a highly selective inhibitor of all PKC isotypes, including atypical PKC-zeta but not Raf-1, blocks MAPK activation by PDGF and PC-PLC , but not that by EGF, suggesting that atypical PKC mediates the PDGF and PC-PLC signal ... Furthermore, dominant negative PKC-zeta inhibits, while ( wild-type ) PKC-zeta overexpression enhances MAPK activation by PDGF and PC-PLC
Berguerand et al., Am J Respir Cell Mol Biol 1997 (Cystic Fibrosis) : The expression of G alpha ( q ) /11 protein was also increased in deltaF508 cells, with increased stimulation of phosphatidylinositol diphosphate-specific phospholipase C (PLC) by bradykinin, and an early, transient activation of mitogen activated protein ( MAP ) kinase
Gagnon et al., J Membr Biol 1999 : P2U/2Y-receptors elicit multiple signaling in Madin-Darby canine kidney ( MDCK ) cells, including a transient increase of [Ca2+ ] i, activation of phospholipases C (PLC) and A2 ( PLA2 ), protein kinase C ( PKC ) and mitogen activated protein kinase ( MAPK ) ... An inhibitor of PLC , U73122, and an inhibitor of MAPK kinase ( MEK ), PD98059, blocked ATP induced inositol-1,4, 5-triphosphate production and MAPK phosphorylation, respectively