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EPHB2 — HSPG2

Text-mined interactions from Literome

Neary et al., J Neurosci 1999 : However, neither inhibition of PI-PLC nor chelation of calcium significantly reduced ATP stimulated ERK activity
Lee et al., Cell Signal 2001 (MAP Kinase Signaling System) : The phospholipase C (PLC) inhibitor, U73122, and EGTA reduced the phosphorylation of both ERK1/2 and MEK1/2 induced by H ( 2 ) O ( 2 )
Eichhorn et al., Endocrinology 2002 : Previously, we had shown that inhibition of PLC activity impaired the ability of insulin to activate ERK in 3T3-L1 adipocytes ... In this study, we confirmed that the insulin receptor and PLC-gamma1 are physically associated in hIRcB fibroblasts, insulin stimulates PLC-gamma1 enzyme activity, and inhibition of PLC activity impairs activation of ERK
Ward et al., J Am Soc Nephrol 2002 : Thus, proximal tubular OK cells express a CaR that mediates Ca ( 2+ ) ( i ) mobilization and PIP ( 2 ) -PLC dependent ERK activation in response to AGAs and thus could play a role in AGA induced nephrotoxicity
Robin et al., Am J Physiol Cell Physiol 2002 : Inhibition of phospholipase C (PLC) by U-73122 or of phosphoinositide (PI) 3-kinase by wortmannin partially reduced ERK activation
Lee et al., Free Radic Biol Med 2002 (MAP Kinase Signaling System) : The phospholipase C (PLC) inhibitor, U73122, or the protein kinase C ( PKC ) inhibitor, Ro-31-8425, blocked H ( 2 ) O ( 2 ) -induced ERK phosphorylation, whereas the same treatment did not inhibit p38 or JNK phosphorylation
Yu et al., Glia 2004 (MAP Kinase Signaling System) : LPA- and S1P induced ERK phosphorylation was dependent on the activation of mitogen activated protein kinase ( MAPK ), phospholipase C (PLC) , and protein kinase C ( PKC ), but was insensitive to pertussis toxin ( PTX )
McMullen et al., Oncogene 2004 : Inhibition of phospholipase C (PLC) resulted in complete inhibition of ERK , while having no affect on p38 activity
Marks et al., Biochem Biophys Res Commun 2003 : However, TCR induced ERK activation was suppressed by inhibitors of PKC and PLC-gamma
Germack et al., Br J Pharmacol 2004 (MAP Kinase Signaling System) : 4. Cl-IB-MECA mediated increases in cAMP accumulation suggest that A ( 3 ) AR-induced ERK1/2 phosphorylation involves adenylyl cyclase activation via phospholipase C (PLC) and PKC stimulation
Hassan et al., Regul Pept 2004 (Prostatic Neoplasms) : The effects of NT on EGFR/ERK/Akt activation and DNA synthesis were attenuated by PLC-inhibitor ( U73122 ), PKC-inhibitors ( bisindolylmaleimide, staurosporine, rottlerin ), MEK inhibitor ( U0126 ) and PI3 kinase inhibitors ( wortmannin, LY 294002 )
Fernández-Tome et al., Biochem Biophys Res Commun 2004 : PGD ( 2 ) also increased phospho-ERK1/2 MAPK in a biphasic-fashion, which was abolished by PLC and PKC inhibitors but not by ethanol, which overincreased phospho-ERK1/2, suggesting that PGD ( 2 ) -induced ERK1/2 activation requires previous PLC-PKC activation while PLD down-regulates it
Keiper et al., J Biol Chem 2004 (MAP Kinase Signaling System) : Finally, we have demonstrated that activation of H-Ras and ERK1/2 requires the lipase activity of PLC-epsilon and the subsequent [ Ca2+ ] i increase, suggesting that H-Ras activation is mediated by a Ca2+ -activated GEF
He et al., J Biol Chem 2004 (Cell Transformation, Neoplastic...) : The presence of the PLC inhibitor U73122 or the calcium chelator 1,2-bis ( 2-aminophenoxy ) ethane-N, N, N ', N'-tetraacetic acid tetrakis ( acetoxymethyl ester ) ( BAPTA-AM ) blocked both ERK and Ras activation, suggesting that both PLC and calcium are required for ERK activation
Cho et al., Mol Cells 2005 (MAP Kinase Signaling System) : These findings indicate that ERK phosphorylation in response to glycated LDL involves the activation of PKC, PLC , and MEK, but is independent of intracellular Ca2+
Mousseaux et al., Br J Pharmacol 2006 : Our results also indicate that phospholipase C (PLC) was involved in GHSR-1a mediated ERK1/2 activation, however, pathways like tyrosine kinases, including Src, and phosphoinositide 3-kinases were not found to be involved
Dehvari et al., Neurosci Lett 2008 : These results demonstrate that PSs regulate Erk activity through a PKCalpha dependent pathway and that disruption of PLC/PKC signaling in the absence of both PS1 and PS2 results in lower downstream activation of Erk
Khundmiri et al., American journal of physiology. Renal physiology 2008 : In the present work utilizing opossum kidney cells, a model of renal proximal tubule, PTH stimulated ERK phosphorylation and membrane translocation of PKCalpha were prevented by inhibition of Src kinase, PLC , and calcium entry
Gomes et al., Biol Chem 2009 : Furthermore, ERK phosphorylation and the mitogenic effect are partially suppressed by a phospholipase C (PLC) inhibitor ... These data suggest that the mitogenic effect of CMS2MS2 on fibroblasts is independent of its proteolytic activity, requires ERK phosphorylation, and involves activation of PLC
Notcovich et al., Exp Cell Res 2010 : On the other hand, H1R induced ERK1/2 activation was inhibited by U73122 but not affected by C3 or beta2-chimaerin, suggesting that ERK1/2 activation was dependent on PLC and independent of RhoA or Rac
Gerilechaogetu et al., Anim Sci J 2009 : These results indicate that the LPS induced phosphorylation of ERK in the chicken heterophils is mediated by PLC , PKC and intracellular calcium, and the PMA stimulated phosphorylation is dependent on intracellular calcium ion and PKC
Leon et al., J Cell Physiol 2011 (Calcium Signaling) : Requirement for PLC?2 in IL-3 and GM-CSF stimulated MEK/ERK phosphorylation in murine and human hematopoietic stem/progenitor cells
Kremer et al., J Immunol 2011 (Calcium Signaling...) : In this study, we demonstrate that PLC activity is required for SDF-1 to induce ERK activation, migration, and CXCR4 endocytosis in human T cells
Abdala-Valencia et al., PloS one 2012 : ERK1/2 activation was blocked by inhibition of XO and PLC but not by inhibition of PKCa, indicating that ERK1/2 is downstream of XO and upstream of PKCa during ICAM-1 signaling
Huang et al., PloS one 2012 (Calcium Signaling...) : In conclusion, our results demonstrate that SKF83959 induced increases in ERK1/2 phosphorylation and astrocyte migration are dependent on PLC-PKCd signals