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EGF — HSPG2

Text-mined interactions from Literome

Meyer zu Heringdorf et al., FEBS Lett 1999 (Calcium Signaling...) : In HEK3 cells, EGF increased [ Ca ( 2+ ) ] ( i ) and stimulated both, SPK and PLC ... In HEK2 cells, EGF similarly stimulated PLC , but did not increase [ Ca ( 2+ ) ] ( i ) or stimulate SPK, suggesting that intracellular SPP production plays a major role for Ca ( 2+ ) signalling by EGF in HEK-293 cells
Schmidt et al., J Biol Chem 2000 : Pretreatment of HEK-293 cells for 2 min with carbachol, a mAChR agonist, lysophosphatidic acid, or ATP, followed by agonist washout, strongly increased ( by 2-3-fold ) maximal PLC stimulation ( measured > /=40 min later ) by epidermal growth factor and platelet derived growth factor, but not insulin, and largely enhanced PLC sensitivity to these RTK agonists
Nojiri et al., Hepatology 2000 : Hepatocytes maintained in primary culture for periods of 1 to 24 hours exhibited a rapid decline in epidermal growth factor (EGF) induced activation of phospholipase C (PLC) , as was evident in a loss of EGF induced inositol 1,4,5-trisphosphate ( IP ( 3 ) ) formation and mobilization of Ca ( 2+ ) from intracellular Ca ( 2+ ) stores ... The loss of PLC activation was not the result of a decrease in EGF receptor or phospholipase C-gamma1 ( PLCgamma1 ) protein levels, nor the result of a loss of tyrosine phosphorylation of these proteins, but was associated with a decrease in EGF induced translocation of PLCgamma1 to the Triton-insoluble fraction, presumably reflecting binding to the actin cytoskeleton
Ward et al., J Biol Chem 2002 : Phospholipase C-gamma (PLC-gamma) is stimulated by epidermal growth factor via activation of the epidermal growth factor receptors
Ramadurai et al., Am J Physiol Lung Cell Mol Physiol 2003 : In conclusion, PLC-gamma expression and activation by EGF in fetal lung are cell specific, corresponding to the development of EGFR expression ... PLC-gamma activation by EGFR in fetal lung fibroblasts may be involved in EGF control of lung development
Liang et al., Mol Pharmacol 1992 : Both of these responses can be abolished by pretreatment with pertussis toxin, suggesting that EGF may regulate phospholipase C (PLC) activity via a guanine nucleotide binding regulatory protein ( G protein ) in liver cells ... In contrast, in A431 human epidermoid carcinoma cells EGF can induce a rapid phosphorylation of PLC-gamma on tyrosine residues that increases the activity of immunoprecipitated PLC-gamma, suggesting that tyrosine phosphorylation of PLC-gamma may be the mechanism for EGF stimulated inositol trisphosphate production in these cells ... To determine the importance of the phosphorylation of PLC-gamma on tyrosine residues in a system where the EGF receptor apparently couples to a G protein, the effect of EGF on tyrosine phosphorylation of PLC-gamma was examined in rat hepatocytes ... Although the amount of PLC-gamma in rat hepatocytes is similar to that in A431 cells and slightly higher than that in Rat1hER cells, EGF causes a barely detectable increase in the phosphorylation of PLC-gamma on tyrosine in hepatocytes, whereas it stimulates a significant degree of phosphorylation of PLC-gamma on tyrosine in Rat1hER or A431 cells
Stope et al., Mol Cell Biol 2004 : EGF induced rapid and sustained GTP loading of Rap2B, binding of Rap2B to PLC-epsilon , and Rap2B dependent translocation of PLC-epsilon to the plasma membrane ... EGF induced tyrosine phosphorylation of RasGRP3, but not RasGRP1, apparently caused by c-Src ; inhibition of c-Src interfered with EGF induced Rap2B activation and PLC stimulation
Song et al., Exp Mol Med 2005 : Inositol 5'-phosphatase, SHIP1 interacts with phospholipase C-gamma1 and modulates EGF induced PLC activity
Ma et al., Mol Cell Biol 2005 : Pharmacological experiments indicate that the EGF induced activation of PKD2 occurs independently of store depletion but requires the activity of phospholipase C (PLC) and phosphoinositide 3-kinase (PI3K)
Yang et al., J Biol Chem 1991 : Pretreatment of the rats with pertussis toxin prior to isolation of the hepatocytes blocked EGF induced tyrosine phosphorylation of PLC-gamma and Ca2+ mobilization but had no effect on autophosphorylation of the EGF receptor or Ca2+ responses elicited by angiotensin II or phenylephrine ... These results indicate that a pertussis toxin-sensitive Gi protein is uniquely involved in the signal transduction pathway mediating EGF induced activation of PLC-gamma and Ca2+ mobilization in hepatocytes
Huckle et al., Endocrinology 1990 : Activation of protein kinase C ( PKC ) with a phorbol ester inhibited ( IC50 = 3-10 nM ) both EGF dependent PtdIns hydrolysis and PLC gamma phosphorylation by more than 90 %
Vega et al., Mol Cell Biol 1992 : Cells expressing mutant epidermal growth factor (EGF) receptors have been used to study mechanisms through which EGF increases phospholipase C (PLC) activity
Li et al., Cell Regul 1991 : The binding of epidermal growth factor (EGF) to its receptor induces tyrosine phosphorylation of phospholipase C gamma (PLC gamma) , which appears to be necessary for its activation leading to phosphatidyl inositol ( PI ) hydrolysis
Yun et al., J Biol Chem 2008 : The interaction of PLC-epsilon with AP2 was responsible for the suppression of EGF receptor down-regulation, since a perturbation in this interaction abolished this effect
Uttamsingh et al., Oncogene 2008 (Cell Transformation, Neoplastic) : Phospholipase C (PLC) and Cox2 induced by EGF plus TGF-beta1 also played a significant role in invasion, whereas PLC was also important for colony formation
van Rheenen et al., J Cell Biol 2007 (Breast Neoplasms...) : We show that EGF induces a rapid loss of PIP ( 2 ) through PLC activity, resulting in a release and activation of a membrane bound pool of cofilin
Everett et al., J Biol Chem 2009 : Analysis of PLC gamma 1 and PLC gamma 2 with point mutations of this residue showed that removal of the negative charge enhanced PLC activity in response to EGF stimulation or activation by Rac
Verheijden et al., Cell Regul 1990 : In contrast, activation of phospholipase C (PLC) by EGF occurs in a GTP independent manner
Payrastre et al., Biochim Biophys Acta 1991 : Using phosphatidyl [ 3H ] inositol 4,5-bisphosphate ( PIP2 ) dispersed with unlabelled phosphatidylethanolamine and phosphatidylserine as an exogenous substrate, no stimulation of PLC activity by EGF could be detected, either with membranes or with membranes plus cytosol
Margolis et al., Mol Cell Biol 1990 : The association between PLC-gamma and wild-type EGF receptor was dependent on the concentration of EGF, but EGF did not enhance the association between PLC-gamma and a kinase negative mutant of the EGF receptor ... Oligomerization of the EGF receptor was not sufficient to induce association of the EGF receptor with PLC-gamma, since the kinase negative mutant receptor underwent normal dimerization in response to EGF yet did not associate with PLC-gamma ... It is concluded that the kinase activity of the EGF receptor is essential for association of PLC-gamma with the EGF receptor, possibly by stimulating receptor autophosphorylation
Teitelbaum et al., J Biol Chem 1990 : In contrast to EGF stimulated PLC activity, stimulation of PLA2 by EGF was not susceptible to inhibition by phorbol 12-myristate 13-acetate
Teitelbaum et al., Am J Physiol 1990 : Similarly, DDA prevents inhibition of epidermal growth factor stimulated PLC by AVP
Wahl et al., Proc Natl Acad Sci U S A 1989 : Previously we have found that in intact cells stimulation of phospholipase C (PLC) activity by EGF is correlated with the retention of increased amounts of PLC activity by a phosphotyrosine immunoaffinity matrix, suggesting that the EGF-receptor tyrosine kinase phosphorylates PLC
Kauffmann-Zeh et al., Science 1995 : Coprecipitation studies revealed an EGF dependent association of PITP with the EGF receptor, with PI-4 kinase, and with PLC-gamma
Chen et al., J Cell Biol 1994 : A specific inhibitor of PLC, U73122 ( 1 microM ) diminished both the EGF induced motility and PLC responses, while its inactive analogue U73343 had no effect on these responses
Yang et al., J Biol Chem 1994 : EGF caused a transient increase of PLC activity in the cytoskeleton fraction which could be abolished by immunoprecipitating PLC-gamma 1
Yang et al., J Biol Chem 1993 : EGF increased phosphoinositide-specific phospholipase C-gamma (PLC-gamma) tyrosine phosphorylation within 1 min, but no effect was observed with vasopressin, insulin, or glucagon after 5 min. EGF also caused a rapid, tyrosine kinase dependent association of G ( i ) alpha with PLC-gamma, which was maximal within 10 min ... In contrast to our previous data on fresh hepatocytes, PT had no effect on the EGF induced tyrosine phosphorylation of PLC-gamma , although Ins-1,4,5-P3 and diacylglycerol production were inhibited
Marino et al., Cell Signal 1996 (Second Messenger Systems) : We investigate the effect of EGF on IP3 production, PLC gamma phosphorylation, calcium transients in rat hepatocytes isolated in quiescent liver ( G0 phase of cell cycle ) and at 4 h ( G1 phase of cell cycle ) and 24 h ( M phase of cell cycle ) after partial hepatectomy
Piiper et al., Am J Physiol 1997 : In the present study, isolated pancreatic acinar membranes were used to investigate the mechanism of epidermal growth factor (EGF) induced activation of phospholipase C (PLC) ... EGF induced activation of PLC was strongly inhibited by pretreatment of the membranes with pertussis toxin, by an antibody raised against a COOH-terminal sequence shared by alpha-subunits of the inhibitory G proteins G ( i ) 1 and G ( i ) 2, and by an anti-PLC-gamma 1 antibody, whereas anti-G(i) alpha 3, anti-Gq/11 alpha, and anti-PLC-beta 1 antibodies had no effect
Saso et al., Gastroenterology 1997 : EGF induced PLC gamma tyrosine phosphorylation and inositol 1,4,5-trisphosphate ( InsP3 ) formation were suppressed, but cytosolic [ Ca2+ ] c elevation was little affected, indicating enhanced InsP3 mediated intracellular Ca2+ release in ethanol fed cells
Bedrin et al., J Cell Physiol 1997 (Second Messenger Systems) : In the nontransformed intestinal cell line IEC-6, expression of EGFR, Src homology and collagen protein (SHC), phospholipase C gamma 1 (PLC gamma) , and their tyrosine phosphorylation in response to EGF was assayed by immunoblot
Piiper et al., Gastroenterology 1997 : Epidermal growth factor (EGF) inhibits bombesin induced activation of phosphoinositide-specific phospholipase C (PLC) in pancreatic acini ... The aim of this study was to investigate the mechanism by which EGF inhibits bombesin induced activation of PLC ... Intact pancreatic acini were pretreated with pertussis toxin to study the role of Gi/o-type heterotrimeric guanosine triphosphate binding regulatory proteins ( G proteins ) in EGF induced modulation of PLC activity ... Pertussis toxin pretreatment of pancreatic acini abolished the inhibitory effect of EGF on bombesin induced PLC activation and amylase release ... Anti-Gi1-2alpha, but not a Gi3alpha-specific antibody, abolished the inhibitory effect of EGF on bombesin induced PLC activity
Van Epps-Fung et al., Endocrinology 1997 : Inhibition of PLC activation did not impair either EGF- or insulin induced activation of glycogen synthase or incorporation of glucose into lipid, supporting the hypothesis that both EGF- and insulin induced glucose disposal can be independent of GLUT4 mediated glucose transport
Hofer et al., Curr Biol 1998 : Ral was activated by the Ca2+ ionophore ionomycin, and activation by LPA or EGF could be blocked by a phospholipase C (PLC) inhibitor