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EGFR — NPY6R

Text-mined interactions from Literome

Cuadrado et al., J Biol Chem 2003 (Breast Neoplasms...) : Aplidin induced apoptosis was only partially blocked by the general caspase inhibitor benzyloxycarbonyl-VAD-fluoromethyl ketone and was also sensitive to AG1478 ( an EGFR inhibitor ), PP2 ( an Src inhibitor ), and SB203580 ( an inhibitor of JNK and p38 MAPK ) in MDA-MB-231 cells
Galve-Roperh et al., Mol Pharmacol 2002 (Astrocytoma) : HU-210 induced ERK activation was inhibited by tyrphostin AG1478 and PP2 , widely employed inhibitors of the epidermal growth factor receptor ( EGF ( R ) ) and the Src family of cytosolic tyrosine kinases, respectively
Li et al., Biochem Biophys Res Commun 2006 : Src tyrosine kinase inhibitor PP2 suppresses ERK1/2 activation and epidermal growth factor receptor transactivation by X-irradiation
Howes et al., J Mol Cell Cardiol 2006 (Hypertrophy) : EGFR phosphorylation is increased in cells expressing Galphaq and this effect is inhibited by PP2 , placing Src upstream of EGFR phosphorylation
Shiraishi et al., Endocrinology 2006 : The LHR mediated phosphorylation of the EGFR and Shc, the activation of Ras, and the phosphorylation of ERK1/2 are inhibited by expression of a dominant negative mutant of Fyn, a member of the Src family kinases (SFKs) expressed in MA-10 cells and by PP2 , a pharmacological inhibitor of the SFKs
Xu et al., Invest Ophthalmol Vis Sci 2006 : Among several inhibitors tested, PP2 blocked wound induced EGFR phosphorylation in THCE cells
Park et al., Cancer Res 2006 (Glioblastoma...) : IR-induced activation of EGFR was suppressed by PP2 , whereas LY294002 and SB203580 did not affect the activations of p38 and PI3K, respectively
Bassa et al., Biochim Biophys Acta 2007 (MAP Kinase Signaling System) : LPC activated Src-kinase and protein kinase C ( PKC ), and both Src kinase inhibitor PP-2 and PKC inhibitor inhibited the activation of EGFR by LPC
Descorbeth et al., J Mol Cell Cardiol 2010 : Pre-treatment of A10 VSMC with high glucose ( 26 mM ) for 3 days, increased the levels of Gqalpha, G11alpha, PLCbeta-1 and PLCbeta-2 proteins which were restored to control levels by AG1478, an inhibitor of EGF-R , AG1295, an inhibitor of PDGF-R and PP2 , an inhibitor of c-Src but not by PP3
Nguyen et al., American journal of physiology. Renal physiology 2011 (Polycystic Kidney, Autosomal Dominant) : Tyrphostin AG1478 and PP2 , inhibitors of EGFR and Src, respectively, blocked ouabain dependent ADPKD cell proliferation
Moody et al., Peptides 2011 (Lung Neoplasms) : The ability of BRS-3 to regulate EGFR transactivation in NCI-H1299-BRS-3 cells was reduced by AG1478 or gefitinib ( EGFR tyrosine kinase inhibitors ), GM6001 ( matrix metalloprotease inhibitor ), PP2 ( Src inhibitor ), N-acetylcysteine ( anti-oxidant ), Tiron ( superoxide scavenger ) and DPI ( NADPH oxidase inhibitor )