◀ Back to EGFR

CAT — EGFR

Text-mined interactions from Literome

Peus et al., Free Radic Biol Med 1999 : Overexpression of catalase strongly inhibited UVB induced EGFR/ERK1/2 pathway activation
Burdick et al., Cancer Res 2003 (Breast Neoplasms) : Overexpression of catalase , but not Cu/Zn superoxide dismutase, reduced the extent of BPQ dependent increased cell number and EGFR pathway activation
Zhou et al., FEBS Lett 2006 (Prostatic Neoplasms) : Antioxidants and catalase inhibited IGF-1 stimulated EGFR phosphorylation, indicating that H ( 2 ) O ( 2 ) is required for EGFR activation
Bełtowski et al., Peptides 2006 : The effect of leptin on ERK and Na ( + ), K ( + ) -ATPase was abolished by catalase , specific inhibitors of epidermal growth factor (EGF) receptor , AG1478 and PD158780, as well as by ERK inhibitor, PD98059, and was mimicked by both exogenous H ( 2 ) O ( 2 ) and EGF
Hyoudou et al., Free Radic Biol Med 2006 (Lung Neoplasms...) : Quantitative RT-PCR and Western blot analyses indicated that PEG-catalase markedly reduced the increase in the expression of epidermal growth factor receptor
Fridrich et al., Mol Nutr Food Res 2007 : In the presence of catalase , suppressing the hydrogen peroxide level to the solvent control, APE effectively suppressed EGFR phosphorylation, even exceeding the effects of AE
Akhtar et al., Int J Pharm 2013 : Dendrimer induced stimulation of EGFR-ERK1/2 signaling could be attenuated by the antioxidants apocynin, catalase and tempol implying that an oxidative stress dependent mechanism was involved
Peus et al., J Invest Dermatol 1998 : Phosphorylation of EGFR was inhibited by the structurally unrelated antioxidants butylated hydroxyanisole, N-acetyl-L-cysteine, and pyrrolidine dithiocarbamate, or by the H2O2 degrading enzyme catalase