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CAT — JUN

Text-mined interactions from Literome

Chung et al., Cancer Res 1999 (Cell Transformation, Neoplastic) : The addition of catalase to the incubation of the cells with EGCG or TFdiG did not prevent the inhibitory effect on AP-1 activity, suggesting that H2O2 does not play a significant role in the inhibition by tea polyphenols
Ding et al., J Biol Chem 2001 : Catalase inhibited phosphorylation of ERKs and p38 kinase, as well as AP-1 activation induced by FFSi, suggesting the involvement of H ( 2 ) O ( 2 ) in the mechanism of silica induced AP-1 activation
Zhou et al., Hepatology 2001 (Ischemia...) : The level of Cu/ZnSOD induced AP-1 activation was significantly reduced by ablation of Kupffer cells or by coexpression of catalase , suggesting that increased H ( 2 ) O ( 2 ) production facilitated by Cu/ZnSOD in hepatocytes and/or Kupffer cells may be responsible for AP-1 activation
Jung et al., Exp Cell Res 2003 (Cell Transformation, Neoplastic...) : DNA binding activity of AP-1 , downstream of ERK1/2, was also inhibited by catalase , N-acetyl-L-cysteine, and the MEK inhibitor PD98059, which significantly blocked arsenite activation of ERK1/2
Zhang et al., Toxicol In Vitro 2007 : JNK inhibitor SP600125 could inhibit ACTX-6 induced apoptosis and catalase could inhibit JNK and c-Jun phosphorylation
Li et al., PloS one 2013 : Furthermore, we found that the presence of NAC, as well as the overexpression of MnSOD, could almost completely abolish the activation of Akt, extracellular-signal regulated kinase ( Erk ) 1/2, c-Jun N-terminal kinase (JNK) , and p38, although only JNK and p38 were affected by overexpression of catalase
Das et al., Am J Physiol 1995 : AP-1 activation was inhibited by catalase ( 500 U/ml ) plus SOD plus ethanol ( 1 mM )
Nilakantan et al., Carcinogenesis 1998 : Ciprofibrate also increased AP-1 activation, but catalase overexpression did not significantly inhibit this increase, although AP-1 activation was 40 % lower in transgenic mice