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CAT — FOS
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
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