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AHSA1 — CAT

Text-mined interactions from Literome

Sen et al., FEBS Lett 2005 : p38 mitogen activated protein kinase ( p38MAPK ) upregulates catalase levels in response to low dose H2O2 treatment through enhancement of mRNA stability
Cao et al., Liver Int 2006 : Up-regulation of leptin receptor and activation of JAK1 and 2 were not affected by DLPC+SAMe, whereas phosphorylation of ERK1/2 and p38 was blocked by DLPC+SAMe or catalase , suggesting an H2O2 dependent mechanism
Gaitanaki et al., Mol Cell Biochem 2006 : Oxidative stress was exemplified by perfusing hearts with 30 microM H ( 2 ) O ( 2 ) for 5 min or with the enzymatic system of xanthine/xanthine oxidase ( 200 microM/10 mU/ml, respectively ) for 10 min. H ( 2 ) O ( 2 ) -induced activation of p38-MAPK ( 7.04 +/- 0.20-fold relative to control values ) was totally attenuated by L-ascorbic acid ( 100 microM ) or catalase ( 150 U/ml )
Gaitanaki et al., J Exp Biol 2007 (MAP Kinase Signaling System) : The p38-MAPK phosphorylation induced by the combined action of CuCl ( 2 ) and hyperthermia was partially inhibited by catalase , indicating that hyperthermia possibly activates the kinase through the production of H ( 2 ) O ( 2 )
Binet et al., J Leukoc Biol 2008 : We found that ATO activates p38 and that, unlike H2O2, this response was not inhibited by exogenous catalase
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