◀ Back to EPHB2
CAT — EPHB2
Text-mined interactions from Literome
Cho et al., Biochem Biophys Res Commun 1999
:
Silica induced
ERK phosphorylation was also effectively
attenuated by
catalase and DPI
Peus et al., Free Radic Biol Med 1999
:
Overexpression of
catalase strongly
inhibited UVB induced
EGFR/ERK1/2 pathway activation
Preston et al., J Biol Chem 2001
:
ERK1/2 phosphorylation was
blocked by
catalase in fibroblasts expressing wild type Neu, however such a response did not occur in cells possessing activated mutant Neu
Cheng et al., J Mol Cell Cardiol 2001
:
This strain activated
ERK phosphorylation was attenuated in the
presence of
catalase
Kulich et al., J Biosci 2003
:
However, exogenously added SOD1 and heat inactivated
catalase had no effect on either toxicity or sustained
ERK phosphorylation
Lin et al., J Mol Cell Cardiol 2004
(MAP Kinase Signaling System) :
Phosphorylation studies of ERK1/2, JNK, and p38, three subgroups of mitogen activator protein kinase demonstrated that
catalase overexpression suppressed JNK phosphorylation and
increased ERK1/2 phosphorylation
Jang et al., Biochem Biophys Res Commun 2004
:
Catalase also
induced activation of NF-kappaB, PI3K, ERKs, p38s, or JNKs. Catalase induced COX-2 expression was abrogated by treatment of MG-132 ( a NF-kappaB inhibitor ) or LY294002 ( a PI3K inhibitor ), but not by treatment of PD98059 ( an
ERK inhibitor ), SB203580 ( a p38 inhibitor ), or SP600125 ( a JNK inhibitor )
Xiao et al., Oncogene 2004
(Prostatic Neoplasms) :
Overexpression of
catalase inhibited DATS mediated activation of JNK1/2, but not
ERK1/2 , and apoptosis induction in DU145 cells suggesting involvement of hydrogen peroxide as a second messenger in DATS induced apoptosis
Hachiya et al., Radiat Res 2005
(Leukemia, Promyelocytic, Acute) :
Moreover, inhibition of
catalase blocked the phosphorylation of
ERK1/2 but not of p38MAPK in HP100-1 cells
Lee et al., Neurochem Res 2005
(Brain Neoplasms...) :
The
ERK activation and cell death induced by H2O2 was
prevented by
catalase , the hydrogen peroxide scavenger, and U0126, an inhibitor of ERK upstream kinase MEK1/2
Cao et al., J Cell Biochem 2006
(MAP Kinase Signaling System) :
ERK1/2 and p38 were activated, and the activation was
blocked by
catalase , consistent with an H2O2 dependent mechanism
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
LeHoux et al., J Mol Endocrinol 2006
:
Overexpression of wild-type ERK1 and
ERK2 significantly
reduced basal as well as Ang II-stimulated human
-2023CYP11B2-CAT activity ; conversely, the two dominant negative mutants increased them
Lin et al., Atherosclerosis 2007
(MAP Kinase Signaling System) :
Phosphorylation studies on ERK1/2, JNK, and p38, three major subgroups of mitogen activator protein kinases, demonstrated that Cu, Zn-SOD and/or
catalase overexpression
suppressed ERK1/2 and JNK phosphorylation
Shim et al., Mol Cells 2006
(Liver Neoplasms...) :
Inhibition of
ERK and p38 MAPK
reduced the induction of
catalase activity resulting from overexpression of CAGE, and inhibition of catalase reduced CAGE promoted motility ... We conclude that CAGE enhances the motility of cancer cells by activating
ERK and p38 MAPK,
inducing catalase activity, and reducing ROS levels
Navarro et al., Ann N Y Acad Sci 2006
:
Deferoxamine ( DFO ; iron chelator ),
catalase ( hydrogen peroxide removing enzyme ), or alpha-tocopherol ( peroxyl-radical scavenger ) did not
affect DOX increased
ERK phosphorylation levels
Osada et al., Cancer Chemother Pharmacol 2008
(Pancreatic Neoplasms) :
But
ERK phosphorylation was not
inhibited by
catalase and was abrogated completely by the thiol antioxidant
Kim et al., J Nutr Biochem 2009
:
However,
catalase partially
blocked the GA-induced phosphorylation of Cx43 and
ERK1/2
Kang et al., J Agric Food Chem 2008
:
Furthermore,
catalase partially
inhibited the EGCG induced inhibition of GJIC and the phosphorylation of Cx43 and
ERK1/2
Wu et al., Arch Biochem Biophys 2009
(MAP Kinase Signaling System) :
Furthermore,
catalase significantly
attenuated the intracellular peroxide production, phosphorylation of
ERK and JNK, and all cytokine gene expressions induced by EGCG
Chang et al., Biomaterials 2009
(MAP Kinase Signaling System) :
Catalase ( 500 and 1000 U/ml ) and U0126 ( 10 and 20 microm, a MEK inhibitor ) effectively
prevented the BisGMA induced
ERK activation, PGE ( 2 ) production and COX-2 expression
Murthy et al., J Biol Chem 2010
(MAP Kinase Signaling System...) :
ERK activation and MMP-9 expression were
recovered by overexpressing
catalase or transfecting siRNA for the mitochondrial iron-sulfur protein, Rieske
Cheng et al., Mol Endocrinol 2010
(Ovarian Neoplasms) :
In addition,
PEG-catalase diminished EGF induced p38 MAPK, but not
ERK1/2 or c-Jun N-terminal kinase, phosphorylation
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
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