◀ Back to MAPK14
MAPK14 — NOX1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Viedt et al., Arterioscler Thromb Vasc Biol 2000
:
JNK and p38
MAPK , but not ERK, activation was
inhibited by an inhibitor of
NAD ( P ) H oxidase
Pomerance et al., J Biol Chem 2000
:
Diphenylene iodonium, a potent inhibitor of
NADPH oxidase ( s ), and ascorbic acid, an effective free radical scavenger,
suppressed TSH- or forskolin stimulated
p38-MAPK phosphorylation, indicating that the generation of reactive oxygen species plays a key role in signaling from cAMP to p38-MAPKs
Brown et al., J Biol Chem 2004
:
Distinct ligand dependent
roles for p38
MAPK in priming and activation of the neutrophil
NADPH oxidase
Tojo et al., J Hypertens 2005
(Hypertension, Renal) :
We hypothesized that p38
MAPK inhibitor, FR167653, may
suppress NAD ( P ) H oxidase and its oxygen radical production and ameliorate renal damage in Dahl salt-sensitive rats with heart failure ( DSHF )
Adachi et al., Hepatology 2005
(Liver Cirrhosis) :
Our data demonstrate that
NAD ( P ) H oxidase derived ROS
induce HSC proliferation mainly through the phosphorylation of p38
MAPK
Chan et al., Circ Res 2005
:
These results suggest that
NADPH oxidase derived O2*- underlies the activation of p38
MAPK or ERK1/2 by Ang II in the ventrolateral medulla
Puntambekar et al., J Neurochem 2005
:
Inhibition of
NADPH oxidase activity also
attenuated NGF dependent p38
MAPK activation
Nishiyama et al., J Pharmacol Sci 2006
(Fibrosis...) :
In RMC, aldosterone induces cellular injuries through
NADPH oxidase dependent ROS production and/or
MAPK activation
Qin et al., Free Radic Biol Med 2006
:
These results suggest that angiotensin II-induced apoptosis is mediated via
NADPH oxidase activation probably through p38
MAPK activation, a decrease in Bcl-2 protein, and caspase activation
Abid et al., J Biol Chem 2007
:
We show that
NADPH oxidase activity is
required for VEGF activation of phosphoinositide 3-kinase-Akt-forkhead, and p38
MAPK , but not ERK1/2 or JNK
Yang et al., Journal of neuroinflammation 2007
(Central Nervous System Diseases) :
Both
NADPH oxidase and mitochondrial electron transfer chain subunit I
play an indispensable role in s-Mtb induced
MAPK activation and pro-inflammatory cytokine production in BV-2 cells and mixed glial cells
Zhu et al., Biochem J 2009
:
NAD ( P ) H oxidase mediated menadione induced ROS production, which then stimulated phosphorylation of p38
MAPK ( mitogen activated protein kinase ) and ERK1/2 ( extracellular-signal regulated kinase 1/2 ), and increased actin polymerization and cytoskeletal protrusions
Quiroga et al., Growth Factors 2009
(Liver Neoplasms...) :
p38
MAPK induced activation of
NADPH oxidase is accomplished by a two-step pathway : first, ROS independent and second ROS- and TGF-beta(1) dependent
Zhang et al., J Hypertens 2010
(Heart Failure...) :
These findings suggest that central inflammation in pathophysiological conditions activates the sympathetic nervous system via
NAD ( P ) H oxidase and p38
mitogen activated protein kinase dependent synthesis of prostaglandin E2
Heo et al., Vascul Pharmacol 2010
(Atherosclerosis) :
Furthermore, the
NADPH oxidase assembly inhibitor, AEBSF, and the blocker of NADPH oxidase, p47(phox) small interference RNA ( siRNA ), also efficiently
blocked LIGHT induced migration, CCR1, CCR2, ICAM-1, and HVEM expression, and p38
MAPK and NF-kB activation
Sancho et al., J Biol Chem 2010
(Carcinoma, Hepatocellular) :
Early
NOX1 activation
induces both a feedback positive loop via an Src-ERK pathway that up-regulates its own levels, and a parallel signaling pathway through p38
MAPK and AKT resulting in EGFR and TGF-alpha up-regulation
Silva et al., J Renin Angiotensin Aldosterone Syst 2010
:
AT1 receptor and
NAD ( P ) H oxidase mediate angiotensin II-stimulated antioxidant enzymes and
mitogen activated protein kinase activity in the rat hypothalamus
Kim et al., Apoptosis 2011
:
Panaxydol induces apoptosis through an increased intracellular calcium level,
activation of JNK and p38
MAPK and
NADPH oxidase dependent generation of reactive oxygen species ... Furthermore, panaxydol was shown to induce apoptosis through an increase in intracellular Ca ( 2+ ) concentration ( [ Ca ( 2+ ) ] ( i ) ),
activation of JNK and p38
MAPK , and generation of reactive oxygen species ( ROS ) initially by
NADPH oxidase and then by mitochondria ... JNK and p38
MAPK play a key role in activation of
NADPH oxidase , since inhibition of their expression or activity abrogated membrane translocation of p47(phox) and p67(phox) subunits and ROS generation
Kodama et al., Genes Cells 2013
:
Furthermore,
Nox1 and Nox4 siRNAs
inhibited both Ras induced DNA damage response and
p38MAPK activation, whereas overexpression of Nox1 and Nox4 alone was able to induce senescence
Dusi et al., Biochem J 1994
:
These results indicate that when FMLP is the agonist, both the tyrosine phosphorylation of p43
MAPK and p75, and the
activation of
NADPH oxidase , are coupled to Ca ( 2+ ) -dependent mechanisms
Ushio-Fukai et al., J Biol Chem 1998
:
However, exogenous H2O2 activates only
p38MAPK ( 14-fold ), and diphenylene iodonium, an
NADH/NADPH oxidase inhibitor , attenuates angiotensin II-stimulated phosphorylation of p38MAPK, but not p42/44MAPK