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FOS — NOX1
Text-mined interactions from Literome
Chou et al., Toxicol Appl Pharmacol 2002
:
Western data showed that
NOx increased the expressions of
c-Fos , c-Jun, and signaling kinases including MEKK1, JNK1, and p38 ( with induction fold of 3.3, 2.8, and 3.2, respectively ) in the cells 12 h after treatment
Yamagishi et al., J Cardiovasc Pharmacol 2004
:
These results demonstrated that azelnidipine inhibited TNF-alpha induced IL-8 expression in HUVEC by blocking
NADPH oxidase mediated ROS generation and subsequent
AP-1 activation
Shiner et al., Free Radic Biol Med 2004
:
The present study demonstrates, for the first time, that PON2 expression increases in monocytes during their maturation into macrophage as a
result of
NADPH-oxidase activation, and this process is partly regulated by the transcription factor
AP-1
Ranjan et al., Antioxid Redox Signal 2006
:
Diphenylene iodonium, an inhibitor of
NADPH oxidase activity, did not affect dosedependent responses of ERK1/2 or Akt to serum, but markedly
inhibited the sequential expression of
c-Fos and Fra-1 required for induction of cyclin D1 during cell cycle re-entry ... These results indicate that Nox1 stimulates cell proliferation in actively cycling cells by reducing the requirement for growth factors to maintain expression of cyclin D1, whereas during cell cycle re-entry,
NADPH oxidase activity is
required for transcriptional activation of
Fos family genes during the immediate early gene response
Becskei et al., J Neuroendocrinol 2008
(Synaptic Transmission) :
Furthermore,
NOX-B11-3 ( 15 mg/kg i.p. ) potently
suppressed ghrelin induced ( 25 microg/kg s.c., 12 h after SPM injection )
c-Fos expression in the Arc
Vendrov et al., J Biol Chem 2010
(Atherosclerosis) :
Thrombin induced CD44 expression is mediated by transcription factor
AP-1 in a
NADPH oxidase dependent manner
Valente et al., Am J Physiol Heart Circ Physiol 2012
(Hyperplasia) :
Similar to ANG II, addition of IL-18 also induced superoxide generation, activated NF-?B and AP-1, and stimulated SMC migration and proliferation, in part via Nox1, and both ANG II and IL-18 induced
NOX1 transcription in an
AP-1 dependent manner
Hsieh et al., Journal of neuroinflammation 2012
:
These results demonstrated that in RBA-1 cells,
activation of
ATF2/AP-1 by the PKC ( a ) -mediated
Nox ( 2 ) /ROS signals is essential for upregulation of MMP-9 and cell migration enhanced by LTA
Lin et al., Cell communication and signaling : CCS 2012
:
These results demonstrated that in RBA-1 cells,
activation of
AP-1 ( c-Fos/c-Jun ) by the PKC-a mediated
Nox2/ROS signals is essential for up-regulation of MMP-9 and cell migration enhanced by BK
Valente et al., Cell Signal 2013
:
IL-18 induced
Nox1 dependent ROS generation, TRAF3IP2 expression, and IKK/NF-?B and
JNK/AP-1 activation