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Zhu et al., Atherosclerosis 1999
:
IL-1 alpha at this dose ( which activates NF-kappa B, but not AP-1 ) also enhanced
LDL activated
AP-1 binding
Zhu et al., Arterioscler Thromb Vasc Biol 2001
:
We previously reported that
LDL activates c-Jun and
AP-1 in ECs
Ares et al., BMC immunology 2002
:
In contrast, oxidized
LDL stimulated
AP-1 and PPARgamma but inhibited NF-kappaB, indicating that the effects of lipid loading with ac-LDL were not due to oxidation of lipids
Zhou et al., Zhonghua Yi Xue Za Zhi 2002
:
Pre-treatment with the different specific kinase inhibitors, the activities of
AP-1 induced by
Ox-LDL were determined by electrophoretic mobility shift assay ( EMSA ) ... The inhibitor of PKC remarkably reduced the activity of
AP-1 induced by
Ox-LDL
Fu et al., J Lipid Res 2003
:
Electrophoretic mobility shift assays further demonstrated that
LDL-ICs stimulated transcription factor
AP-1 activity
Ziouzenkova et al., J Biol Chem 2003
(Inflammation) :
Here we demonstrate that
LDL ( - )
increases tumor necrosis factor alpha (TNFalpha) induced inflammatory responses through NF kappa B and
AP-1 activation with corresponding increases in vascular cell adhesion molecule-1 ( VCAM1 ) expression ... LPL treated
LDL ( - )
suppressed NF kappa B and
AP-1 activation, increasing expression of the PPAR alpha target gene I kappa B alpha, although only in the genetic presence of PPAR alpha and with intact LPL hydrolysis
Wu et al., Cell Biochem Funct 2003
:
The present study showed that
ox-LDL strongly
induced AP-1 binding activity in rat mesangial cells ( RMCs ) in a dose- and time dependent manner, reaching the maximal activation at 250 microg ml(-1) within 24 h ... This study demonstrates that multiple kinase activities are involved in the mechanism of
ox-LDL induced
AP-1 activation in mesangial cells, and ox-LDL stimulates AP-1 through JNK-c-Jun other than MEK-c-Fos signalling pathway
Ryoo et al., Biochem Biophys Res Commun 2004
:
Pretreatment of hAoSMCs with fenofibrate abolishes the
effects of
LDL on
AP-1 activation without affecting nuclear factor (NF)-kappaB
Ares et al., Arterioscler Thromb Vasc Biol 1995
:
In the present study we demonstrated that
Ox-LDL activates
activator protein-1 (AP-1) , a transcription factor generally induced by mitogenic substances
Lin et al., Atherosclerosis 1996
(Arteriosclerosis) :
In contrast, the binding activities of
AP-1 and GATA, on the other hand, are
increased by
LDL
Zhu et al., Arterioscler Thromb Vasc Biol 1998
:
This study demonstrates that ( 1 )
LDL is an endothelial agonist distinct from other cell stimulators, such as cytokines, endotoxin, and phorbol 12-myristate 13-acetate, because LDL appears to activate human umbilical vein endothelial cells predominantly through the transcription factor AP-1 and not NF-kappaB ; and ( 2 ) LDL
increases AP-1 via mechanisms involving multiple kinase activities and c-Jun transcription
Zhu et al., Biochim Biophys Acta 1999
:
We have reported previously that native
low-density lipoprotein (LDL) activates c-Jun and transcription factor
AP-1 in human umbilical vein endothelial cells ( HUVEC ) ... The aim of this study was to elucidate the upstream signaling mechanisms mediating
LDL activation of
c-Jun/AP-1