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AKT3 — ICAM1
Text-mined interactions from Literome
Lin et al., J Cell Physiol 2007
(Lung Neoplasms) :
We initially observed that IL-1beta induced
ICAM-1 promoter activity was
attenuated by the inhibitors of Src ( PP1 ), PDGFR ( AG1296 ), PI3-K ( LY294002 and wortmannin ), and
Akt ( SH-5 ), revealed by reporter gene assay, Western blotting, and RT-PCR analyses ... The
involvement of Src and
PI3-K/Akt in IL-1beta induced
ICAM-1 expression was significantly attenuated by transfection of A549 cells with dominant negative plasmids of Src, p85 and Akt, respectively ... These results suggested that
Akt phosphorylation mediated through transactivation of Src/PDGFR promotes the transcriptional p300 activity and eventually
leads to
ICAM-1 expression induced by IL-1beta
Hur et al., Stem Cells 2007
(Ischemia) :
In vitro and in vivo experiments using adenoviral vector for constitutively active or dominant negative Akt genes showed that activated
Akt enhanced
intercellular adhesion molecule 1 ( ICAM-1 ) expression on ECs
Yoon et al., PloS one 2008
(Neoplasm Metastasis...) :
In neuroblastoma cell lines,
ICAM-2 expression did not
affect AKT activation, tumorigenic potential or chemosensitivity, as has been reported for some types of transfected cells
Minhajuddin et al., J Biol Chem 2009
:
Furthermore, we observed that expression of the constitutively active form of PKC-delta or
Akt was
sufficient to induce NF-kappaB activation and
ICAM-1 expression, and that co-expression of mTOR suppressed these responses ... In reciprocal experiments, inhibition/depletion of mTOR augmented NF-kappaB activation and
ICAM-1 expression
induced by PKC-delta or
Akt
Wong et al., Arthritis Res Ther 2010
(Arthritis, Rheumatoid) :
Further investigations showed that the expression of
ICAM-1 , VCAM-1 and chemokines stimulated by IL-27 was differentially
regulated by intracellular activation of phosphatidylinositol 3-OH
kinase-AKT , c-Jun amino-terminal kinase and Janus kinase pathways
Liu et al., Blood 2012
:
ICAM-1 activation also
stimulated phosphorylation of
Akt ( p-Ser473 ) and eNOS ( p-Ser1177 ), thereby increasing NO production
Park et al., Br J Pharmacol 2013
:
A PI3K specific inhibitor ( LY294002 ),
Akt inhibitor VIII ( Akti ) and NF-?B inhibitors ( Bay-11-7082 and MG-132 )
attenuated the induction of
ICAM-1 by PGE2