◀ Back to ICAM1
ICAM1 — TCF3
Text-mined interactions from Literome
Lawson et al., J Immunol 1999
:
ICAM-1 cross linking
caused activation of Erk-1 and the AP-1
transcription factor complex, without any increase in NF-kappaB activity, in contrast to TNF stimulation
Hoffmann et al., Clin Exp Immunol 1999
:
Since PDTC is known to be a potent inhibitor of NF-kappaB, the stimulating effects of neopterin on
ICAM-1 gene expression and protein generation may be
mediated by activation of this
transcription factor
Hess et al., Stroke 2000
(Reperfusion Injury) :
We determined whether a NF-kappaB
transcription factor decoy ( TFD ) could
block intercellular adhesion molecule (ICAM)-1 upregulation, an indicator of endothelial cell activation
Blaber et al., J Am Soc Nephrol 2003
:
Only AP-1 activation, however, was calcium dependent, suggesting the central
involvement of this
transcription factor in
ICAM-1 and RANTES induction after the ligation of ICAM-1
Ishihara et al., Dig Dis Sci 2006
:
ICAM-1 expression, stimulated by neutrophil elastase, was partially reduced by a diacylglycerol kinase inhibitor and protein kinase C inhibitor, but was completely
inhibited by a phospholipase C inhibitor, cytosolic Ca ( 2+ ) chelator, calmodulin antagonist, and nuclear
transcription factor kappa B inhibitor
Sun et al., International journal of biological sciences 2008
:
The expression of HO-1, iNOS ( Western blot ) and
ICAM-1 ( cell ELISA ) proteins and
activation of inflammation-relevant
transcription factor , NF-kappaB ( EMSA ) were assessed
Grether-Beck et al., Proc Natl Acad Sci U S A 1996
:
Activation of
transcription factor AP-2
mediates UVA radiation- and singlet oxygen induced expression of the human
intercellular adhesion molecule 1 gene
Jaeschke et al., Hepatology 1999
(Endotoxemia...) :
However, there was no significant difference in other critical parameters, e.g.,
activation of the
transcription factor , nuclear factor-kappaB (NF-kappaB), and soluble
intercellular adhesion molecule-1 ( sICAM-1 ), parenchymal cell apoptosis, and neutrophil sequestration in the liver