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FOS — ICAM1

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
Toyoshima et al., Biochem Biophys Res Commun 1999 (Carcinoma, Squamous Cell...) : These findings indicate that NO up-regulates ICAM-1 expression on cancer cells by a regulatory mechanism involving PKC and suggest that NF-kappaB, but not AP-1 , might be involved in induction of ICAM-1 by NO in cancer cells
Wang et al., Arterioscler Thromb Vasc Biol 1999 : Adenovirus mediated overexpression of c-Jun and c-Fos induces intercellular adhesion molecule-1 and monocyte chemoattractant protein-1 in human endothelial cells
Liao et al., Endothelium : journal of endothelial cell research 2000 : We have demonstrated that PDTC not only induced AP-1 binding and ICAM-1 expression by itself, but it also augmented AP-1 activation and ICAM-1 induction in low-dose IL-1alpha treated cells
Chang et al., J Surg Res 2001 (Disease Models, Animal...) : Therapeutic effect of dimethyl sulfoxide on ICAM-1 gene expression and activation of NF-kappaB and AP-1 in septic rats ... We investigated the therapeutic effect of DMSO on intercellular adhesion molecule 1 ( ICAM-1 ) gene expression and activation of nuclear factor-kappaB (NF-kappaB) and activating protein-1 (AP-1) in a rat model of peritonitis sepsis ... The levels of ICAM-1 mRNA expression and activation of NF-kappaB and AP-1 in livers were determined at 3 and 6 h post-CI ... At 3 h post-CI surgery ( early sepsis ), DMSO treatment at 30 and 60 min post-CI surgery significantly inhibited sepsis induced ICAM-1 mRNA expression and activation of NF-kappaB and AP-1 ... DMSO has no effect on ICAM-1 gene expression and activation of NF-kappaB and AP-1 when administered at 90 min post-CI surgery
Schuringa et al., Cytokine 2001 : Overexpression of c-Jun and c-Fos strongly enhanced STAT3-driven IRE transactivation as well as transactivation of the human intercellular adhesion molecule (ICAM)-1 promoter
Wang et al., Arterioscler Thromb Vasc Biol 2001 : In the present study, a regulated adenovirus expressing a dominant negative mutant of c-Jun ( TAM-67 ) was used to examine the role of AP-1 in the LDL induced ICAM-1 activation
Chen et al., Mol Pharmacol 2004 : TNF-alpha induced ICAM-1 promoter activity was attenuated using an activator protein-1 (AP-1) site deletion mutant, indicating the involvement of AP-1 in ICAM-1 expression ... The inhibitory effects of apigenin and luteolin on ICAM-1 expression are mediated by the sequential attenuation of the three MAPKs activities, the c-fos and c-jun mRNA expressions, and the AP-1 transcriptional activity
Franscini et al., Circulation 2004 (Vasculitis) : Our study revealed a novel antiinflammatory mechanism of APC dependent gene regulation in HCAECs since c-Fos dependent induction of MCP-1 and ICAM-1 was suppressed
Böhm et al., Exp Dermatol 2004 : Functional studies have shown that alpha-MSH exerts anti-inflammatory actions in human fibroblastic skin cells by suppressing interleukin-1 (IL-1) induced IL-8 production, activation of the transcription factor activator protein-1 (AP-1) and induction of intercellular adhesion molecule-1 by interferon-alpha
Yang et al., J Cell Physiol 2010 (Arthritis, Rheumatoid) : IL-1beta induced ICAM-1 expression, extracellular signal regulated kinase ( ERK ) and c-Jun-N-terminal kinase (JNK) phosphorylation, AP-1 activation, and nuclear factor-kappaB (NF-kappaB) p65 translocation were attenuated by the inhibitors of MEK1/2 ( U0126 ), JNK ( SP600125 ), AP-1 ( tanshinone IIA ), and NF-kappaB ( helenalin ) or transfection with respective short hairpin RNA plasmids ... These results suggest that in human RASFs, activation of ERK, JNK, AP-1 , and NF-kappaB are essential for IL-1beta induced ICAM-1 expression and leukocyte adhesion
Yang et al., J Biol Chem 2010 (Mouth Neoplasms) : PGE ( 2 ) -induced expression of ICAM-1 and migration activity were inhibited by a specific inhibitor, siRNA, and mutants of PKCd, c-Src, and AP-1
Zhang et al., Zhonghua Jie He He Hu Xi Za Zhi 2010 (Ventilator-Induced Lung Injury) : To study the expression of intercellular cell adhesion molecule-1 ( ICAM-1 ), Interleukin-10 (IL-10) and the activation of transcription factor activator protein-1 (AP-1) in a rabbit model of ventilator induced lung injury ( VILI ) and therefore to explore their possible role in VILI
Fong et al., J Cell Physiol 2012 (Bone Neoplasms...) : In addition, activator protein-1 (AP-1) inhibitors suppressed the cell migration and ICAM-1 expression enhanced by CCN6
Muñoz et al., J Immunol 1996 : Taken together, these results indicate that the antioxidant PDTC induces transcriptional activation of ICAM-1 and that this induction is mediated at least in part by the transcription factor AP-1
Koyama et al., J Immunol 1996 : Cross linking of intercellular adhesion molecule 1 ( CD54 ) induces AP-1 activation and IL-1beta transcription ... In this study, we provide the first evidence that ICAM-1 engagement induces activation of the transcription factor AP-1 and transcription of the IL-1beta gene using a specific Ab to cross-link ICAM-1 on a rheumatoid synovial cell line ( E11 cells )
Kupatt et al., J Mol Cell Cardiol 1997 : Because upregulation of AP-1 through hypoxia alone did not affect ICAM-1 expression, we conclude that redox-sensitive NFkappaB activation triggers ICAM-1 upregulation
Ishizuka et al., Clin Exp Immunol 1998 : These findings suggest that ICAM-1 or ELAM-1 expression of HUVEC stimulated via TXA2 receptors is augmented by induction of NF-kappaB and AP-1 binding activity through the PKC system, and that VCAM-1 expression is augmented by induction of NF-kappaB binding activity