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NFKB1 — SELE
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Kayal et al., Mol Microbiol 1999
:
By infecting in vitro human umbilical vein endothelial cells ( HUVEC ) with L. monocytogenes, we found that wild-type bacteria
induced the expression of the adhesion molecules ( ICAM-1 and
E-selectin ), chemokine secretion ( IL-8 and monocyte chemotactic protein-1 ) and
NF-kappa B nuclear translocation
Madge et al., J Biol Chem 2000
:
Although Akt has been reported to activate NFkappaB, LY294002 does not prevent TNF- or IL-1 induced degradation of IkappaBalpha, beta, or epsilon, transcription of
NFkappaB dependent
E-selectin or ICAM-1 promoter-reporter genes, or surface expression of E-selectin or ICAM-1 in human EC
Russell et al., Am J Physiol Gastrointest Liver Physiol 2000
(Ischemia) :
These findings suggest that superoxide and TNF-alpha mediate gut I/R induced
E-selectin expression via an
NF-kappaB dependent mechanism ; this upregulation of E-selectin contributes significantly to I/R induced neutrophil recruitment
Tsuyuki et al., J Immunol 2001
:
It is known that
NF-kappa B activation is
required for transcription of
E-selectin , and the current data show that the suppression of E-selectin expression by S-nitroso-N-acetyl-penicillamine pretreatment and thiol deprivation was associated with reduced NF-kappa B DNA binding activity in PAEC
Ochi et al., Eur J Immunol 2002
:
Because induction of both VCAM-1 and
E-selectin by these cytokines is
NF-kappaB dependent , we investigated whether the inhibitory effect of hyperosmotic medium might involve IRF-1
Ishii et al., Toxicol Appl Pharmacol 2002
:
These results suggest that BLM can directly
induce E-selectin expression with an increase in transcription in endothelial cells through activation and nuclear translocation of
NF-kappaB/Rel without mediation of inflammatory cytokines
Li et al., J Immunol 2003
:
In surviving cells, TRAIL activates
NF-kappaB ,
induces expression of
E-selectin , ICAM-1, and IL-8, and promotes adhesion of leukocytes
Uchiba et al., Thromb Haemost 2004
:
These observations suggested that AT
inhibited the TNF-alpha induced increase in
E-selectin expression in HUVECs by inhibiting the interaction of
NF-kappaB with CBP/p300 through cAMP dependent protein kinase A-induced CREB activation
Yu et al., Blood 2005
(Arteriosclerosis) :
Endothelial expression of
E-selectin is induced by the platelet-specific chemokine platelet factor 4 through LRP in an
NF-kappaB dependent manner
Lee et al., J Biol Chem 2005
:
FBI-1 enhanced
NF-kappaB mediated transcription of
E-selectin genes in HeLa cells upon phorbol 12-myristate 13-acetate stimulation and overcame gene repression by IkappaB alpha or IkappaB beta ... Confocal microscopy showed that FBI-1 increased NF-kappaB movement into the nucleus and increased the stability of NF-kappaB in the nucleus, which enhanced
NF-kappaB mediated transcription of the
E-selectin gene
Reed et al., Dig Dis Sci 2005
(Colitis...) :
Colon tissue was collected for assessment of histological changes,
NF-kappa B activation , myeloperoxidase (MPO) activity, and expression of NK-1R, SP, TNFalpha, IL-1beta, VCAM-1, ICAM-1,
E-selectin , CINC-1, MIP-1alpha, and iNOS
Chiu et al., Blood 2007
:
Gel shifting and chromatin immunoprecipitation assays showed that SMC coculture increased the nuclear factor-kappaB (NF-kappaB)-promoter binding activity in ECs ; inhibition of
NF-kappaB activation by p65-antisense, lactacystin, and N-acetyl-cysteine
blocked the coculture induced
E-selectin promoter activity
Li et al., Molecular vision 2007
:
Inhibition of
NF-kappaB partially
prevented the induction of IL-1alpha, IL-8, and
ELAM-1 , but not IL-6
Rajan et al., J Cell Biochem 2008
:
We further demonstrated that inhibition of
NF-kappaB completely
blocked TNF-alpha induced expression of ICAM-1, VCAM-1 and
E-selectin
Song et al., Br J Pharmacol 2009
:
Down-regulation of VCAM and
E-selectin expression induced by CORM-3 was independent of HO-1 up-regulation and was predominantly
due to inhibition of sustained
NF-kappaB activation
Katada et al., Inflammation 2010
(Inflammatory Bowel Diseases...) :
The obtained results indicate that tissue levels of TNF-alpha,
E-selectin and ICAM-1 protein expression,
activation of
NF-kappaB , and subsequent accumulation of PMN were elevated in I/R challenged jejunum
Lewis et al., Mol Cell Biol 1994
:
Cytokine induced expression of the
E-selectin gene
requires the promoter binding and interaction of the transcription factors
NF-kappa B and ATF
Weber et al., Circulation 1995
:
Our data suggest that aspirin inhibits
NF-kappa B mobilization,
induction of VCAM-1 and
E-selectin , and subsequent monocyte adhesion in endothelial cells stimulated by TNF, thereby providing an additional mechanism for therapeutic effects of aspirin
Weber et al., J Immunol 1995
:
Our data suggest that specific phosphorylation following protein tyrosine kinase activation may be required for
NF-kappa B mobilization and
induction of VCAM-1 and
ELAM-1 by TNF
Cockerill et al., Blood 1995
:
CsA also suppressed E-selectin, but not vascular cell adhesion molecule-1 ( VCAM-1 ) expression in endothelial cells, even though the
E-selectin promoter is
activated by
NF-kappa B rather than NFAT
Kaszubska et al., Mol Cell Biol 1993
:
We previously reported that
NF-kappa B and a complex we referred to as NF-ELAM1
play a central role in cytokine induced expression of the
E-selectin gene
Hallahan et al., Biochem Biophys Res Commun 1995
:
These data demonstrate that
E-selectin expression does not require cytokine synthesis, but
involves NFkB activation
Zhou et al., Eur J Immunol 1996
:
Since it has been documented that the expression of
E-selectin and Mac-1 is
regulated either directly or indirectly by the transcription factor
NF kappa B , our studies provide in vivo evidence that tepoxalin is a potent inhibitor of NF kappa B-mediated events in animal models and this novel molecular mechanism clearly defines it as a new class of anti-inflammatory compounds
Essani et al., J Immunol 1996
:
However, the fact that hepatic parenchymal cells, despite NF-kappa B activation do not express E- selectin mRNA, suggests that
NF-kappa B activation alone is not
sufficient for
E-selectin gene transcription in vivo
Lee et al., Immunol Lett 1996
:
The
NF-kappa B inhibitor, tepoxalin,
suppresses surface expression of the cell adhesion molecules
CD62E , CD11b/CD18 and CD106
Palmetshofer et al., Transplantation 1998
:
BS-I strongly induced
E-selectin , P-selectin, intercellular adhesion molecule-1, and interleukin-8 mRNA in an
NF-kappaB dependent manner
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