Other 16931033

Following TNF-α stimulation, IκB is phosphorylated, ubiquitinated, and degraded by a proteasome, resulting in the release of cytoplasmic NF-κB, which then translocates to the nucleus

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p(RGD:Tnf) increases complex(SCOMP:"Nfkb Complex")
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297e9fc34d
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PubMed 12878589

To explore how LPL negatively regulates LDL(-)/Tnf induction of the Vcam1 promotor ...Tnfa induced Nfkb binding, a response augmented in the presence of LDL(-). In the presence of LPL, however, LDL(-) significantly decreased Nfkb binding; WY14163 had similar effects.% In our study LDLR overexpression significantly increased LDL(-) activation of the VCAM1 promotor but not PPARa ligand binding domain activation.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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65d7b03063
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PubMed 15545623

Wild-type and Jnk1-/- Jnk2-/- (Jnk-/-) fibroblasts....Furthermore, TNF-stimulated NF-kB DNA binding activity was detected in nuclear extracts prepared from wild-type and Jnk-/- fibroblasts, but not from wild-type (N-IkBa) or Jnk-/- (N-IkBa) fibroblasts,

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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4bb4b3648b
Networks

PubMed 16633352

Besides inducing interleukin-1 beta (IL-1beta) and interleukin-10 (IL-10) production, MSP triggers an enhanced tumor necrosis factor-alpha release, especially in healthy and pulmonary fibrosis smokers.

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act(complex(SCOMP:"Nfkb Complex"), ma(tscript)) increases p(RGD:Tnf)
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95403546f8
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PubMed 12960163

Nuclear factor kappaB (NF-kappaB) plays an important role in the transcriptional regulation of genes involved in inflammation and cell survival. In this study, we demonstrated that NF-kappaB-dependent gene expression was inhibited by E1A in poly(ADP)-ribose polymerase-1 knock out (PARP-1 (-/-)) cells complemented with wild type PARP-1 after tumor necrosis factor alpha (TNFalpha) or lipopolysaccharide (LPS) treatment. PARP-1 and p300 synergistically coactivated NF-kappaB-dependent gene expression in response to TNFalpha and LPS. Furthermore, PARP-1 interacted directly with p300 and enhanced the interaction of NF-kappaB1/p50 to p300. The C terminus, harboring the catalytic domain of PARP-1 but not its enzymatic activity, was required for complete transcriptional coactivation of NF-kappaB by p300 in response to TNFalpha and LPS. Together, these results indicate that PARP-1 acts synergistically with p300 and plays an essential regulatory role in NF-kappaB-dependent gene expression.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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74ad991aaa
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PubMed 15217635

Exposure to TNF-alpha activates transcription factors NF-kappaB, Smad3/4, and PPARalpha/gamma

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
d3ae841f89
Anatomy
epithelium
Cell
fibroblast
CellLine
COS-1 cell
CellStructure
Cell Nucleus
Disease
estrogen-receptor negative breast cancer
Species
10116
Networks
BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
12e2bfdad5
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PubMed 9794459

Treatment of Rat VSMCs with IL1beta (10 ng/ml) and Tnf alpha (100ng/ml) induced the iNos expression by 8-10 fold. The subsequent production of Nox were blocked by adding a proteasome inhibitor MG115 (40 M). this suggest that Tnf alpha and Il 1 beta stimulated NO production and iNos expression via Nfkb.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
6e66c47631
Anatomy
blood vessel smooth muscle
Cell
kidney epithelial cell
CellLine
293 cell
CellStructure
Cell Nucleus
Disease
atherosclerosis
MeSHAnatomy
Sputum
MeSHDisease
Head and Neck Neoplasms
Species
10116
Networks

PubMed 20339581

Well known is the case of TNF?, produced by tumor and immune cells, which leads to the survival of cancer cells by the upregulation of antiapoptotic proteins, that is, Bcl-2 [13?15], via the activation of the nuclear factor kappa B (NF?B) [16].

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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7529ca8599
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PubMed 19338980

As expected, NF-kB binding was induced by TNF-a treatment compared to untreated control (Mock) (Fig. 3; lanes 2 and 1, respectively).....the same DNA-protein complex was significantly down-regulated when HUVEC were infected with AdVshRNAIFI16 before TNF-a treatment (lane 4).

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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80cf9013b9
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PubMed 15833768

we sought to assess whether TSP-1 is able to activate NF-?B. Using a NF-?B-dependent promoter construct, we monitored NF-?B activity after EC treatment with TSP-1 (Fig. 6A). We found that TSP-1 induced a threefold increase in promoter activity (normalized to control). In agreement with the literature (49), TNF-? provided a fivefold increase of NF-?B-dependent promoter activity.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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5255c3fa48
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PubMed 14766535

TNF-alpha-induced increase in Caco-2 TJ permeability correlated with Caco-2 NF-kappa B activation. Inhibition of TNF-alpha-induced NF-kappa B activation by selected NF-kappa B inhibitors, curcumin and triptolide, prevented the increase in Caco-2 TJ permeability, indicating that NF-kappa B activation was required for the TNF-alpha-induced increase in Caco-2 TJ permeability.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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93efdfe6f8
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PubMed 9748323

To circumvent this problem, we developed an alternative procedure which allowed us to show that in neutrophils, LPS and TNFalpha induce a NF-kappaB DNA-binding activity which essentially consists of p50/RelA dimers,

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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e23087e7a3
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PubMed 9242696

Although IL-1a and TNFa caused induction of NF-kB DNA binding activity in both cell types,(By EMSA)

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
451be7a439
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PubMed 15602009

TNF activates NFKB transcriptional activity in macrophages and epithelial cells . TNF similarly activates p38 MAPK.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
25cb6662df
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PubMed 15456740

We, therefore, examined the transactivation of NF-kB in response to H2O2 and CSC in A549 cell stably transfected with the NF-kB-dependent promoter. TNF-a treatment was used as a positive control. H2O2 and TNF-a treatments significantly increased NF-kB transactivation, compared with the control values at 24 h in A549 cells (Fig. 7A).

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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e0921d6bce
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PubMed 10391896

NF-kappaB activation by tumor necrosis factor alpha (TNFalpha) provides a survival signal that impairs the TNFalpha-induced apoptotic response. We show here that expression of Par-4 inhibits the TNFalpha-induced nuclear translocation of p65 as well as the kappaB-dependent promoter activity.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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85306e42e0
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PubMed 19273391

Inflammatory stimuli such as tumour necrosis factor alpha (TNFalpha) and lipopolysaccharides (LPS) trigger rapid NFkappaB activation in an IKKbetadependent manner (canonical pathway). Alternatively, a subset of TNF family members can induce the activation of a specific form of NFkappaB by a slower process dependent on the IKKalpha subunit (noncanonical pathway) (99).

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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c6f8c4bcbe
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PubMed 19842832

In vitro treatment of AM isolated from COPD patients and healthy subjects with TNF-a resulted in significantly increased NF-kB activity in AM of COPD patients when compared with those of healthy subjects.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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45e8014baa
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PubMed 9727009

Stimulation of myocytes with TNFalpha resulted in a 2.1-fold increase (p < 0.001) in NFkappaB-dependent gene transcription and nuclear DNA binding.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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eb0d415a59
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PubMed 12490536

Inhibition of AR attenuated TNF-alpha and hyperglycemia-induced activation of protein kinase C (PKC), phosphorylation of the inhibitory subunit of nuclear factor-kappaB (NF-kappaB), and stimulation of NF-kappaB

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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f1257e9572
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PubMed 12700228

Transient transfection of BRCA1 significantly enhances the ability of the tumor necrosis factor-alpha or interleukin-1beta to activate transcription from the promoters of NF-kappaB target genes.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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1f2961c08b
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PubMed 14656721

Stimulation of neutrophils with TNF-a resulted in increased nuclear levels of NF-kB. Addition of H2O2 to neutrophil cultures containing TNF-a potently inhibited NF-kB activation compared with that seen in neutrophils incubated with TNF-a alone (Fig. 4B).

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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029dd5ac5c
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PubMed 15687488

When overexpressed, CPAP enhanced NF-kappaB-dependent transcription induced by tumor necrosis factor-alpha (TNFalpha).

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
6b4dc03889
Networks

PubMed 15489375

TNF-? stimulated NF-?B-dependent promoter activity (Fig. 5D), that rottlerin had little effect on TNF-?-induced NF-?B-dependent promoter activity, and that PDTC diminished NF-?B-dependent promoter activity

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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46bdc5a0e3
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PubMed 1912581

A TNF-inducible protein also bound to this fragment and resulted in a different mobility pattern. Binding of the TNF-induced nuclear protein to the -419 to -304 fragment was inhibited by an oligonucleotide containing the nuclear factor-kappa B (NF-kappa B) consensus sequence. DNA footprinting demonstrated protection of an NF-kappa B binding site at positions -377 to -368. Methylation interference assays showed that the TNF-induced protein made contact points with guanine residues in the same NF-kappa B sequence.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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2ea8563145
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PubMed 11597930

In contrast, TNF-alpha activation of the IL-8 promoter was mediated almost entirely through the nuclear factor-?B and activation protein-1 response elements present between -70 and -133 bp of the IL-8 promoter.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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0671f173e9
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PubMed 15936183

One major molecular effect of TNF-a is the activation of NFKB

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
6488fa10cf
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PubMed 17062602

We showed that pretreatment of neutrophils with NF-kB blockers profoundly inhibits the induction of early-response genes encoding TNF-a, IL-1b, CXCL8, CCL3, and CCL4 in neutrophils and hinders the release of the corresponding proteins. Thus, NF-kB appears to be a key player in the induction of inflammatory cytokines and chemokines in neutrophils.

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act(complex(SCOMP:"Nfkb Complex"), ma(tscript)) increases p(RGD:Tnf)
Hash
78e3b26e2f
Networks

PubMed 18363837

TNF-alpha-induced increase in MLCK promoter activity was mediated by NF-kappaB activation. There were eight kappaB binding sites on MLCK promoter. The NF-kappaB1 site at +48 to +57 mediated TNF-alpha-induced increase in MLCK promoter activity. The NF-kappaB2 site at -325 to -316 had a repressive role on promoter activity. The opposite effects on promoter activity were due to differences in the NF-kappaB dimer type binding to the kappaB sites. p50/p65 dimer preferentially binds to the NF-kappaB1 site and up-regulates promoter activity; while p50/p50 dimer preferentially binds to the NF-kappaB2 site and down-regulates promoter activity.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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2bc77f2621
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PubMed 8717528

NF-kappa B can be activated by exposure of cells to LPS or inflammatory cytokines such as TNF or IL-1, viral infection or expression of certain viral gene products, UV irradiation, B or T cell activation, and by other physiological and nonphysiological stimuli.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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02a59eba6f
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PubMed 15284221

antisense ablation of AR prevented both TNF-alpha-induced PKC and NF-kappaB activation

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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46f14b9b13
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PubMed 12859951

TNFalpha, a strong NF-kappaB activator required for hepatocyte proliferation during liver regeneration, triggered the expression of S100A6 mRNA in human hepatoblastoma cell line HepG2

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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5df88687a0
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PubMed 10616907

We report that TNF induces DNA replication in growth-arrested LE6 cells and that its effect involves the activation of NFkappaB and STAT3 and an increase in c-myc and IL-6 mRNAs. We conclude that NFkappaB is an essential component of the TNF proliferative pathway and that TNF-induced changes in IL-6 mRNA, STAT3, and c-myc mRNA are dependent on NFkappaB activation.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
19202d5a13
Anatomy
liver
Cell
hepatic stellate cell
CellLine
RIN-m5F cell
CellStructure
Cell Membrane
Disease
osteosarcoma
Species
10116
Networks
BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
97cdfe3af4
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PubMed 10946303

TNF-a rapidly (10 min) activated NF-kB, similar activation being seen after 1 and 24 h (Fig. 10A).

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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688664f92f
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PubMed 11799112

We found that the reintroduction of PTEN into prostate cells inhibited TNF-stimulated NF-kappaB transcriptional activity.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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441e7ad01f
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PubMed 10699758

Simultaneous overexpression of selenophosphate synthetase and phospholipid-hydroperoxide GSH peroxidase (PHGPx) [250] blocks activation of NF-kB by IL-1. Overexpression of SOD [84] or GSH peroxidase [81, 211] abolished NF-kB activation by preventing degradation of IkB after stimulation with TNF-a. The precise mechanism(s) through which oxidants and reductants influence activation of NF-kB is presently unknown; however, there is evidence that antioxidant enzyme (AOE372), a redox-sensitive thioredoxin peroxidase, regulates IkB phosphorylation [246]. Phosphatases The phosphatases are an important component of most signal transduction pathways, because failure to reverse kinase actions can disrupt normal cellular functions. For example, transfection of human fibroblasts with constitutively active ras (hRasV12) inhibits cell growth and ultimately results in a senescentlike phenotype [441]. Similarly, constitutive ERK activation has an inhibitory effect on cell cycle progression [442,443]. Both the serine/threonine phosphatases and the PTPs are known to be redox-sensitive [82,144,153,156,271,281, 444-449]. The mechanism of redox effects on activity is probably best understood for the PTPs. Without exception, the PTPs contain a highly conserved region of 11 amino acid residues in their catalytic domain; specifi- cally, (Ile/Val)-His-Cys-X-Ala-Gly-X-X-Arg-(Ser/Thr)- Gly, where X is a nonconserved amino acid [17]. Either oxidation or mutation of the cysteine renders these molecules inactive [17,281]. H2O2 is a potent inhibitor of PTPs. As in the case of other oxidants, H2O2 probably oxidizes the thiolate anion at the catalytic site [280]. Because formation of a phosphorylcysteine intermediate seems to be critical to PTP activity [450-452], blocking it through oxidation of the cysteine inactivates the molecules. In many cases, treatment of cells with H2O2 stimulates increases in protein phosphorylation by inhibiting phosphatase-catalyzed removal of phosphate groups. Furthermore, mitogens that increase cellular ox- idant production may stimulate phosphorylation indirectly by decreasing phosphatase activity. Additional mechanisms are involved in stimulation of pathways activated by growth factors that increase oxidant production, however, because there are known instances in which the oxidants they produce have no effect on protein phosphorylation. For example, TGF-b1 stimulates phosphorylation of numerous proteins and has been shown to cause a large increase in H2O2 production; however, its effects on protein phosphorylation are not blocked by catalase [453]. Furthermore, H2O2 is effective in promoting phosphorylation of phospholipase D, the PDGF receptor, and PKC-a even after pretreatment of Swiss 3T3 fibroblasts with orthovanadate to inhibit phosphatases [454]. Thus, although diminished phosphatase activity may partially account for increased phosphorylation in some cases, it cannot totally account for oxidation effects on phosphorylation in every case. SPECIFICITY In general, there is good agreement between studies on redox effects on any given gene; albeit, not all oxidizing or reducing treatments exert equivalent effects. This is clearly demonstrated in studies of pag , which encodes a protein associated with cellular proliferation. Pag protein inhibits the tyrosine kinase activity of the Abelson (abl ) protein by binding to its SH3-binding domain [455]. BSO, menadione, sodium arsenate, and diethyl maleate all stimulate pag expression, but H2O2 does not [269]. Conversely, H2O2 stimulates c-fos expression (Table 1), although 4-hydroynonenal (a product of v-6-polyunsaturated fatty acid peroxidation) not only fails to induce c-fos expression but is actually inhibitory to c-fos induction by EGF and PDGF [185]. Similarly, some oxidants such as diamide decrease hypoxia-induced signals [201], although others such as H2O2 increase them [124]. As might be expected, the effects of any stimu...

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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41c6abc840
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PubMed 11978627

Nuclear factor-kappaB (NF-kappaB) was activated within 15 min of TNF-alpha addition.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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e2c6ac79fc
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PubMed 12897154

Although TRAF2 is known to be required for TNF-induced JNK and NF-kappaB activation

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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fec641bee1
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PubMed 12631585

NF-kappaB inhibitor, sulfasalazine, inhibited neuromelanin induced synthesis of proinflammatory mediator molecules Nitric oxide, TNF-alpha and IL-6 in a dose-and time-dependent manner.

BEL
complex(SCOMP:"Nfkb Complex") increases p(RGD:Tnf)
Hash
8bfeb7a773
Anatomy
colon
Cell
mesangial cell
CellLine
293T/17 cell
CellStructure
Cytoplasm
Disease
B-cell lymphoma
Species
10116
Networks

PubMed 18337563

TNF also induces the notch ligand jagged-1, through an NFkappaB-dependent mechanism

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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231f249736
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PubMed 19842832

The activation of NF-kB therefore leads to a coordinated increase in the expression of many genes whose products mediate inflammatory and immune responses. For example, the coordinated stimulation of the expression of the genes for E-selectin, IL-8, and TNF-a results in the recruitment and activation of neutrophils [32].

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act(complex(SCOMP:"Nfkb Complex"), ma(tscript)) increases p(RGD:Tnf)
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df51527c3c
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PubMed 19842832

In vitro treatment of AM isolated from COPD patients and healthy subjects with TNF-a resulted in significantly increased NF-kB activity in AM of COPD patients when compared with those of healthy subjects. Pyrrolidine dithiocarbamate (PDTC) and N-acetyl-L-cysteine (NAC; precursor for glutathione) significantly inhibited the activation of NF-kB induced by TNF-a [149].

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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12385cda92
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PubMed 12193701

The cells treated with a neutralizing anti-TNF-alpha Ab attenuated IFN-gamma induced DNA binding activity of NFkB. The supershift analysis using Antibodies to the p50 and p65 showed the activation of both subunits of NF-kB, confirming that IFN-gamma induced NFkB activation was due to induction and subsequent autocrine/paracrine action of TNF-alpha.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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3a298b8bba
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PubMed 9446586

Nuclear extracts from LPS, TNF-alpha, and IL-1beta-treated VSMCs, IL-1beta-treated human hepatoma HepG2, and human lung fibroblast IMR-90 cells showed strong inducible binding activity to the NF-kappaB-like site by gel shift assays. These results demonstrated that NF-kappaB-like nuclear factor was involved in the inducible expression of the human bradykinin B1 receptor gene during inflammatory processes.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
a8f8403040
Anatomy
blood vessel smooth muscle
Cell
hepatocyte
CellLine
32D cell
CellStructure
Extracellular Matrix
Disease
atherosclerosis
MeSHAnatomy
Sputum
MeSHDisease
Head and Neck Neoplasms
Species
10116
Networks
BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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e66a392ddb
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PubMed 10460762

These data indicate that TNF-a or Fas ligation induces activation of NF-kB p65 hetero- or homodimers in bronchiolar epithelial cells.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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3bfc41796c
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PubMed 8849369

TNFa-induced NF-KB activation in synovial cells. The ability of TNFa to induce NF-KB binding in synovial cells was analyzed by EMSA

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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67282b2efc
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PubMed 14754897

ZNF216 also inhibited tumor necrosis factor (TNF)-, interleukin-1-, and Toll-like receptor 4-induced NFkappaB activation in a dose-dependent manner. overexpression of ZNF216 sensitized cells to TNF-induced apoptosis.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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062538b1e4
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PubMed 12391248

To determine the optimal concentrations of SCF, anti-IgE and TNF- required to activate NF-B to its active form (NF-Ba), five preliminary experiments were performed in which mast cells were incubated with the stimulants for 4 h and the percentage of cells staining positive for immunoreactive NF-Ba was determined.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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PubMed 17034424

Toll-like receptors (TLRs) signal through two main pathways: a myeloid differentiation factor (MyD)88-dependent pathway that acts via nuclear factor kappaB (NF-kappaB) to induce proinflammatory cytokines such as tumour necrosis factor-alpha (TNF-alpha); In this study we have shown that, whilst NF-kappaB activation and production of TNF-alpha and interleukin-12 by murine RAW264.7 and J774.2 cells in response to stimulation by TLR4, -5, -7 or -9,

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act(complex(SCOMP:"Nfkb Complex"), ma(tscript)) increases p(RGD:Tnf)
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36ab97e18d
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PubMed 15837949

TNF-{alpha} induces transcription of AGT via the transcription factor nuclear factor-{kappa}B, which is known to be involved in the production of numerous proinflammatory markers.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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PubMed 10637272

Mouse bone marrow cells treated with 20 ng/ml of TNF-alpha for 1 hour activated NFkB. Nuclear extracts were prepared and analyzed by an ESMA with an NF-kB binding oligonucleotide probe.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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6e7ae57e40
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PubMed 11062238

# Ariadne: Activation of NF-kappaB by TNF alpha is attenuated by RhoB. [Regulation]

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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e3ac90d104
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PubMed 12684057

Therefore, in the present study we investigated whether IL-18 expression is regulated by cytokines and oxidative stress in cardiomyocytes. TNF-alpha induced rapid and sustained activation of NF-kappaB whereas H(2)O(2) induced delayed and transient activation. Both TNF-alpha and H(2)O(2) induced IL-18 mRNA and precursor protein in cardiomyocytes, and IL-18 release into culture supernatants.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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PubMed 19189937

These results show that NF-kB is required for enhancing the expression of human ACAT1 gene by TNFa in the differentiating THP-1 monocytes.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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3d0b7cf9af
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PubMed 20937831

Indoxyl sulfate treatment enhanced the activation of JNK, p38 MAPK, and NF-kB in TNF-alpha-activated HUVEC. Inhibitors of JNK and NF-kB attenuated indoxyl sulfate-induced E-selectin expression in HUVEC and subsequent THP-1 adhesion.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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0ac1ed66f6
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PubMed 16865089

NF-kB may be activated by cytokines, such as tumor necrosis factor-A (TNFa) and protein kinase C (PKC), which has been demonstrated in many inflammatory cells.4

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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6e8db55027
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PubMed 17322026

normal primary HBE cells were cultured and then infected with an adenovirus carrying an NF-B-dependent luciferase reporter construct. These cells were then pretreated with PS-1145 or ML120B before stimulation with IL-1 or TNF (Fig. 7). Analysis of luciferase activity revealed a strong induction by either IL-1 or TNF.

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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c686a3a94c
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PubMed 16603398

The receptor interacting protein kinase 1 (RIP1) is essential for the activation of nuclear factor kappaB (NF-kappaB) by tumor necrosis factor alpha (TNFalpha).

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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5ded6c8fd1
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PubMed 15602009

There is increased COX-2 expression in alveolar macrophages from patients with COPD compared with normal control subjects (Taha et al., 2000Go). This is presumably a result of induction by inflammatory cytokines such as TNF-{alpha} and IL-1{beta}, which activate NF-{kappa}B, the key regulator of COX-2 (Newton et al., 1997Go

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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a1aeebca16
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PubMed 11390371

5-lipoxygenase inhibitors attenuate TNF-alpha- and IL-1beta-stimulated NF-kappaB activation

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
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a0fbd16e66
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PubMed 14732733

TNF is a major activator of NF.54

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p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
67fce9df45
Networks

PubMed 9405367

The TNF-induced death of mouse primary fibroblasts expressing deregulated c-Myc was inhibited by transient overexpression of the p65 subunit of NF-kappaB, which increased NF-kappaB activity in the cells.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
2bf07ae1d8
Networks

PubMed 11585904

We show here that RKIP also antagonizes the signal transduction pathways that mediate the activation of the transcription factor nuclear factor kappa B (NF-kappaB) in response to stimulation with tumor necrosis factor alpha (TNF-alpha) or interleukin 1 beta.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
09ef5b421e
Networks

PubMed 8849369

We were also able to demonstrate that NF-KB was activated by TNFa in synovial cells from patients with RA as well as from patients with noninflammatory joint injury

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
f5451ae0ec
Networks

PubMed 16143316

Parallel with inhibitory effect on cell growth, HCA dose dependency inhibited TNF-alpha-induced activation of NF-kappaB accompanied with inhibition of the translocation of p50.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
e8dcf14a4e
Networks

PubMed 8870666

The sentence from Jubilant Ceramide activated both PKC zeta and NFKB in terminally differentiated 3T3-L1 adipocytes after TNF treatment.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
0ec6ede368
Networks

PubMed 9388244

Activation of NF-kappaB by TNF-alpha occurred within 15 min and coincided with rapid degradation of IkappaBalpha. Co-treatment with NO donors did not prevent IkappaBalpha phosphorylation or degradation. However, after 2 h of TNF-alpha stimulation, NO donors inhibited NF-kappaB activation and augmented IkappaBalpha resynthesis and nuclear translocation by 2.5- and 3-fold, respectively. This correlated with a 75% reduction in TNF-alpha-induced VCAM-1 expression. In a time-dependent manner, NO donors alone caused the nuclear translocation of IkappaBalpha

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
ab74ff9822
Networks

PubMed 10893342

We tested the hypothesis that the TNF-alpha-stimulated transcription factor nuclear factor (NF)-kappaB could, in part, mediate TNF-alpha action by inhibiting the transcriptional potency of the VDR and RXR at their cognate cis regulatory sites.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
cabbb3d789
Anatomy
artery
Cell
osteoblast
CellLine
PC-12 cell
CellStructure
Cell Nucleus
Disease
multiple myeloma
Species
10116
Networks
BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
cc01c10527
Networks

PubMed 16214042

Overexpression of USP31 in HEK 293T cells inhibited TNFalpha, CD40, LMP1, TRAF2, TRAF6 and IKKbeta-mediated NF-kappaB activation, but did not inhibit Smad-mediated transcription activation. In addition, both USP31 isoforms interact with p65/RelA.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
dbae88db8b
Networks

PubMed 17947699

Using EMSA, both IL-1b- and TNF-a-dependent NF-kB DNA binding was attenuated by overexpression of an IKK2 (KA) dominant-negative construct and a truncated version of IkBa (IkBadeltaN),...Again, overexpression of the IKK2 dominant-negative construct and IkBadeltaN inhibited both IL-1b- and TNF-a-induced NF-kB activation (Fig. 4B).

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
fc586e0bd2
Networks

PubMed 10540155

The EMSAs indicated that sodium butyrate suppressed TNF-alpha-induced nuclear factor (NF)-kappaB- and activation protein (AP)-1-DNA binding activity, but enhanced TNF-alpha-induced activation of CCAAT/enhancer-binding protein (C/EBP)beta (NF-IL-6)-DNA binding activity

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
539bee97fd
Networks

PubMed 20492675

In Fig.5A, the ability of anti-TNFa and anti-IL-1b neutralizing antibodies to block activation of NF-kB in RLE cells by their respective cytokine targets is demonstrated by Western blot analysis of IkBa.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
301fcfa252
Networks

PubMed 15140884

Nuclear factor-kappaB (NF-kappaB) is a transcription factor critical for key cellular processes, including immune response, apoptosis, and cell cycle progression. A yeast two-hybrid screening, using the Rel homology domain (RHD) of the p65 subunit (RelA) of NF-kappaB as bait, led to the isolation of PIAS3, previously identified as a specific inhibitor of STAT3. We show that PIAS3 can directly associate with p65 using an in vitro pull-down and in vivo coimmunoprecipitation assays. When overexpressed, PIAS3 inhibits NF-kappaB-dependent transcription induced by treatment with tumor necrosis factor alpha (TNF-alpha) or interleukin-1beta or by overexpression of TNF family receptors such as RANK, TNFR1, and CD30 or signal transducers of TNF receptor-associated factors (TRAFs), including TRAF2, TRAF5, and TRAF6. Downregulation of PIAS3 by RNA interference reverses its effect on TNF-alpha-mediated NF-kappaB activation. We found that an N-terminal region of PIAS3 is necessary for both the interaction with p65 and the transcriptional suppression activity. In addition, we found that an LXXLL coregulator signature motif located within the N-terminal region of PIAS3 is the minimal requirement for the interaction with p65. Furthermore, we demonstrate that PIAS3 interferes with p65 binding to the CBP coactivator, thereby resulting in a decreased NF-kappaB-dependent transcription. Taken together, these data suggest that PIAS3 may function in vivo as a modulator in suppressing the transcriptional activity of p65.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
a4435070aa
Networks

PubMed 12897149

HSP27 overexpression increases NF-kappaB nuclear relocalization, DNA binding, and transcriptional activity induced by etoposide, TNF-alpha, and interleukin 1beta.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
0b77ef9f5c
Networks

PubMed 12547194

Furthermore, we found that the MAP3K TAK1, which has been implicated in IL-1-induced activation of the NF-kappaB pathway, was also critical for TNFalpha-induced activation of the NF-kappaB pathway

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
4db21830c8
Networks

PubMed 9681829

Human oligodendroma cells treated with TNF-alpha increased the reporter gene activity of the MBP transfected cells by four fold. A mutant construct of NFKB when introduced at the promoter of MBP failed to increase the reporter activity suggesting that TNF-alpha induced MBP gene activity is mediated through NFKB.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
95c4695738
Networks

PubMed 20369072

TNF was shown to increase tight junction permeability via NF-kB activation in brain microvascular endothelial cells and Caco2 intestinal epithelial cells

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
35861fc0af
Networks

PubMed 9032466

In order to determine the functionality of the TNF-a released in cell supernatants in terms of NF-kB inducibility, we treated ACH-2 cells with equivalent TNF-a concentrations to those released in supernatants after treatment with H2O2 or HOCl, i.e. 100 and 33 pg/ml respectively (or 16.6 and 5 units/ml). Nuclear extracts were prepared 30, 60 and 120 min after induction and analysed by EMSA. As shown in Figure 7(A), a rather important specific NF-kB induction was detectable in the nucleus of ACH-2 cells treated under these conditions.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
f7df618502
Networks

PubMed 15310755

A PERIOD-like domain (amino acids 591-719) of AIP1 binds to the intact RING finger of TRAF2, and specifically enhances TRAF2-induced ASK1 activation. At the same time, the binding of AIP1 to TRAF2 inhibits TNF-induced IKK-NF-kappaB signaling.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
9c0334728c
Networks

PubMed 16989870

Transient transfection with an [NF-kappaB]x4 luciferase reporter construct showed that AS-6 inhibition of TNF-alpha-stimulated NF-kappaB activation was PPARgamma-dependent.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
030cc3b140
Anatomy
blood vessel smooth muscle
Cell
fibroblast
CellLine
HCT 116 cell
CellStructure
Cell Membrane
Disease
ovarian cancer
MeSHAnatomy
Sputum
MeSHDisease
Head and Neck Neoplasms
Species
10116
Networks
BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
7d2f7bb686
Networks

PubMed 19052556

mechanism involved a host-dependent increase in circulating levels of TNF that led to the upregulation of NF-?B-regulated antiapoptotic factors, such as BCL-XL, cIAP1 and cIAP2, in the tumour cells116.

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
56827ac8e8
Networks

PubMed 12409315

TNF-alpha induces phosphorylation of AKT, activation of NF-kappaB, and the phosphorylation of JUN kinase

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
2225e2b592
Anatomy
heart
Cell
cardiac muscle cell
CellLine
HUVEC cell line
CellStructure
Cell Nucleus
Disease
squamous cell carcinoma
Species
10116
Networks
BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
e3b031ef0b
Networks

Other

There was significant activation of NF-κB when hASM cells were stimulated with TNF-α. These data support a large body of evidence demonstrating that TNF-α receptor stimulation leads to activation of NF-κB (47, 48).

BEL
p(RGD:Tnf) increases complex(SCOMP:"Nfkb Complex")
Hash
29a8779f9f
Networks

PubMed 12969251

The NFKB SN50 inhibitor peptide showed a strong inhibition of NO production when added simultaneously or in the first hour after AGE activation, suggesting that NFKB translocation is a very early event in the AGE-NO pathway and NFKB SN50 also inhibited TNF alpha and IL 6 production.

BEL
act(complex(SCOMP:"Nfkb Complex"), ma(tscript)) increases p(RGD:Tnf)
Hash
712d1ed96b
Networks

PubMed 12168567

Tumour necrosis factor-alpha (TNF-alpha) or endotoxin induce the activation of two major transcription factors, NF-kappa B (nuclear factor-kappaB) and AP-1 (activating protein-1)

BEL
p(RGD:Tnf) increases act(complex(SCOMP:"Nfkb Complex"), ma(tscript))
Hash
29827340a1
Networks

PubMed 17615396

In support of activation of NF-kB in COPD, NF-{kappa}B was clearly responsible for enhancing the levels of IL-1 and TNF-{alpha}, via depletion of GSH and generation of ROS in the human macrophage-like cell line MonoMac6 stimulated by aqueous CSE (361).

BEL
act(complex(SCOMP:"Nfkb Complex"), ma(tscript)) increases p(RGD:Tnf)
Hash
06ccce7953
Networks

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of the open source project, PyBEL. Please feel free to contact us here to give us feedback or report any issues.