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p(HGNC:TNF)

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Entity

Name
TNF
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 14

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0

Anti-inflammatory activity of anatabine via inhibition of STAT3 phosphorylation v1.0.0

Tau protein aggregation is associated with cellular senescence in the brain v1.0.0

Inflammasome activation and innate immunity in Alzheimer’s disease v1.0.2

Anatabine lowers Alzheimer's Aβ production in vitro and in vivo v1.0.0

The Spleen Tyrosine Kinase (Syk) Regulates Alzheimer Amyloid-β Production and Tau Hyperphosphorylation* v1.0.0

Increased NF-κB signalling up-regulates BACE1 expression and its therapeutic potential in Alzheimer's disease. v1.0.0

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 59

a(CHEBI:nicotine) decreases sec(p(HGNC:TNF)) View Subject | View Object

Notably, nicotine pretreatment of rat adipocytes (279) reduces the release of TNF-alpha as well as free fatty acids and the adipokine adiponectin (whose function is not known, although its levels change in metabolic syndrome). PubMed:19126755

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MeSH
Adipocytes
Text Location
Review

a(CHEBI:nicotine) regulates act(p(HGNC:TNF)) View Subject | View Object

Nicotine may regulate the neuroprotective secretion of TNFalpha by microglia through enhancement of lowlevel TNF secretion and suppression of lipopolysaccharide- induced TNFalpha secretion (Suzuki et al., 2006; Park et al., 2007) via alpha7-dependent activation of JNK and MAPK pathways. PubMed:19293145

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a(HBP:HBP00089) increases sec(p(HGNC:TNF)) View Subject | View Object

The plaque-associated microglia secrete a variety of cytotoxic species including the inflammatory cytokines, INF-g, TNF-a, IL-1b and IL-6 and chemokines, most prominently CCL2 [10-12]. PubMed:21718217

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Confidence
High
MeSH
Microglia

a(GO:"neurofibrillary tangle") increases p(HGNC:TNF) View Subject | View Object

NFT containing neurons upregulated genes involved in cell survival and viability, inflammation, cell cycle progression and molecular transport and downregulated apoptosis, necrosis and cell death pathways (Figure 1a). NFkB, a pro-survival master transcriptional regulator of inflammation, was the highest predicted upstream regulator of the NFT-gene expression profile. In agreement with inflammatory activation, other predicted upstream regulators included IFNG, TNF, TLR4, IL1B and CXCL1 (Figure 1b) PubMed:30126037

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Annotations
Confidence
Medium
MeSH
Neurons
MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta") increases sec(p(HGNC:TNF)) View Subject | View Object

NLRP3 inflammasome formation and subsequent activation of caspase-1 cleavage capacity was instrumental for Abeta-induced nitric oxide production and TNF-a release PubMed:28019679

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Annotations
Confidence
High
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Tumor necrosis factor subgraph

complex(GO:"NLRP3 inflammasome complex") increases sec(p(HGNC:TNF)) View Subject | View Object

NLRP3 inflammasome formation and subsequent activation of caspase-1 cleavage capacity was instrumental for Abeta-induced nitric oxide production and TNF-a release PubMed:28019679

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Annotations
Confidence
High
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Tumor necrosis factor subgraph

act(p(HGNC:CASP1)) increases sec(p(HGNC:TNF)) View Subject | View Object

NLRP3 inflammasome formation and subsequent activation of caspase-1 cleavage capacity was instrumental for Abeta-induced nitric oxide production and TNF-a release PubMed:28019679

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Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Tumor necrosis factor subgraph

composite(a(CHEBI:Nilvadipine), p(HGNC:TNF)) hasComponent p(HGNC:TNF) View Subject | View Object

Appears in Networks:

composite(p(FPLX:RHO), p(HGNC:ROCK1)) increases act(p(HGNC:TNF)) View Subject | View Object

For instance, the small GTPase Rho and its downstream effector Rho-associated coiled-coil containing protein kinase (ROCK) have been shown to contribute to TNFα induction of NFkB activation (45). PubMed:25331948

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a(CHEBI:"amyloid-beta") increases p(HGNC:TNF) View Subject | View Object

Furthermore, Amyloid-β actuates NF-κB – dependent pro-inflammatory pathways in microglia culminating in TNFα expression and subsequently TNFα effectuated neurotoxicity PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(a(MESH:Microglia)) increases p(HGNC:TNF) View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

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Annotations
MeSH
Alzheimer Disease

a(CHEBI:"1,8-cineole") decreases p(HGNC:TNF) View Subject | View Object

The expression of pro-inflammatory cytokines such as TNF-, IL-1 and IL-6 were significantly reduced by treatment of 1,8-cineole in A 25-35-induced cells [250]. PubMed:29179999

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(GO:"NF-kappaB complex") regulates p(HGNC:TNF) View Subject | View Object

Another known target of NF-κB, TNFα [266, 267] is also up-regulated in the cortex [268], cerebrospinal fluid, and the serum of Alzheimer’s disease patients PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(GO:"NF-kappaB complex") increases p(HGNC:TNF) View Subject | View Object

Furthermore, Amyloid-β actuates NF-κB – dependent pro-inflammatory pathways in microglia culminating in TNFα expression and subsequently TNFα effectuated neurotoxicity PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(GO:"NF-kappaB complex") increases p(HGNC:TNF) View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:TNF) View Subject | View Object

Another known target of NF-κB, TNFα [266, 267] is also up-regulated in the cortex [268], cerebrospinal fluid, and the serum of Alzheimer’s disease patients PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta") increases sec(p(HGNC:TNF)) View Subject | View Object

Glial activation, pro-inflammatory gene expression and elevated secretion of IL-1, IL-6 and TNF- are consequences of high A levels [30,31]. PubMed:29179999

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a(CHEBI:Geniposide) decreases p(HGNC:TNF) View Subject | View Object

Geniposide considerably suppressed RAGE-related signaling such as ERK and IB/NF-B, the expression of TNF-, IL-1 and cerebral A accumulation in vivo[245] PubMed:29179999

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a(CHEBI:curcumin) decreases p(HGNC:TNF) View Subject | View Object

Curcumin showed several anti-inflammatory characteristics. It deploys various cytokine-inhibitory, anti-inflammatory activities and decreases the expression levels of COX-2, LOX, and iNOS. Moreover, the expression of the pro-inflammatory cytokines, for instance, TNF-, IL-1, -2,-6, -8, and -12 and the neurotoxic factors were suppressed by curcumin in lipopolysaccharide (LPS)-stimulated monocytes and alveolar macrophages [103]. PubMed:29179999

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a(CHEBI:resveratrol) decreases p(HGNC:TNF) View Subject | View Object

Resveratrol crossed the blood-brain barrier (BBB) [111,112] and down-regulated several inflammatory biomarkers such as TNF-, COX2 and interleukins [113,114]. PubMed:29179999

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a(PUBCHEM:102336202) decreases p(HGNC:TNF) View Subject | View Object

Xanthoceraside decreased the expression of A 25-35/IFN--stimulated NO, IL-1,and TNF- in microglia, which implicated the down-regulation of the activities of MAPK and NF-B pathways [248] PubMed:29179999

Appears in Networks:
Annotations
Cell Ontology (CL)
microglial cell

a(PUBCHEM:14193399) decreases p(HGNC:TNF) View Subject | View Object

Glaucocalyxin B, found in Rabdosia japonica, considerably atten-uated the expression of NO, TNF-, IL-1, COX-2 and iNOS in LPS-induced microglia cells [169–172]. Moreover, the activation of NF-B, p38 MAPK and ROS generation was interrupted by glauco- calyxin B in LPS-induced microglia cells [172]. PubMed:29179999

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Annotations
Cell Ontology (CL)
microglial cell

a(PUBCHEM:440312) decreases p(HGNC:TNF) View Subject | View Object

LPS-activated expression of pro-inflammatory and neurotoxic factors like NO, TNF-, PGE2, NO synthase and COX2 production and LOX activity were inhibited by dihydroasparagusic acid in microglia cells [243]. PubMed:29179999

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Annotations
Cell Ontology (CL)
microglial cell

a(PUBCHEM:441923) decreases p(HGNC:TNF) View Subject | View Object

The expression of the protein and mRNA of TLR3, TLR4, NF-B and TNF receptor associated factor 6 (TRAF-6) were substantially decreased by ginsenoside Rg1, and it also decreased the expression of TNF- and IFN- [227] PubMed:29179999

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a(PUBCHEM:442534) decreases p(HGNC:TNF) View Subject | View Object

It attenuated the development of AD by inhibiting glycogen synthase kinase 3 (GSK-3) and NF-B activation, and sup-pressing the NLRP3 inflammasome and cytokines such as TNF-and IL-1 [1]. PubMed:29179999

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a(PUBCHEM:444795) decreases p(HGNC:TNF) View Subject | View Object

Retinoic acid showed anti-inflammatory qualities via suppressing the expression of the inflammatory mediators IL-6, IL-12 and TNF- [216–219] and mod-ulating NF-B signaling [220,221]. PubMed:29179999

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a(PUBCHEM:73078) decreases p(HGNC:TNF) View Subject | View Object

It ameliorated spatial learning and memory disorder, which was caused by A 1-42 and was associated with the inter-ference of NF-B activity and the inhibition of IL-1 and TNF-expression [183]. PubMed:29179999

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a(MESH:Lipopolysaccharides) increases p(HGNC:TNF) View Subject | View Object

LPS treatment induced the nuclear translocation of NF-κB and increased the expression and secretion of TNF-α and IL-1β [63]. PubMed:27288790

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a(MESH:Lipopolysaccharides) increases sec(p(HGNC:TNF)) View Subject | View Object

LPS treatment induced the nuclear translocation of NF-κB and increased the expression and secretion of TNF-α and IL-1β [63]. PubMed:27288790

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act(p(FPLX:NFkappaB)) increases p(HGNC:TNF) View Subject | View Object

Then the stimulation of RAGE is able to activate the mitogen-activated protein kinase signaling cascades which converge in IκB kinase complex to phosphorylate IκB, thereby release and activate NF-κB, thus trigger NF-κB dependent gene transcription including IL-1β and TNF-α, which in turn induce the translocation of NF-κB to the nucleus [50]. PubMed:27288790

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path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:TNF) View Subject | View Object

TNF-α [27], IL-1β [28], IL-18 [29], CXCL10 [30] and TGF-β1 [31] are known to be elevated in the AD brain. PubMed:27288790

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Annotations
MeSH
Brain

complex(GO:"NF-kappaB complex") increases p(HGNC:TNF) View Subject | View Object

Increased presence of NF-κB mediated IL-1β, IL-6, and TNF-α cytokines have been reported in the affected tissues, serum and CSF of AD patients PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

composite(a(MESH:"amyloid beta-protein (25-35)"), complex(GO:"NF-kappaB complex")) increases sec(p(HGNC:TNF)) View Subject | View Object

Stimulation with the Aβ25-35 fragments induces secretion of cytokines such as TNF-α and of neurotrophic factors such as nerve growth factor (NGF) and brain derived nerve factor (BDNF) in NF-κB-dependent manner PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:TNF) View Subject | View Object

Increased presence of NF-κB mediated IL-1β, IL-6, and TNF-α cytokines have been reported in the affected tissues, serum and CSF of AD patients PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"N-acetyl-L-cysteine") decreases p(HGNC:TNF) View Subject | View Object

Similarly, NAC prevented increased expression of MHCII, CD14, TNFα, IL-6, IL-1β, and CD86 and mildly compensated for the decrease of CD206 and IL-10 following heme treatment (Figure 4D; supplemental Figure 5). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Spleen
MeSH
Anemia, Sickle Cell
Text Location
Results

a(CHEBI:TEMPO) decreases p(HGNC:TNF) View Subject | View Object

mROS scavenger (Mito-TEMPO) and NADPH oxidases inhibitors (apocynin and DPI) block TNF production induced by heme. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

a(CHEBI:apocynin) decreases p(HGNC:TNF) View Subject | View Object

mROS scavenger (Mito-TEMPO) and NADPH oxidases inhibitors (apocynin and DPI) block TNF production induced by heme. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

a(CHEBI:dibenziodolium) decreases p(HGNC:TNF) View Subject | View Object

mROS scavenger (Mito-TEMPO) and NADPH oxidases inhibitors (apocynin and DPI) block TNF production induced by heme. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

a(CHEBI:heme) increases p(HGNC:TNF) View Subject | View Object

. Heme activates macrophages inducing the production of TNF, KC (Figueiredo et al., 2007), IL-1β (unpublished), and LTB4 (Monteiro et al., 2011). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Review

a(CHEBI:heme) increases p(HGNC:TNF) View Subject | View Object

On the other hand, TNF secretion induced by heme is essential for the activation of the programed necrotic cell death pathway, which is denominated necroptosis (Fortes et al., 2012). PubMed:24904418

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Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Review

a(CHEBI:heme) increases p(HGNC:TNF) View Subject | View Object

Moreover, heme amplifies MyD88- (TNF and IL-6) and TRIF-dependent (IP-10) cytokines. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Malaria
Text Location
Review

a(CHEBI:heme) increases p(HGNC:TNF) View Subject | View Object

Haem also induces tumour necrosis factor (TNF) secretion in monocyte/macrophages through TLR4 and the adaptor molecule, MYD88 (Figueiredo et al, 2007). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

a(CHEBI:heme) increases p(HGNC:TNF) View Subject | View Object

In addition, we observed increased ROS production ( Figure 2I; supplemental Figure 2), as well as an enhanced expression of IL-6 and TNFα in cells treated with heme-albumin compared with heme-Hx (Figure 2J-K). PubMed:26675351

Appears in Networks:
Annotations
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

a(CHEBI:heme) increases p(HGNC:TNF) View Subject | View Object

Taken sequentially, it appears that the release of heme under hemolytic conditions initiates the extrinsic pathway of coagulation through the upregulation of TF on endothelial cells and leukocytes, but subsequently blocks the propagation of coagulation by inhibiting FVIII and FV, and by inhibiting the conversion of fibrinogen into fibrin and fibrin clots. PubMed:26875449

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Review

a(CHEBI:protoporphyrin) causesNoChange p(HGNC:TNF) View Subject | View Object

Importantly, protoporphyrin did not induce TNFα, suggesting a critical proinflammatory role for iron within the heme moiety (supplemental Figure 8). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

a(MESH:"Reactive Oxygen Species") increases p(HGNC:TNF) View Subject | View Object

However, ROS is necessary to induce TNF secretion and MAPK activation. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

a(MESH:"ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate") decreases p(HGNC:TNF) View Subject | View Object

In hepatic macrophages, TAK-242 also diminished heme-driven induction of IL-6 and TNFα and NAC partially recovered CD206 downregulation ( Figure 5B-C). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

a(MESH:Monocytes) positiveCorrelation p(HGNC:TNF) View Subject | View Object

For example, monocytes from SCD patients show an enhanced state of activation, with increased expression of interleukin (IL)-15 and production of TNFα and IL-1β. PubMed:26675351

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Introduction

complex(a(CHEBI:heme), a(MESH:"ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate")) decreases p(HGNC:TNF) View Subject | View Object

Cotreatment of M0 BMDMs with heme and TAK-242 attenuated the increase of the M1 markers MHCII, CD14, TNFα, IL-6, IL-1β, and CD86 and the decrease of the M2 marker CD206, IL-10, and Ym1 in comparison with heme treatment alone ( Figure 4A; supplemental Figures 5 and 12). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Spleen
MeSH
Anemia, Sickle Cell
Text Location
Results

complex(a(CHEBI:heme), a(MESH:Lipopolysaccharides)) increases p(HGNC:TNF) View Subject | View Object

In vivo, injection of heme and LPS induces a significant increase in the concentrations of TNF and IL-6 when compared to the challenge with LPS alone (Fernandez et al., 2010). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Cerebral Hemorrhage
Text Location
Review

p(HGNC:HPX) decreases p(HGNC:TNF) View Subject | View Object

In addition, Hx and DFO prevented the heme- and ironmediated induction of the M1 markers MHCII, CD86, CD14, and TNFα and the decrease of some M2 markers, such as CD206, IL-10, and Arginase-1 (the last for FeNTA only) in M0 BMDMs (Figure 6A; supplemental Figure 15A). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

p(HGNC:TLR4) increases p(HGNC:TNF) View Subject | View Object

Haem also induces tumour necrosis factor (TNF) secretion in monocyte/macrophages through TLR4 and the adaptor molecule, MYD88 (Figueiredo et al, 2007). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

complex(p(HGNC:MAPK1), p(HGNC:MAPK14), p(HGNC:MAPK8)) increases p(HGNC:TNF) View Subject | View Object

TLR4 activation leads to MAPKs and NFκB activation, which are necessary to TNF secretion. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

p(HGNC:FTH1) decreases p(HGNC:TNF) View Subject | View Object

Cells deficient on FtH are more susceptible to oxidative damage, while increased amounts of FtH protects cells from death induced by challenges such as Fe, tumor necrosis factor (TNF), heme, heme plus TNF, or oxidized low-density lipoprotein (LDL; Juckett et al., 1995; Pham et al., 2004; Gozzelino et al., 2012). PubMed:24904418

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Text Location
Review

p(HGNC:NFKB1) increases p(HGNC:TNF) View Subject | View Object

TLR4 activation leads to MAPKs and NFκB activation, which are necessary to TNF secretion. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

p(HGNC:MYD88) increases p(HGNC:TNF) View Subject | View Object

Haem also induces tumour necrosis factor (TNF) secretion in monocyte/macrophages through TLR4 and the adaptor molecule, MYD88 (Figueiredo et al, 2007). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

act(p(HGNC:NFKB1)) increases p(HGNC:TNF) View Subject | View Object

Only under protein-free conditions did we observe a limited heme-induced TNF-alpha response in cultured macrophages, which was triggered via signaling of the classical TLR4–MyD88–TRIF pathway of NF-kB activation.28 PubMed:29610666

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Annotations
Cell Ontology (CL)
macrophage
MeSH
Mitochondria
Text Location
Discussion

path(MESH:Fever) positiveCorrelation p(HGNC:TNF) View Subject | View Object

Moreover, IL-1β and TNF modifies the hypothalamus threshold of the body temperature causing fever. PubMed:24904418

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Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Review

path(MESH:Hemolysis) increases p(HGNC:TNF) View Subject | View Object

Second, immune hemolysis is accompanied by production of TNF- which induces tissue factor expression in endothelial cells and also decreases the endothelial expression of thrombomodulin, a potent modulator of thrombin activity [62]. PubMed:28458720

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Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Veins
MeSH
beta-Thalassemia
Text Location
Review

Out-Edges 47

p(HGNC:TNF) increases bp(GO:"MAPK cascade") View Subject | View Object

Furthermore, TNF-alpha strongly promotes ligand-mediated upregulation of alpha4beta2 nAChRs through a mechanism that requires p38 mitogen-activated protein kinase (MAPK) signaling (163). PubMed:19126755

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Text Location
Review

p(HGNC:TNF) increases act(a(CHEBI:nicotine)) View Subject | View Object

There is evidence that nicotine’s neuroprotective effects can be mediated through tumor necrosis factor-alpha (TNF-alpha). Application of either nicotine or TNF-alpha protects cultured mouse embryonic cortical neurons from N-methyl-D-aspartate (NMDA) toxicity, but coapplication of both does not. PubMed:19293145

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p(HGNC:TNF) decreases act(a(CHEBI:"N-methyl-D-aspartic acid")) View Subject | View Object

There is evidence that nicotine’s neuroprotective effects can be mediated through tumor necrosis factor-alpha (TNF-alpha). Application of either nicotine or TNF-alpha protects cultured mouse embryonic cortical neurons from N-methyl-D-aspartate (NMDA) toxicity, but coapplication of both does not. PubMed:19293145

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p(HGNC:TNF) increases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

Following this 15 mins of stimulation with TNFa, an increased p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, P=0.021) without a noticeable increase in STAT3 phosphorylation (Mann–Whitney U=7, Z=-0.289, P=0.773) was observed compared to the control conditions (Fig. 1) PubMed:23178521

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Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

p(HGNC:TNF) increases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

An increased in both STAT3 (Mann–Whitney U=0, Z=-2.309, P=0.021) and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, P=0.021) was observed following 24 h of treatment with TNFa PubMed:23178521

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Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

p(HGNC:TNF) increases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

TNFa significantly stimulated STAT3 (Mann–Whitney U=0, Z=-2.309, P=0.021) and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, P=0.021) PubMed:23178521

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Experimental Factor Ontology (EFO)
HEK293

p(HGNC:TNF) causesNoChange p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

Following this 15 mins of stimulation with TNFa, an increased p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, P=0.021) without a noticeable increase in STAT3 phosphorylation (Mann–Whitney U=7, Z=-0.289, P=0.773) was observed compared to the control conditions (Fig. 1) PubMed:23178521

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

p(HGNC:TNF) increases p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

An increased in both STAT3 (Mann–Whitney U=0, Z=-2.309, P=0.021) and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, P=0.021) was observed following 24 h of treatment with TNFa PubMed:23178521

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

p(HGNC:TNF) increases p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

TNFa significantly stimulated STAT3 (Mann–Whitney U=0, Z=-2.309, P=0.021) and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, P=0.021) PubMed:23178521

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Annotations
Experimental Factor Ontology (EFO)
HEK293

p(HGNC:TNF) increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

We observed that anatabine dose dependently inhibited NFκB activation by TNFα in HEK293 NFκB luciferase reporter cells (Fig. 5) whereas nicotine was ineffective PubMed:21958873

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Experimental Factor Ontology (EFO)
CHO cell

p(HGNC:TNF) increases p(HGNC:BACE1) View Subject | View Object

As expected, TNFα greatly stimulated BACE-1 transcription whereas anatabine fully prevented the increase in BACE-1 mRNA levels induced by TNFα (Fig. 7A). PubMed:21958873

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Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

p(HGNC:TNF) increases p(HGNC:BACE1) View Subject | View Object

Tumor necrosis factor-α (TNFα) has been shown to induce BACE-1 expression and to contribute to brain accumulation of Aβ peptides PubMed:25331948

Appears in Networks:

p(HGNC:TNF) increases p(HGNC:BACE1) View Subject | View Object

We found that both (-)-nilvadipine and racemic nilvadipine reduce BACE-1 mRNA expression (Fig. 1C) induced by TNFα PubMed:25331948

Appears in Networks:

p(HGNC:TNF) increases a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Tumor necrosis factor-α (TNFα) has been shown to induce BACE-1 expression and to contribute to brain accumulation of Aβ peptides PubMed:25331948

Appears in Networks:
Annotations
MeSH
Brain

p(HGNC:TNF) increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

For instance, the small GTPase Rho and its downstream effector Rho-associated coiled-coil containing protein kinase (ROCK) have been shown to contribute to TNFα induction of NFkB activation (45). PubMed:25331948

Appears in Networks:

p(HGNC:TNF) increases bp(GO:"NIK/NF-kappaB signaling") View Subject | View Object

TNF-a is a strong activator of NF-kB signalling pathways. PubMed:21329555

Appears in Networks:

p(HGNC:TNF) increases r(HGNC:BACE1) View Subject | View Object

Compared to controls, TNF-a treatment resulted in significant increase in luciferase activity in the cells transfected with the human BACE1 promoter pB1P- N1 plasmid (p<0.005) and addition of aspirin in- hibited the BACE1 transcriptional activation induced by TNF-a (p<0.005 relative to TNF-a and p>0.05 relative to controls) (Fig. 6a). PubMed:21329555

Appears in Networks:

p(HGNC:TNF) increases r(HGNC:BACE1) View Subject | View Object

Consistent with pB1P-N1 plasmid results, TNF-a significantly induced BACE1-NF-kB promoter activation (p<0.005) and the NSAIDs aspirin, ibuprofen and indomethacin significantly blocked the TNF-a-induced BACE1- NF-kB promoter activation (p<0.005) (Fig. 6b). PubMed:21329555

Appears in Networks:

p(HGNC:TNF) increases act(p(FPLX:NFkappaB), ma(tscript)) View Subject | View Object

Our data clearly demonstrate that NSAIDs inhibit TNF-a-induced BACE1 transcription via its NF-kB cis-acting elements. PubMed:21329555

Appears in Networks:

p(HGNC:TNF) increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

The trophic factors that evoke proliferation of NPC by inducing activation of NF-κB include epidermal growth factor (EGF) [155-161], basic fibroblast growth factor (bFGF) [155-161], vascular endothelial growth factor (VEGF) [162], tumor necrosis factor α (TNFα) [163], and erythropoietin (EPO) PubMed:28745240

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

p(HGNC:TNF) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Another known target of NF-κB, TNFα [266, 267] is also up-regulated in the cortex [268], cerebrospinal fluid, and the serum of Alzheimer’s disease patients PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:TNF) increases path(HBP:neurotoxicity) View Subject | View Object

Furthermore, Amyloid-β actuates NF-κB – dependent pro-inflammatory pathways in microglia culminating in TNFα expression and subsequently TNFα effectuated neurotoxicity PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:TNF) increases bp(GO:"neuron death") View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:TNF) increases act(p(FPLX:NFkappaB)) View Subject | View Object

It inhibited the activation of NF-B in TNF- induced HepG2 cells [193]. PubMed:29179999

Appears in Networks:

p(HGNC:TNF) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

TNF-α [27], IL-1β [28], IL-18 [29], CXCL10 [30] and TGF-β1 [31] are known to be elevated in the AD brain. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Brain

p(HGNC:TNF) increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

Nuclear local- ization of NF-κB in differentiated neuron progenitor cells (NPCs) is in- creasing following exposure to IL-1β and TNF-α, strong inducers of the NF-κB pathway with increase in the phosphorylation of IKK and p65 while decrease in the level of IκB [32]. PubMed:27288790

Appears in Networks:

p(HGNC:TNF) increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

Then the stimulation of RAGE is able to activate the mitogen-activated protein kinase signaling cascades which converge in IκB kinase complex to phosphorylate IκB, thereby release and activate NF-κB, thus trigger NF-κB dependent gene transcription including IL-1β and TNF-α, which in turn induce the translocation of NF-κB to the nucleus [50]. PubMed:27288790

Appears in Networks:

p(HGNC:TNF) increases act(p(FPLX:NFkappaB)) View Subject | View Object

NSAIDs inhibit BACE1 tran- scriptional activation induced by strong NF-κB activator TNF-α. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

p(HGNC:TNF) increases p(FPLX:"IKK_complex", pmod(Ph)) View Subject | View Object

Nuclear local- ization of NF-κB in differentiated neuron progenitor cells (NPCs) is in- creasing following exposure to IL-1β and TNF-α, strong inducers of the NF-κB pathway with increase in the phosphorylation of IKK and p65 while decrease in the level of IκB [32]. PubMed:27288790

Appears in Networks:

p(HGNC:TNF) increases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

Nuclear local- ization of NF-κB in differentiated neuron progenitor cells (NPCs) is in- creasing following exposure to IL-1β and TNF-α, strong inducers of the NF-κB pathway with increase in the phosphorylation of IKK and p65 while decrease in the level of IκB [32]. PubMed:27288790

Appears in Networks:

p(HGNC:TNF) decreases p(FPLX:IKB) View Subject | View Object

Nuclear local- ization of NF-κB in differentiated neuron progenitor cells (NPCs) is in- creasing following exposure to IL-1β and TNF-α, strong inducers of the NF-κB pathway with increase in the phosphorylation of IKK and p65 while decrease in the level of IκB [32]. PubMed:27288790

Appears in Networks:

p(HGNC:TNF) increases a(MESH:Cytokines) View Subject | View Object

Inhibition of NF-κB leads to decreased induction of cytokines and chemokines by IL-1β and TNF-α. PubMed:27288790

Appears in Networks:

p(HGNC:TNF) increases a(MESH:Chemokines) View Subject | View Object

Inhibition of NF-κB leads to decreased induction of cytokines and chemokines by IL-1β and TNF-α. PubMed:27288790

Appears in Networks:

p(HGNC:TNF) increases act(p(HGNC:BACE1)) View Subject | View Object

NSAIDs inhibit BACE1 tran- scriptional activation induced by strong NF-κB activator TNF-α. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

p(HGNC:TNF) increases act(p(FPLX:ERK)) View Subject | View Object

Omega-6 phospholipids, e.g. dilinoleoylphosphatidylcholine (DLPC), have been shown to block TNF-α and H 2 O 2 activation of MAPK as well as blocks IκBα phosphorylation in the SH-SY5Y cells and prevents the phosphorylation and activation of NF-κB. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

p(HGNC:TNF) increases p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

What's more, DLPC complete- ly abolishes TNF-α and H 2 O 2 induced neuronal tau phosphorylation, re- duces cellular APP levels and Aβ expression and secretion in SH-SY5Y cells [91,92] (Table 1). PubMed:27288790

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y
MeSH
Cerebral Cortex
MeSH
Hippocampus

p(HGNC:TNF) increases p(HGNC:NGF) View Subject | View Object

Stimulation of neuronal cells by TNF-α has been shown to upregulate transactivation of anti-apoptotic gene products and neurotrophins such as Bcl-2 and NGF respectively PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Alzheimer Disease

p(HGNC:TNF) increases p(HGNC:BCL2) View Subject | View Object

Stimulation of neuronal cells by TNF-α has been shown to upregulate transactivation of anti-apoptotic gene products and neurotrophins such as Bcl-2 and NGF respectively PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Alzheimer Disease

p(HGNC:TNF) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Increased presence of NF-κB mediated IL-1β, IL-6, and TNF-α cytokines have been reported in the affected tissues, serum and CSF of AD patients PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:TNF) increases act(p(HGNC:RIPK1)) View Subject | View Object

WhileMAPK8 increases ROS generation, TNF induces RIP1–RIP3 necrosome which triggers necroptosis. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

p(HGNC:TNF) increases act(p(HGNC:RIPK3)) View Subject | View Object

WhileMAPK8 increases ROS generation, TNF induces RIP1–RIP3 necrosome which triggers necroptosis. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

p(HGNC:TNF) positiveCorrelation path(MESH:Fever) View Subject | View Object

Moreover, IL-1β and TNF modifies the hypothalamus threshold of the body temperature causing fever. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Review

p(HGNC:TNF) increases path(MESH:Inflammation) View Subject | View Object

Although KC and IL-1β functions were not investigated during heme-induced inflammatory effects, TNF and LTB4 were described as essential inflammatory mediators during inflammatory events induced by heme. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Review

p(HGNC:TNF) increases path(MESH:Inflammation) View Subject | View Object

Pro-inflammatory cytokines and chemokines [e.g., inter leukin 1B (IL1B), CXCL8 (also termed IL8), TNF and chemokine (C-C motif) ligand 2 (CCL2, also termed MCP1)], are upregulated in haemolytic disorders such as SCD (Qari et al, 2012). This pro-inflammatory cytokine milieu is crucial in mediating the pro-coagulant effects of vascular endothelial cells and promotes localized inflammation and thrombosis (Qari et al, 2012). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

p(HGNC:TNF) increases bp(GO:"necroptotic process") View Subject | View Object

On the other hand, TNF secretion induced by heme is essential for the activation of the programed necrotic cell death pathway, which is denominated necroptosis (Fortes et al., 2012). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Text Location
Review

p(HGNC:TNF) increases path(MESH:Thrombosis) View Subject | View Object

Pro-inflammatory cytokines and chemokines [e.g., inter leukin 1B (IL1B), CXCL8 (also termed IL8), TNF and chemokine (C-C motif) ligand 2 (CCL2, also termed MCP1)], are upregulated in haemolytic disorders such as SCD (Qari et al, 2012). This pro-inflammatory cytokine milieu is crucial in mediating the pro-coagulant effects of vascular endothelial cells and promotes localized inflammation and thrombosis (Qari et al, 2012). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

p(HGNC:TNF) positiveCorrelation a(MESH:Monocytes) View Subject | View Object

For example, monocytes from SCD patients show an enhanced state of activation, with increased expression of interleukin (IL)-15 and production of TNFα and IL-1β. PubMed:26675351

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Introduction

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 PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.