| + |
SIRT6 | up-regulates 
deacetylation
|
TNF |
0.321 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-201658 |
Lys19 |
LAEEALPkKTGGPQG |
Homo sapiens |
|
| pmid |
sentence |
| 23552949 |
Sirt6 regulates tnf-alfa secretion through hydrolysis of long-chain fatty acyl lysine |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-201662 |
Lys20 |
AEEALPKkTGGPQGS |
Homo sapiens |
|
| pmid |
sentence |
| 23552949 |
Sirt6 regulates tnf-alfa secretion through hydrolysis of long-chain fatty acyl lysine |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates quantity by expression 
transcriptional regulation
|
SCN3A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253485 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
SERPINA3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254809 |
|
|
Homo sapiens |
Astrocyte Cell Line |
| pmid |
sentence |
| 11027208 |
We characterize a molecular mechanism responsible for both IL-1 and TNF-induced expression of ACT gene in astrocytes. We identify the 5' distal IL-1/TNF-responsive enhancer of the ACT gene located 13 kb upstream of the transcription start site. This 413-bp-long enhancer contains three elements, two of which bind nuclear factor kB (NF-kB) and one that binds activating protein 1 (AP-1). All of these elements contribute to the full responsiveness of the ACT gene to both cytokines, as determined by deletion and mutational analysis. The 5' NF-kB high-affinity binding site and AP-1 element contribute most to the enhancement of gene transcription in response to TNF and IL-1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
SCN10A |
0.28 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253484 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
NOD2 |
0.428 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252407 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18647246 |
NOD2, toll-like receptor 4 (TLR4) and the adapter protein receptor-interacting protein 2 (RIP2) are induced by tumor-necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in the bronchial epithelial cell line BEAS-2B. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates activity
|
GCH1 |
0.25 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252210 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9204951 |
The de novo synthesis of 6-BH4 depends on the induction of GTP-CH-1, e.g., by tumor necrosis factor-alpha (TNF alpha). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates activity
|
SCN3A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253494 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates
|
ARDS |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261034 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32446778 |
Taken together, these data clearly indicate that, in SARS-CoV in-fection, ARDS is the ultimate result of a cytokine storm. In this scenario,the release by immune effector cells of large amounts of pro-in-flammatory cytokines (IFNα, IFNγ, IL-1β, IL-6, IL-12, IL-18, IL-33,TNFα, TGFβ) and chemokines (CXCL10, CXCL8, CXCL9, CCL2, CCL3,CCL5) precipitates and sustains the aberrant systemic inflammatoryresponse. The cytokine storm is readily followed by theimmune system “attacking” the body, which in turn will cause ARDSand multiple organ failure, the final result being death, at least in themost severe cases of SARS-CoV-2 infection |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
TNF | up-regulates
|
MPO-ANCA |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270588 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 15972951 |
Second, LPS-mediated aggravation of anti-MPO IgG-induced glomerulonephritis was attenuated, but not prevented, by pretreatment with neutralizing anti-TNF-α antibodies. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Tissue: |
Blood Serum |
| + |
TNF | up-regulates activity
binding
|
TNFRSF1B |
0.928 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-88216 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12040173 |
The binding of tnf to tnf-r1 triggers a series of intracellular events that ultimately result in the activation of two major transcription factors, nuclear factor kb (nf-kb) and c-jun. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253594 |
|
|
|
|
| pmid |
sentence |
| 14732063 |
[...] two distinct types of TNF-Rs have been identified and molecularly cloned: TNF-R55 (also referred to as TNFR1, p55 or CD120a) and TNF-R75 (also called TNFR2, p75 or CD120b) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253592 |
|
|
|
|
| pmid |
sentence |
| 17151142 |
These data indicate that myogenic activation of p38 requires TNF-alpha receptor-mediated signaling |
|
| Publications: |
3 |
Organism: |
Homo Sapiens, |
| + |
FUBP1 | down-regulates quantity by repression 
transcriptional regulation
|
TNF |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259130 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19637194 |
FBP1 down-regulates cell cycle inhibitors and proapoptotic genes. Interestingly, we also observed the up-regulation of proapoptotic genes following FBP1 knockdown in Hep3B cells. In addition, mRNA levels of the death ligands tumor necrosis factor (TNF) α and tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) were significantly increased. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | down-regulates quantity by repression
transcriptional regulation
|
DNAH10 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265551 |
|
|
Homo sapiens |
Keratinocyte |
| pmid |
sentence |
| 31836722 |
The protein expression of DNAH10 was assessed by Western blot analysis after stimulation of primary keratinocytes (P4) with inflammatory cytokine TNFα or growth factor TGF-β1 and their combination (Fig. 5C). Treatment with TNFα, TGF-β1, and their combination down regulated the expression of DNAH10 in keratinocytes after a 24-h-stimulation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates activity
binding
|
TNFRSF1A |
0.923 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-226676 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10634209 |
TNF-induced apoptosis is mediated primarily through the activation of type I receptors |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-199091 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23070005 |
For TNFR1, the cytokine TNFα binds to the receptor and triggers its trimerization, which leads to the assembly of the receptor complex and initiation of signaling. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256025 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21133840 |
TNF alpha and IFN gamma exhibit a cross-talk at the level of TNFR1 to induce activation of macrophages |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253593 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14732063 |
Tumour necrosis factor (TNF) exerts two main effects: a beneficial one as an anti-infection, anti-tumour cytokine, and a detrimental one in the systemic inflammatory response syndrome (SIRS). Two receptors (TNF-R) mediate these effects. two distinct types of TNF-Rs have been identified and molecularly cloned: TNF-R55 (also referred to as TNFR1, p55 or CD120a) and TNF-R75 (also called TNFR2, p75 or CD120b) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253591 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17151142 |
TNF-α has two distinct plasma membrane receptors known as p55 and p75. These data indicate that myogenic activation of p38 requires TNF-alpha receptor-mediated signaling |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-109716 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11502070 |
Binding of tnf to the extracellular domain of tnfrsf1a leads to homotrimerization. |
|
| Publications: |
6 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Inhibition of Apoptosis, Mitochondrial Control of Apoptosis, Multiple sclerosis, NF-KB Canonical, P38 Signaling, P38 Signaling and Myogenesis, SARS-COV APOPTOSIS, TNF-alpha Signaling |
| + |
Golimumab (Simponi) | down-regulates activity 
binding
|
TNF |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272491 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33369527 |
Golimumab is a transgenic anti-TNF monoclonal antibody that acts primarily by targeting and neutralizing TNF, thus preventing inflammation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates
|
AKT2 |
0.324 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-106596 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11287630 |
Tumor necrosis factor (tnf) inhibited insulin-promoted tyrosine phosphorylation of irs-1 and activated the akt/protein kinase b serine-threonine kinase, a downstream target for phosphatidylinositol 3-kinase |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | P38 Signaling and Myogenesis |
| + |
TNF | down-regulates quantity by repression
transcriptional regulation
|
BMP4 |
0.321 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266085 |
|
|
Homo sapiens |
A-549 Cell |
| pmid |
sentence |
| 17350185 |
TNF-alpha represses the activity of a human Bmp4 promoter-luciferase construct, transfected into A549 and H441 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RBM10 | up-regulates quantity by expression
transcriptional regulation
|
TNF |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259153 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30403180 |
These data indicated that RBM10 overexpression induced osteosarcoma cell apoptosis via promoting the production of TNF-α that appear to act as an autocrine factor regulating osteosarcoma programmed cell death. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates
|
AKT |
0.496 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-244458 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11287630 |
Tumor necrosis factor (tnf) inhibited insulin-promoted tyrosine phosphorylation of irs-1 and activated the akt/protein kinase b serine-threonine kinase, a downstream target for phosphatidylinositol 3-kinase |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, Inhibition of Apoptosis, MTOR Signaling, SARS-COV APOPTOSIS, SARS-CoV INFLAMMATORY RESPONSE, Thyroid Hormone Metabolism |
| + |
Adalimumab (Imraldi) | down-regulates activity
binding
|
TNF |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272493 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33125196 |
Adalimumab is a recombinant human immunoglobulin monoclonal antibody that specifically binds to tumor necrosis factor α (TNF-α) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | down-regulates
|
IRS1 |
0.406 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-106599 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11287630 |
Irs-1 tyrosine phosphorylation by tnf was blocked by rapamycin, an inhibitor of the mammalian target of rapamycin (mtor), a downstream target of akt. these results suggest that tnf impairs insulin signaling through irs-1 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | MTOR Signaling |
| + |
TNF | up-regulates activity
|
SCN9A |
0.254 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253488 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
NOTCH1 |
0.489 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253606 |
|
|
Homo sapiens |
Rheumatoid Arthritis Disease Specific Synovial Fibroblast |
| pmid |
sentence |
| 14586405 |
We found that TNF induced the expression of Notch-1, Notch-4, and Jagged-2 in RSF. The expression of these proteins was detected in the RA synovial tissues. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates activity
|
MAPK14 |
0.631 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-147369 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16813528 |
These observations suggest that tnf-alpha activates p38 map kinase during the inflammatory response at the injured growth plate, and tnf-alpha-p38 signaling seems to be required for marrow mesenchymal cell proliferation and migration at the growth plate injury site and in cell culture. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | P38 Signaling, P38 Signaling and Myogenesis, TNF-alpha Signaling |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
SCN8A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253482 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
UVB radiation | up-regulates
|
TNF |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252208 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19005488 |
UVB and proinflammatory cytokines synergistically activate TNF-alpha production in keratinocytes through enhanced gene transcription. UVB and IL-1alpha treatment synergistically enhanced TNF-alpha secretion and mRNA levels in human keratinocytes, similar to the findings reported previously in human fibroblasts. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
etanercept | down-regulates activity
binding
|
TNF |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272490 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25455504 |
Etanercept is a recombinant human TNF receptor p75Fc fusion protein that binds with high affinity to the soluble and transmembrane forms of TNF, thereby acting as a decoy receptor for TNF and, prevents TNF-mediated inflammatory cellular responses by competitive inhibition |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
SCN9A |
0.254 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253479 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
HES1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253605 |
|
|
Homo sapiens |
Rheumatoid Arthritis Disease Specific Synovial Fibroblast |
| pmid |
sentence |
| 22190977 |
Exposure of RA FLSs to TNF-α (10 ng/ml) led to increase of Hes-1, a target gene of Notch signaling, and a marked upregulation of Notch 2, Delta-like 1, and Delta-like 3 mRNA levels. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates activity
|
SCN1A |
0.261 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253487 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
SCN1A |
0.261 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253478 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | down-regulates
|
Adipogenesis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-173421 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21514273 |
Tumor necrosis factor-? (TNF-alpha) Is known to suppress adipocyte differentiation via a Beta-catenin-dependent pathway. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | MTOR Signaling, Thyroid Hormone Metabolism |
| + |
FCGR3A | up-regulates quantity by expression
|
TNF |
0.339 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249526 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 10728755 |
This study suggests a dominant role for FcgammaRIIIA in the induction of both TNFalpha and IL-1alpha production by human macrophages in rheumatoid arthritis following receptor ligation by small immune complexes. The signaling of TNFalpha production may require the ligation of either 3 FcgammaRIIIA receptors or only 2 FcgammaRIIIA receptors, where one interaction must involve binding via an Fc domain. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
A9/b1 integrin | up-regulates quantity by expression
|
TNF |
0.317 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253315 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24241034 |
Importantly, autocrine and paracrine interactions of alpha9beta1 integrin and tenascin-C induced the expression of MMPs and IL-6 in synovial fibroblasts, as well as TNF-alpha± and IL-1beta in synovial macrophages. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
chloroquine | down-regulates quantity
|
TNF |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260853 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32283152 |
Chloroquine inhibits the production and release of TNF and IL-6, which indicates that chloroquine may suppress the cytokine storm in patients infected with COVID-19. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV CYTOKINE STORM |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
NOTCH4 |
0.317 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253607 |
|
|
Homo sapiens |
Rheumatoid Arthritis Disease Specific Synovial Fibroblast |
| pmid |
sentence |
| 14586405 |
We found that TNF induced the expression of Notch-1, Notch-4, and Jagged-2 in RSF. The expression of these proteins was detected in the RA synovial tissues. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates
|
REL |
0.425 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-77547 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 10823840 |
C-rel emerges as the main nf-kb family member stimulated by tnf_ in the context of physiologic activation of resting t cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates activity
|
NfKb-p65/p50 |
0.666 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255689 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 8530143 |
Data from our laboratory demonstrate that the TNF signal transduction pathway-mediating NF-kappa B activation involves two phospholipases, a phosphatidylcholine-specific phospholipase C (PC-PLC) and an endosomal acidic sphingomyelinase (aSMase). The aSMase activation by TNF is secondary to the generation of 1,2-diacylglycerol (DAG) produced by a TNF-responsive PC-PLC. SMase and its product ceramide induce degradation of the NF-kappa B inhibitor I kappa B as well as NF-kappa B activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, Inhibition of Apoptosis, Multiple sclerosis, NF-KB Canonical, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE, TNF-alpha Signaling |
| + |
TNF | down-regulates quantity by repression
transcriptional regulation
|
DIO |
0.261 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267811 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 9397972 |
From the results in Figs. 1-3, it is clear that several cytokines reduce the expression of 5’-DI mRNA and enzymatic activity in FRTL-5 cells grown in TSH-containing medium. These include TNF-a, IL-lb and INF-g but not TGF-b. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270239 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 9397972 |
From the results in Figs. 1-3, it is clear that several cytokines reduce the expression of 5’-DI mRNA and enzymatic activity in FRTL-5 cells. These include TNF-a, IL-lb and INF-y. |
|
| Publications: |
2 |
Organism: |
Rattus Norvegicus |
| + |
TNF | up-regulates activity
|
PI3K |
0.324 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252733 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 10485710 |
Tnf activates phosphatidylinositol-3-oh kinase (pi(3)k). |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE, Thyroid Hormone Metabolism |
| + |
TNF | up-regulates activity
|
SCN2A |
0.261 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253489 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
M1_polarization | up-regulates
|
TNF |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263826 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 32454942 |
Macrophages and microglia show a high plasticity and have been arbitrarily classified into “M1” (proinflammatory) and “M2” (prorepair, anti-inflammatory) phenotypes depending on their activation state, although it is now widely accepted that this classification is hugely oversimplified, particularly for microglia, and only partially reflects the real situation. According to the M1/M2 model, M1 polarized cells are characterized by the release of proinflammatory mediators, such as TNF, IL-1β, and IFNγ |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
CTSK |
0.367 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253317 |
|
|
|
|
| pmid |
sentence |
| 11920402 |
This is supported by our finding that inflammatory cytokines such as IL-1b and TNFa increase the expres- sion of cathepsin K mRNA 6–8-fold and increase the secretion of the mature enzyme. |
|
| Publications: |
1 |
| + |
Phagocytosis | down-regulates quantity
|
TNF |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255446 |
|
|
|
Macrophage |
| pmid |
sentence |
| 22933625 |
Furthermore, phagocytosis of apoptotic neutrophils by M1 macrophages increased production of the Th2 cytokine TGFβ by the macrophages, while reducing expression of the Th1 cytokines IL-1β and TNF-α, reflecting a shift toward an M2 phenotype |
|
| Publications: |
1 |
| + |
TNF | down-regulates quantity by repression
transcriptional regulation
|
COMT |
0.295 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251963 |
|
|
Rattus norvegicus |
Astrocyte |
| pmid |
sentence |
| 19291302 |
COMT gene expression is downregulated by TNFα in primary rat astrocytes at both protein and mRNA levels. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
TNF | down-regulates quantity by repression
transcriptional regulation
|
SCNN1A |
0.311 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251954 |
|
|
Homo sapiens |
Alveolar Epithelial Cell |
| pmid |
sentence |
| 16877633 |
TNF, a proinflammatory cytokine present in several lung pathologies, decreases the expression and activity of the epithelial Na(+) channel (ENaC) by approximately 70% in alveolar epithelial cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | down-regulates quantity by repression
transcriptional regulation
|
LPL |
0.401 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251853 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 3063839 |
Cytokines, notably TNF and IL-1, suppress synthesis of lipoprotein lipase which decreases the rate of TGFA clearance. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251855 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16106106 |
TNF-α and IL-6 inhibit lipoprotein lipase |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates
|
AKT1 |
0.496 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-106593 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11287630 |
Tumor necrosis factor (tnf) inhibited insulin-promoted tyrosine phosphorylation of irs-1 and activated the akt/protein kinase b serine-threonine kinase, a downstream target for phosphatidylinositol 3-kinase |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | P38 Signaling and Myogenesis |
| + |
Infliximab (Remicade) | down-regulates activity
binding
|
TNF |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272489 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26092578 |
Infliximab [IFX] is a monoclonal antibody designed to intercept and neutralise tumour necrosis factor alpha [TNFα], a key inflammatory cytokine |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ADAM17 | up-regulates quantity
cleavage
|
TNF |
0.693 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-46754 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 9034190 |
We have now purified and cloned a metalloproteinase that specifically cleaves precursor TNF-alpha. [...]This enzyme (called the tnf-alpha-converting enzyme, or tace) is a new member of the family of mammalian adamalysins (or adams), for which no physiological catalytic function has previously been identified. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | P38 Signaling and Myogenesis |
| + |
TNF | up-regulates
|
PIK3CD |
0.268 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-70622 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10485710 |
Tnf activates phosphatidylinositol-3-oh kinase (pi(3)k) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
S | up-regulates quantity
|
TNF |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260280 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 17412287 |
The ability of S-protein to induce TNF-a |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-COV APOPTOSIS, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE |
| + |
TNF | up-regulates activity
|
SCN10A |
0.28 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253493 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates
binding
|
PIK3CG |
0.301 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-70625 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10485710 |
Tnf activates phosphatidylinositol-3-oh kinase (pi(3)k) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates
binding
|
TNFRSF21 |
0.344 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-59745 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9714541 |
We report the identification and initial characterization of dr6, a new member of the tnf receptor family possessing a cytoplasmic death domain. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Brain |
| Pathways: | Multiple sclerosis |
| + |
TNF | down-regulates activity
transcriptional regulation
|
MC1R |
0.294 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252381 |
|
|
Homo sapiens |
Melanocyte |
| pmid |
sentence |
| 9767234 |
MSH receptor (MSH-R) binding activity was upregulated by UVB, IL-1alpha, -1beta and ET-1, but was downregulated by TNF-alpha.Northern blotanalysis showed that MC1-R mRNA expression was induced 24 h after UVB irradiation in a dose-dependent manner, and that 24-h treatment with ET-1 also induced an expression of MC1-R mRNA,whereas TNF-a downregulated the expression. In addition, IL-1a and -1b have a small but real inductiveeffect on MC1-R mRNA expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TLR8 | up-regulates quantity
|
TNF |
0.461 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259249 |
|
|
Homo sapiens |
Myeloid Dendritic Cell, Monocyte-derived Dendritic Cell |
| pmid |
sentence |
| 15661881 |
TLR8 functions in monocytes and myeloid DC and is involved in the production of proinflammatory cytokines such as TNF-α. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates activity
|
PIK3CA |
0.277 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-70616 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 10485710 |
Tnf activates phosphatidylinositol-3-oh kinase (pi(3)k). |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | MTOR Signaling |
| + |
TNF | up-regulates
|
Inflammation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260258 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18231581 |
Induction and over-production of proinflammatory cytokines and chemokines, such as IL-6, IL-8, TNF-a and INF-c, were considered to be main mediators in the pathogenesis of SARS |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, Multiple sclerosis, NF-KB Canonical, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE, TNF-alpha Signaling |
| + |
MFGE8 | down-regulates quantity by repression
transcriptional regulation
|
TNF |
0.317 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260650 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 22114683 |
Our study demonstrated the direct anti-inflammatory role of MFG-E8 in terms of attenuating TNF-α production in mouse peritoneal macrophages and RAW264.7 cells treated with LPS |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
IL1A | up-regulates quantity by expression
transcriptional regulation
|
TNF |
0.507 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252209 |
|
|
Homo sapiens |
Keratinocyte |
| pmid |
sentence |
| 19005488 |
UVB and proinflammatory cytokines synergistically activate TNF-alpha production in keratinocytes through enhanced gene transcription. UVB and IL-1alpha treatment synergistically enhanced TNF-alpha secretion and mRNA levels in human keratinocytes, similar to the findings reported previously in human fibroblasts. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates activity
|
SCN4A |
0.26 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253490 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
ANXA1 | up-regulates quantity by expression
transcriptional regulation
|
TNF |
0.34 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261941 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 27426034 |
Our study demonstrates that ANXA1 can be phosphorylated by PKC and is subsequently translocated to the nucleus of BV-2 microglial cells after OGD/R, resulting in the induction of pro-inflammatory cytokines. we set out to examine the relationship between the different subcellular distributions of ANXA1 and the upregulation of inflammatory cytokines. When BV-2 microglial cells were transfected with ANXA1-S27A constructs following by OGD/R treatment, the pro-inflammatory cytokines, IL-1β, IL-6, and TNF-α, were found to be expressed at lower levels than those of control groups |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates activity
|
SCN11A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253492 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
HBB | up-regulates quantity by expression
transcriptional regulation
|
TNF |
0.305 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251752 |
|
|
Homo sapiens |
Monocyte |
| pmid |
sentence |
| 11901318 |
Free hemoglobin enhances tumor necrosis factor-alpha production in isolated human monocytes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates
|
Demyelination |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263834 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24507514 |
TNF-a is the most comprehensively studied cytokine in both EAE and MS. Most TNF-a overexpressing transgenic animals showed spontaneous pathology, characterized by progressive demyelination and macrophage infiltration |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
TNF | up-regulates activity
|
SCN5A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253486 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates activity
|
SCN8A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253491 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates
|
PIK3CB |
0.257 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-70619 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10485710 |
Tnf activates phosphatidylinositol-3-oh kinase (pi(3)k). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
RIPK2 |
0.361 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252409 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18647246 |
NOD2, toll-like receptor 4 (TLR4) and the adapter protein receptor-interacting protein 2 (RIP2) are induced by tumor-necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in the bronchial epithelial cell line BEAS-2B. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Certolizumab (Cimzia) | down-regulates activity
binding
|
TNF |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272492 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32207094 |
Certolizumab pegol (Cimzia®) is a PEGylated, Fab'-only, recombinant humanized antibody against TNF-α. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
SCN5A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253477 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
JAG2 |
0.324 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253608 |
|
|
Homo sapiens |
Rheumatoid Arthritis Disease Specific Synovial Fibroblast |
| pmid |
sentence |
| 14586405 |
We found that TNF induced the expression of Notch-1, Notch-4, and Jagged-2 in RSF. The expression of these proteins was detected in the RA synovial tissues. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
TNF |
0.666 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255354 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20219869 |
Once in the nucleus, NF-kB can induce the transcription of iNOS, TNF-alpha, and IL-1, which may then promote further NF-kB activation, as well as elevate the expression of other inflammatory mediators such as CCL2 and IL-6. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Skeletal Muscle |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, Inhibition of Apoptosis, Multiple sclerosis, NF-KB Canonical, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE, TNF-alpha Signaling |
| + |
STAG2 | up-regulates
|
TNF |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-119988 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14660624 |
Stag2 is able to enhance the activity of the tumor necrosis factor alpha, the cd69, and the human immunodeficiency virus long terminal repeat promoters in a nf-kappab-dependent manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
doramapimod | down-regulates
chemical inhibition
|
TNF |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-190335 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
HNRNPU | up-regulates quantity by stabilization
post transcriptional regulation
|
TNF |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262281 |
|
|
|
|
| pmid |
sentence |
| 17174306 |
In the present study, we show that hnRNP-U specifically enhances the expression of tumor necrosis factor alpha mRNA by increasing its stability, possibly through binding to the 3' untranslated region. We also show that hnRNP-U enhances the expression of several other genes as well, including GADD45A, HEXIM1, HOXA2, IER3, NHLH2, and ZFY, by binding to and stabilizing these mRNAs. |
|
| Publications: |
1 |
| + |
KLF4 | down-regulates quantity by repression
transcriptional regulation
|
TNF |
0.338 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254520 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 22378047 |
KLF4 cooperates with Stat6 to induce M2 genes (Arg-1, Mrc1, Fizz1, PPARγ) and inhibit M1 genes (TNFa, Cox-2, CCL5, iNOS) via sequestration of coactivators required for NF-κB activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
SCN4A |
0.26 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253481 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
MC1R | down-regulates quantity by repression
transcriptional regulation
|
TNF |
0.294 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252375 |
|
|
Homo sapiens |
HaCaT Cell |
| pmid |
sentence |
| 19656324 |
Constitutive expression of MC1R in HaCaT keratinocytes inhibits basal and UVB-induced TNF-alpha production. the constitutive activity of MC1R results in elevated intracellular cAMP level, reduced NF-kappaB activity and decreased TNF-alpha transcription |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates activity
|
Inflammation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258988 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 23685857 |
Tumor necrosis factor α (TNF-α, also known as cachectin) is a strong pro-inflammatory cytokine which plays an important role in the immune system during inflammation, cell proliferation, differentiation and apoptosis |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, Multiple sclerosis, NF-KB Canonical, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE, TNF-alpha Signaling |
| + |
TNF | down-regulates quantity by repression
transcriptional regulation
|
DIO1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267485 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 9397972 |
From the results in Figs. 1-3, it is clear that several cytokines reduce the expression of 5’-DI mRNA and enzymatic activity in FRTL-5 cells. These include TNF-a, IL-lb and INF-y. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| Pathways: | Thyroid Hormone Metabolism |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
SNAI2 |
0.313 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255152 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20509143 |
we show that TNFα treatment of human breast cancer cells up-regulates SLUG with a dependency on canonical NF-κB/HIF1α signaling, which is strongly enhanced by p53 inactivation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
SCN2A |
0.261 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253480 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
TNF | up-regulates
|
Angiogenesis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252285 |
|
|
|
|
| pmid |
sentence |
| 17326328 |
More than a dozen different proteins have been identified as angiogenic activators, including vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), angiogenin, transforming growth factor (TGF)-α, TGF-β, tumor necrosis factor (TNF)-α, platelet-derived endothelial growth factor, granulocyte colony-stimulating factor, placental growth factor, interleukin-8, hepatocyte growth factor, and epidermal growth factor |
|
| Publications: |
1 |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
IL6 |
0.52 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260856 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32446778 |
Interleukin-6 (IL-6) deserves a more extensive discussion in view of its involvement in the coronavirus-induced cytokine storm. The production of this cytokine is increased by IL-1β and tumor necrosis factor (TNF- α) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Multiple sclerosis, SARS-CoV CYTOKINE STORM |
| + |
HBA1 | up-regulates quantity by expression
transcriptional regulation
|
TNF |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251753 |
|
|
Homo sapiens |
Monocyte |
| pmid |
sentence |
| 11901318 |
Free hemoglobin enhances tumor necrosis factor-alpha production in isolated human monocytes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | down-regulates quantity by destabilization
|
LZTR1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253612 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16356934 |
Induction of Apoptosis by Staurosporine, TNFα, and TRAIL Induces Degradation of LZTR-1 by Caspase- and Proteasome-dependent Pathways |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Degranulation | up-regulates quantity
|
TNF |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255347 |
|
|
Homo sapiens |
Mast Cell |
| pmid |
sentence |
| 24232182 |
Particularly, damage-activated mast cells almost instantly begin to secrete TNFa, histamine and tryptase and then initiate the de novo synthesis of other cytokines, such as interleukin (IL)6 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IRF5 | up-regulates quantity by expression
transcriptional regulation
|
TNF |
0.465 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254518 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21240265 |
Among the genes with differences in expression in the M1 and M2 subsets are those regulated by IRF5, including IL12A, IL12B, IL23A, IL1B, TNF, CCL3(encoding MIP-1α), RANTES, CD1A, CD40, CD86 and CCR7 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNF | up-regulates quantity by expression
transcriptional regulation
|
SCN11A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253483 |
|
|
Mus musculus |
Cerebral Cortical Neuron |
| pmid |
sentence |
| 26112872 |
TNF-α increases Na(+) currents by accelerating the channel activation as well as increasing the expression of VGSCs in a mechanism dependent upon NF-κB and p38 MAPK signal pathways in CNS neurons. TNF-α increased Na(+) currents by accelerating the activation of VGSCs. The threshold for action potential (AP) was decreased and firing rate were increased. VGSCs were up-regulated at both the mRNA and protein levels. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
3.0
TNF
- 
- 