| + |
NfKb-p65/p50 | up-regulates quantity by expression 
transcriptional regulation
|
CCR3 |
0.258 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254660 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16604092 |
Rosmarinic acid also inhibited TNF-alpha-induced phosphorylation and degradation of IkappaB-alpha, as well as nuclear translocation of NF-kappaB heterodimer induced by TNF-alpha. This suggests that rosmarinic acid downregulates the expression of CCL11 and CCR3 via the inhibition of NF-kappaB activation signaling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates
|
Inflammation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260445 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24168260 |
NF-κB, which can be activated by mitogen-activated protein kinases (MAPKs) (12), is responsible for the transcription of inflammatory factors and profibrotic cytokines, which promote an inflammatory response and fibrosis |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-245039 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20457564 |
The nuclear factor NF-kappaB pathway has long been considered a prototypical proinflammatory signaling pathway, largely based on the role of NF-kappaB in the expression of proinflammatory genes including cytokines, chemokines, and adhesion molecules. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255489 |
|
|
|
|
| pmid |
sentence |
| 25309941 |
Following GSK3β activation, NF-κB is translocated from the cytoplasm to the nucleus and binds transcriptional sites with CBP leading to an increase in the transcription of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6). |
|
| Publications: |
3 |
Organism: |
Homo Sapiens, |
| Pathways: | B-cell activation, COVID-19 Causal Network, EBV infection, Fibrosis, Glucocorticoid receptor Signaling, Innate Immune Response, IL1 Signaling , Inflammosome Activation, Multiple sclerosis, NF-KB Canonical, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV CYTOKINE STORM, SARS-CoV FIBROSIS, SARS-CoV INFLAMMATORY RESPONSE, SARS-CoV INNATE RESPONSE TO dsRNA, TNF-alpha Signaling |
| + |
PPP2CA | down-regulates 
dephosphorylation
|
NfKb-p65/p50 |
0.449 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217421 |
|
|
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 11591705 |
Rela was dephosphorylated by a purified pp2a core enzyme, a heterodimer formed by the catalytic subunit of pp2a (pp2ac) and pr65, in a concentration-dependent manner.These data suggest that the constitutive activation of rela in melanoma cells could be due, at least in part, to the deficiency of pp2a, which exhibits decreased dephosphorylation of nf-kappa b/rela. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV STRESS GRANULES |
| + |
CASP8AP2 | up-regulates 
binding
|
NfKb-p65/p50 |
0.246 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217385 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22075988 |
In addition, both cleavage products of c-flip turned out to be inducers of nf-kb activity by binding to the ikk complex. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
HYAL1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253880 |
|
|
Homo sapiens |
253J Cell |
| pmid |
sentence |
| 18718911 |
In 253J-Lung and HT1376 bladder cancer cell lines, which show high HYAL-1 expression, transcription factors Egr-1, AP-2, and NFκB bind the HYAL-1 promoter. Because both SP1 and Egr-1 have two overlapping binding sites within the promoter (Fig. 5), it appears that although SP1 binding to the methylated HYAL-1 promoter turns off transcription, binding of Erg-1 (and also AP-2) to the unmethylated promoter turns on transcription. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
LCN2 |
0.349 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254796 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15536164 |
Biglycan, NGAL, and MMP-9 are transcriptionally up-regulated by NF-kappaB, a transcription factor that is activated in FAP nerves and SG. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TNFRSF17 | up-regulates
|
NfKb-p65/p50 |
0.283 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-79510 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10903733 |
Bcma overexpression induces nf-kb activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates
transcriptional regulation
|
IL6 |
0.635 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254511 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 20086235 |
Both NF-κBs bind to a conserved DNA motif (80) that is found in numerous IL-1–responsive genes, in particular the ones encoding IκBα (81), IL-6 (82), IL-8 (18, 83,84), monocyte chemoattractant protein 1 (MCP1) (28), and cyclooxygenase 2 (COX2) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Multiple sclerosis, SARS-CoV CYTOKINE STORM |
| + |
RELA | form complex 
binding
|
NfKb-p65/p50 |
0.709 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-55381 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9450761 |
Here we report the crystal structure at 2.9 a resolution of the p50/p65 heterodimer bound to the kappab dna |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
GSK3B | up-regulates activity
|
NfKb-p65/p50 |
0.374 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255485 |
|
|
|
|
| pmid |
sentence |
| 25309941 |
Following GSK3β activation, NF-κB is translocated from the cytoplasm to the nucleus and binds transcriptional sites with CBP leading to an increase in the transcription of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6). |
|
| Publications: |
1 |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
S100A6 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254803 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12859951 |
NF-kappaB transcription factor contributes to the activation of S100A6 gene expression in response to TNFalpha in HepG2 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
IL17R complex | up-regulates activity
|
NfKb-p65/p50 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261338 |
|
|
Mus musculus |
NIH-3T3 Cell |
| pmid |
sentence |
| 8777726 |
3T3 cells were preincubated with an IL-17Rspecific antiserum and then assayed for NF-KB activation by HVS13. Preincubation with the IL-1 7R antiserum dramatically decreased the NF-KB activity induced by HVSl3 as compared with cells preincubated with an irrelevant rat antiserum (Figure 5C). This result indicated that the engagement of the IL-17R by its ligands induced NF-KB activity. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Multiple sclerosis |
| + |
NfKb-p65/p50 | up-regulates
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-245043 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11359934 |
The nuclear factor-kappaB (NF-kappaB) family of transcription factors has been shown to regulate proliferation in several cell types. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255692 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22021368 |
In normal hematopoiesis, AML1 suppresses NF-κB signaling and thus may contribute to inhibition of excessive proliferation of hematopoietic cells. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML, B-cell activation, COVID-19 Causal Network, EBV infection, FLT3-ITD signaling, Glucocorticoid receptor Signaling, NF-KB Canonical, Pancreatic ductal adenocarcinoma (PDA), TNF-alpha Signaling |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
SOD2 |
0.498 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-172392 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21357467 |
The nfkb p65/p50 heterodimer increases sod2, and p50/p50 suppresses it nf-kb p65/p50 binds to the enhancer and is important for cytokine-induced sod2 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates
transcriptional regulation
|
NOS2 |
0.453 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256250 |
|
|
|
|
| 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 |
| Tissue: |
Skeletal Muscle |
| + |
GSK3B | up-regulates
phosphorylation
|
NfKb-p65/p50 |
0.374 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217367 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17183360 |
Rela is phosphorylated at: ser276 by the catalytic subunit of protein kinase a (pkac), msk1 and msk2; at ser311 by the atypical pkczeta; at ser468 by ikkbeta, ikkepsilon and glycogen-synthase kinase-3beta (gsk3beta); at ser529 by ck2; and at ser536 by ikkbeta, ikkalfa, ikkepsilon, nf-kb activating kinase (nak, also known as tank-binding kinase-1 tbk1)) and rsk1 (also known as p90 ribosomal protein s6 kinase (p90s6k) . |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217430 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 16407239 |
Rela is phosphorylated at: ser276 by the catalytic subunit of protein kinase a (pkac), msk1 and msk2; at ser311 by the atypical pkczeta; at ser468 by ikkbeta, ikkepsilon and glycogen-synthase kinase-3beta (gsk3beta); at ser529 by ck2; and at ser536 by ikkbeta, ikkalfa, ikkepsilon, nf-kb activating kinase (nak, also known as tank-binding kinase-1 tbk1)) and rsk1 (also known as p90 ribosomal protein s6 kinase (p90s6k) . |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3-ITD signaling |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
EBNA1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266803 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29659505 |
We found that EBV-encoded Qp-EBNA1 can be upregulated by NF-κB, while EBNA1 protein expression has been shown to negatively regulate NF-κB activation by inhibiting IKKα/β phosphorylation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | EBV infection |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
BIRC2 |
0.536 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-64100 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9916987 |
The iaps have been shown to be induced by nf-kappab or v-rel in multiple cell lines and conversely, hiap1 and hiap2 have been shown to activate nf-kappab possibly forming a positive feed-back loop. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAP3K7 | up-regulates activity
|
NfKb-p65/p50 |
0.652 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-55710 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9480845 |
Overexpression of tak1 together with its activator protein, tak1 binding protein 1 (tab1), induced the nuclear translocation of nf-kappa b p50/p65 heterodimer accompanied by the degradation of i kappa b alpha and i kappa b beta, and the expression of kappa b-dependent reporter gene...[]...These Results suggest that tak1 induces nf-kappa b activation through a novel nik-independent signaling pathway |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, IL1 Signaling , Inflammosome Activation, Inhibition of Apoptosis, NF-KB Canonical, SARS-CoV INFLAMMATORY RESPONSE, Toll like receptors |
| + |
NSD1 | up-regulates
methylation
|
NfKb-p65/p50 |
0.466 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217388 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20080798 |
Fbxl11 and nsd1 have opposite effects on nf-kb; both bind to p65 subunit after activation of nf-kb. / nsd1 activates nf-kb and reverses the inhibitory effect of fbxl11 / these data confirm that fbxl11 and nsd1 constitute an enzyme pair that methylates and demethylates p65 on k218 and 221 in response to cytokine stimulation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
BGN |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254797 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15536164 |
Biglycan, NGAL, and MMP-9 are transcriptionally up-regulated by NF-kappaB, a transcription factor that is activated in FAP nerves and SG. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SOCS3 | down-regulates 
|
NfKb-p65/p50 |
0.392 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253052 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16543409 |
Suppressor of cytokine signaling (SOCS)-3 was shown to inhibit IL-1-induced transcription and activation of NFkappaB and the MAPKs JNK and p38, but the mechanism is unknown |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TBK1 | up-regulates activity
phosphorylation
|
NfKb-p65/p50 |
0.589 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260157 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15489227 |
Constitutive and interleukin-1-inducible Phosphorylation of p65 NF-{kappa}B at Serine 536 Is Mediated by Multiple Protein Kinases Including I{kappa}B Kinase (IKK)-{alpha}, IKK{beta}, IKK{epsilon}, TRAF Family Member-Associated (TANK)-binding Kinase 1 (TBK1). Overexpressed ikkepsilon and tbk1 phosphorylate ser-536 in vivo and in vitro. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Innate Immune Response, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE, SARS-CoV INNATE RESPONSE TO dsRNA, Toll like receptors |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
F3 |
0.25 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254810 |
|
|
Homo sapiens |
HUVEC Cell |
| pmid |
sentence |
| 12744731 |
In conclusion, NF-kappaB could be activated promptly after HUVEC incubated with TNF-alpha, then it was bound to TF promotor to start the TF transcription, TF mRNA expression was upregulated, that leaded to the increase of TF expression on the HUVEC surface and activated the coagulation cascade. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CCND1 |
0.487 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235648 |
|
|
Mus musculus |
C2C12 Cell, Myoblast |
| pmid |
sentence |
| 10409765 |
Nf-kappab regulation of cyclin d1 occurs at the transcriptional level and is mediated by direct binding of nf-kappab to multiple sites in the cyclin d1 promoter. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Tissue: |
Muscle, Skeletal Muscle |
| Pathways: | Acute Myeloid Leukemia |
| + |
RPS6KA4 | up-regulates
phosphorylation
|
NfKb-p65/p50 |
0.275 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217373 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17183360 |
Rela is phosphorylated at: ser276 by the catalytic subunit of protein kinase a (pkac), msk1 and msk2; at ser311 by the atypical pkczeta; at ser468 by ikkbeta, ikkepsilon and glycogen-synthase kinase-3beta (gsk3beta); at ser529 by ck2; and at ser536 by ikkbeta, ikkalfa, ikkepsilon, nf-kb activating kinase (nak, also known as tank-binding kinase-1 tbk1)) and rsk1 (also known as p90 ribosomal protein s6 kinase (p90s6k) msk 1 and 2 can directly phosphorylate and activate transcription factors such as creb, atf1, the nf-kb isoform p65 and stat 1 and 3. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOD1 | up-regulates
|
NfKb-p65/p50 |
0.296 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252411 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18079694 |
Nod1 and Nod2 stimulation activates NF-kappaB through RICK, a caspase-recruitment domain-containing kinase. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
TNF |
0.678 |
| 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 |
| + |
IKK-complex | up-regulates
phosphorylation
|
NfKb-p65/p50 |
0.819 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216341 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15489227 |
Chromatographic fractionation of cell extracts allowed the identification of two distinct enzymatic activities phosphorylating ser-536. Peak 1 represents an unknown kinase, whereas peak 2 contained ikkalpha, ikkbeta, ikkepsilon, and tbk1. collectively, our results provide evidence for at least five kinases that converge on ser-536 of p65 and a novel function for this phosphorylation site in the recruitment of components of the basal transcriptional machinery to the interleukin-8 promoter. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216365 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 19609947 |
Our data suggest that the stimulation of nfkb by akt is dependent on the phosphorylation of p65 at s534, mediated by ikk (ikb kinase) alfa and beta. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | B-cell activation, COVID-19 Causal Network, EBV infection, FLT3-ITD signaling, Innate Immune Response, IL1 Signaling , Inflammosome Activation, Inhibition of Apoptosis, Macrophage polarization, Multiple sclerosis, NF-KB Canonical, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV INFLAMMATORY RESPONSE, SARS-CoV INNATE RESPONSE TO dsRNA, TNF-alpha Signaling, T cell activation, Toll like receptors |
| + |
PRKACA | up-regulates
phosphorylation
|
NfKb-p65/p50 |
0.508 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217391 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17959673 |
In this study, we demonstrate that the phosphorylation of p50 and p65 by the catalytic subunit of protein kinase a (pkac) is essential for nf-kappab dna binding and transactivation activity. treatment with h89 and knockdown of pkac in cells led to the inhibition of phosphorylation at p50 ser(337) and p65 ser(276) and loss of dna binding by nf-kappab. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217364 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9660950 |
The transcriptional activity of nf-kappa b is stimulated upon phosphorylation of its p65 subunit on serine 276 by protein kinase a (pka). |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
FTH1 |
0.339 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254792 |
|
|
Homo sapiens |
T-lymphoma Cell Line |
| pmid |
sentence |
| 19258503 |
We show that inhibition of constitutively active NF-kappaB causes down-regulation of ferritin heavy chain (FHC) that leads to an increase of free intracellular iron, which, in turn, induces massive generation of ROS. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAP3K14 | up-regulates
|
NfKb-p65/p50 |
0.354 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-46212 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9020361 |
Nik stimulates nf-kappab activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Innate Immune Response |
| + |
IFNG | down-regulates activity
|
NfKb-p65/p50 |
0.447 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255937 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 23667107 |
Early inhibition of IL-1β expression by IFN-γ is mediated by impaired binding of NF-κB to the IL-1β promoter but is independent of nitric oxide. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Macrophage polarization, Multiple sclerosis, SARS-CoV CYTOKINE STORM |
| + |
STAT6 | down-regulates activity
binding
|
NfKb-p65/p50 |
0.418 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249553 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 10982806 |
STAT6 mediates suppression of STAT1 and NF-kB-dependent transcription by distinct mechanisms. Both processes are dependent upon the STAT6 transactivation domain and may involve sequestration of necessary but different transcriptional coactivator proteins. These two suppressive mechanisms are controlled differentially by the nature of the STAT6 DNA-binding site |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization |
| + |
CHUK | down-regulates
phosphorylation
|
NfKb-p65/p50 |
0.796 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217397 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10469655 |
All residues of p105 phosphorylated by ikka are c-terminal; the major phosphorylation region contains three serines (ser923; ser927;ser932) and two threonines (thr927 and thr391). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMAD3/SMAD4 | down-regulates activity
|
NfKb-p65/p50 |
0.332 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249554 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 10973958 |
NF-kB-, AP-1-, and Smad3-driven promoters all require p300/CREB-binding protein for their transactivation. Previous studies have suggested that NF-kB- and AP-1-driven promoters can be inhibited by competitive recruitment of coactivators such as p300/CPB to other unrelated promoters. We hypothesized that NF-kB and AP-1 compete with Smad3 for limiting quantities of p300. This hypothesis predicts that added p300 should alleviate TGF-b1/Smad3-mediated inhibition of inflammatory genes. Conversely, increasing doses of TGF-b1/Smad3 would compete away even overexpressed p300 from NF-kB/AP- 1-driven promoters. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV FIBROSIS |
| + |
IKBKB | down-regulates
phosphorylation
|
NfKb-p65/p50 |
0.869 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217400 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10469655 |
Ikkbeta phosphorylates p105 resulting in its degradation, which releases tpl2 resulting in activation of the pro-proliferative map kinase- pathway. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217403 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11158290 |
Ikkbeta phosphorylates p105 resulting in its degradation, which releases tpl2 resulting in activation of the pro-proliferative map kinase- pathway. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling |
| + |
NFKBIA | down-regulates activity
binding
|
NfKb-p65/p50 |
0.813 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217394 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 1340770 |
Nf-kappa b is an inducible transcription factor comprised of a 50-kd (p50) and a 65-kd (p65) subunit. Induction of nf-kappa b activity, which is a critical event in many signal transduction pathways, involves release from a cytoplasmic inhibitory protein, i kappa b, followed by translocation of the active transcription factor complex into the nucleus. we demonstrate by in vitro and in vivo methods that the recently cloned i kappa b/mad-3 interacts with both the p50 and p65 subunits of nf-kappa b |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-64092 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9914500 |
In nonstimulated cells, nf-kappab is present in the cytosol where it is complexed to its inhibitor ikappab however, we found that only one of the activities, namely the ikk1/2 complex, exists as a pre-assembled kinase-substrate complex in which the ikks are directly or indirectly associated with several nf-kappab-related and ikappab-related proteins: rela, relb, crel, p100, p105, ikappa balpha, ikappa bbeta and ikappa bepsilon. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, FLT3-ITD signaling, IL1 Signaling , Inhibition of Apoptosis, Multiple sclerosis, NF-KB Canonical, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV STRESS GRANULES, TNF-alpha Signaling, T cell activation, Toll like receptors |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
|
PTGS2 |
0.368 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260262 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17705188 |
Inflammatory stimuli can activate IkappaB kinase (IKK) signalsome and subsequently the nuclear factor kappa B (NF-kappaB), which influences gene expression of cyclooxygenase-2 (Cox-2) along with other transcription factors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, SARS-CoV INFLAMMATORY RESPONSE |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CCL11 |
0.263 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254661 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16604092 |
Rosmarinic acid also inhibited TNF-alpha-induced phosphorylation and degradation of IkappaB-alpha, as well as nuclear translocation of NF-kappaB heterodimer induced by TNF-alpha. This suggests that rosmarinic acid downregulates the expression of CCL11 and CCR3 via the inhibition of NF-kappaB activation signaling. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates
|
Survival |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-96834 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14585074 |
Activation of the nf-kb pathway regulates a variety of ant-apoptotic factors |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Inhibition of Apoptosis, Pancreatic ductal adenocarcinoma (PDA) |
| + |
NfKb-p65/p50 | down-regulates quantity by repression
transcriptional regulation
|
EPCAM |
0.284 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254790 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11505407 |
The current results provide the first insights into the regulation of EpCAM expression, which is regulated negatively by TNFalpha and TPA through the activation of NF-kappaB. The repression may rely on the competition of NF-kappaB for p300/CBP histone acetyl transferase activity, because the overexpression of p300 reverts TNFalpha effects. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | down-regulates quantity by repression
transcriptional regulation
|
BHMT |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254659 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16953798 |
SAM and MTA down-regulate BHMT expression in HepG2 cells in part by inducing NF-kappaB, which acts as a repressor for the human BHMT gene. While SAM's mechanism is NF-kappaB-dependent, MTA has both NF-kappaB-dependent and -independent mechanisms. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
|
TP53 |
0.49 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-123602 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15044535 |
These results indicate that nf-kb actions occur upstream of p53 to regulate both p53 levels and activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML, EBV infection, FLT3-ITD signaling, Pancreatic ductal adenocarcinoma (PDA) |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
IL1B |
0.585 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255355 |
|
|
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, IL1 Signaling , Inflammosome Activation, Multiple sclerosis, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE |
| + |
TNF | up-regulates activity
|
NfKb-p65/p50 |
0.678 |
| 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 |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
SLC25A27 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268984 |
|
|
|
|
| pmid |
sentence |
| 20385226 |
We present the first direct evidence that UCP4 is regulated by NF-kappaB, mediated via a functional NF-kappaB site in its promoter region, and that UCP4 has a significant role in NF-kappaB prosurvival signaling, mediating its protection against MPP(+) toxicity.|NF-kappaB inhibition significantly suppressed the MPP(+)-induced increase in UCP4 expression. |
|
| Publications: |
1 |
| + |
IKBKE | up-regulates activity
phosphorylation
|
NfKb-p65/p50 |
0.425 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217379 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15489227 |
Constitutive and interleukin-1-inducible Phosphorylation of p65 NF-{kappa}B at Serine 536 Is Mediated by Multiple Protein Kinases Including I{kappa}B Kinase (IKK)-{alpha}, IKK{beta}, IKK{epsilon}, TRAF Family Member-Associated (TANK)-binding Kinase 1 (TBK1). Overexpressed ikkepsilon and tbk1 phosphorylate ser-536 in vivo and in vitro. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Innate Immune Response, SARS-CoV INNATE RESPONSE TO dsRNA, Toll like receptors |
| + |
NfKb-p65/p50 | up-regulates
|
Fibrosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260446 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24168260 |
NF-κB, which can be activated by mitogen-activated protein kinases (MAPKs) (12), is responsible for the transcription of inflammatory factors and profibrotic cytokines, which promote an inflammatory response and fibrosis |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
NfKb-p65/p50 | down-regulates
|
MYOD1 |
0.281 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255352 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20219869 |
Furthermore, NF-kB activation can cause destabilization of MyoD mRNA and degradation of MyoD protein (35, 49), which would further impede muscle differentiation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Skeletal Muscle |
| + |
IKBKB |
phosphorylation
|
NfKb-p65/p50 |
0.869 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217376 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15489227 |
Chromatographic fractionation of cell extracts allowed the identification of two distinct enzymatic activities phosphorylating ser-536. Peak 1 represents an unknown kinase, whereas peak 2 contained ikkalpha, ikkbeta, ikkepsilon, and tbk1. collectively, our results provide evidence for at least five kinases that converge on ser-536 of p65 and a novel function for this phosphorylation site in the recruitment of components of the basal transcriptional machinery to the interleukin-8 promoter. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217427 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16046471 |
Rela is phosphorylated at ser536 by ikkbeta, ikkalfa, ikkepsilon, nf-kb activating kinase (nak, also known as tank-binding kinase-1 tbk1) and rsk1 (also known as p90 ribosomal protein s6 kinase (p90s6k) .we now present evidence that suggests that the upstream kinase ikkbeta plays an important role in tax-induced p53 inhibition through phosphorylation of p65/rela at ser-536. .Ikkbeta Plays an important role in tax-induced p53 inhibition through phosphorylation of p65/rela at ser-536. . |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling |
| + |
PRKCZ | up-regulates
phosphorylation
|
NfKb-p65/p50 |
0.494 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217370 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17183360 |
Rela is phosphorylated at: ser276 by the catalytic subunit of protein kinase a (pkac), msk1 and msk2; at ser311 by the atypical pkczeta; at ser468 by ikkbeta, ikkepsilon and glycogen-synthase kinase-3beta (gsk3beta); at ser529 by ck2; and at ser536 by ikkbeta, ikkalfa, ikkepsilon, nf-kb activating kinase (nak, also known as tank-binding kinase-1 tbk1)) and rsk1 (also known as p90 ribosomal protein s6 kinase (p90s6k) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TLR2 | down-regulates activity
|
NfKb-p65/p50 |
0.559 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260973 |
|
|
Homo sapiens |
Peripheral Blood Mononuclear Cell |
| pmid |
sentence |
| 19185596 |
S protein is a ligand for human TLR2. S protein utilizes toll-like receptor 2(TLR 2) to increase IL-8 production.Our results show that SARS S protein in a soluble form increased IL-8 production through hTLR2 ligand interaction. we have provided evidence that S protein induces IL-8 in PBMC in vitro and in THP-1 cells. The ability of S protein to increase IL-8 mRNA was mediated by activation of NF-κB possibly via TLR2 ligand and could be inhibited by the NF-κB inhibitor TPCK. The ability to detect elevated NF-κB transcription factor activity in the nucleus in response to S protein suggests that this most likely occurs by the mechanism of induction. Moreover increased secretion of IL-8 and IL-6 cytokines indicated that levels of proinflammatory mediators could be enhanced by S protein interaction with monocyte macrophages and could stimulate NK, neutrophil and monocyte migration to the site of infection. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | EBV infection, SARS-CoV CYTOKINE STORM |
| + |
NfKb-p65/p50 | down-regulates quantity by repression
transcriptional regulation
|
EGR1 |
0.399 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254258 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 21983014 |
In conclusion we demonstrated that treatment of HeLa cells with DMC leads to an enhanced formation of a complex consisting of NF-κB and HDAC1 that binds to the EGR1 promoter resulting in downregulation of EGR1 expression which plays a major role for transcriptional inhibition of mGPES-1 expression. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
MDM2 |
0.374 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-168296 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20921405 |
Nf-kb activation following t-cell receptor engagement induces the expression of mdm2 through interaction with nf-kb sites in its p1 promoter |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML, FLT3-ITD signaling, Pancreatic ductal adenocarcinoma (PDA) |
| + |
RPGRIP1L | down-regulates
demethylation
|
NfKb-p65/p50 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217412 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20080798 |
Fbxl11 and nsd1 have opposite effects on nf-kb; both bind to p65 subunit after activation of nf-kb. / nsd1 activates nf-kb and reverses the inhibitory effect of fbxl11 / these data confirm that fbxl11 and nsd1 constitute an enzyme pair that methylates and demethylates p65 on k218 and 221 in response to cytokine stimulation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DPF2 | up-regulates activity
binding
|
NfKb-p65/p50 |
0.303 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261964 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 20460684 |
REQ is required for the oncogenic activity induced by RelB/p52. . Through in vitro binding experiments, REQ was found to bind to several SWI/SNF complex subunits and also to the p52 NF-κB subunit through its nuclear localization signal containing the N-terminal region. In this study, we present evidence that REQ is a specific adaptor protein that links RelB/p52 with Brm-type SWI/SNF complexes and thereby plays pivotal roles at the most downstream stages of the noncanonical NF-κB pathway. We further show that REQ is required for oncogenesis in several human tumor cell lines in which the noncanonical NF-κB pathway is aberrantly regulated.REQ and Brm specifically promote RelB/p52-dependent transcriptional activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | down-regulates quantity by repression
transcriptional regulation
|
THBD |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253909 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15677570 |
We further show evidence suggesting that NF-κB inhibits TM expression indirectly by competition for the coactivator p300/CBP. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
IL4 |
0.424 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254497 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 15048722 |
We demonstrate that NF-kappa B binds to the IL-4 promoter in vivo upon T cell activation. Inhibition of NF-kappa B nuclear translocation in living cells blocked binding of NF-kappa B to the IL-4 promoter. The data provide first evidence that NF-kappa B is directly involved in IL-4 transcription |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization, Multiple sclerosis |
| + |
IKBKG | up-regulates
phosphorylation
|
NfKb-p65/p50 |
0.79 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217382 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15489227 |
Chromatographic fractionation of cell extracts allowed the identification of two distinct enzymatic activities phosphorylating ser-536. Peak 1 represents an unknown kinase, whereas peak 2 contained ikkalpha, ikkbeta, ikkepsilon, and tbk1. collectively, our results provide evidence for at least five kinases that converge on ser-536 of p65 and a novel function for this phosphorylation site in the recruitment of components of the basal transcriptional machinery to the interleukin-8 promoter. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | EBV infection, IL1 Signaling , Inhibition of Apoptosis, NF-KB Canonical, Toll like receptors |
| + |
HDAC1 | down-regulates
binding
|
NfKb-p65/p50 |
0.544 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217409 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17183360 |
Phosphorylation at thr505 by the chk1 inhibits rela transactivation and results in its increased association with hdac1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CD86 |
0.293 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254782 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19164127 |
We found that upon TLR7 and TLR8 activation, JNK and NF-kappaB positively regulated the expression of CCR7, CD86, CD83, and CD40 and the production of IL-6 and IL-12p40. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CCL20 |
0.304 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271680 |
|
|
|
|
| pmid |
sentence |
| 22319003 |
Combined stimulation with IL-6, sIL-6R, and IL-17 increased the recruitment of phosphorylated NF-B to the CCL20 promoter, increased binding of coactivators such as p300 and CBP, and enhanced H3 and H4 histone acetylation, consistent with a transcriptionally active gene. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-278041 |
|
|
Homo sapiens |
Pancreatic Cancer Cell |
| pmid |
sentence |
| 31561620 |
CCL20 is a NF-κB target gene in PDAC cells. |
|
| Publications: |
2 |
Organism: |
, Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CD80 |
0.299 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254783 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12860928 |
Upon CD40 signaling, transcription of the CD80 gene is induced by the nuclear factor (NF)-kappaB transcription factor. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | down-regulates
binding
|
MAP3K8 |
0.554 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216289 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22435554 |
Tpl-2 is stoichiometrically complexed with the nf-kb inhibitory protein, nf-kb1 p105, and the ubiquitin-binding protein abin-2, both of which are required to maintain tpl-2 protein stability. Binding to p105 also prevents tpl-2 from phosphorylating mek |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Toll like receptors |
| + |
NfKb-p65/p50 | down-regulates quantity by repression
transcriptional regulation
|
LTC4S |
0.258 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254799 |
|
|
Homo sapiens |
Mononuclear Phagocyte |
| pmid |
sentence |
| 12574384 |
activation of NF-kappaB and p50/p65 overexpression down-regulated the LTC(4) synthase gene. LPS down-regulates cysteinyl LT release and LTC(4) synthase gene expression in mononuclear phagocytes by an NF-kappaB-mediated mechanism. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates
|
Immune_response |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216319 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12692549 |
The transcription factors interferon regulatory factor 3 (IRF3) and NF-B are required for the expression of many genes involved in the innate immune response. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | B-cell activation, COVID-19 Causal Network, EBV infection, Innate Immune Response, Inflammosome Activation, Multiple sclerosis, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE, SARS-CoV INNATE RESPONSE TO dsRNA, SARS-CoV STRESS GRANULES, T cell activation, Toll like receptors |
| + |
NfKb-p65/p50 | up-regulates
binding
|
EGR1 |
0.399 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216328 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10671503 |
The early growth response transcription factor egr-1 can also interact with rela in vitro and regulate nf-kappab transcriptional activity in vivo |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity
transcriptional regulation
|
IL1B |
0.585 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255938 |
|
|
Homo sapiens |
U-937 Cell |
| pmid |
sentence |
| 8021507 |
In these studies, we show that NF-kappa B induces transcription from the human pro-IL-1 beta (IL-1 beta) gene. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, IL1 Signaling , Inflammosome Activation, Multiple sclerosis, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
SERPINA3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254805 |
|
|
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 |
| + |
LMP1 | up-regulates activity
|
NfKb-p65/p50 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267616 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26428373 |
Soon, it has been recognized that TES1 and 2 coincide with two regions named C-terminal activating regions (CTAR) 1 and 2, respectively, that are responsible for interaction of LMP1 with cellular signaling molecules. Early studies revealed that both CTAR1 and CTAR2 contribute to the activation of NF-κB, Later, it became evident that CTAR1 primarily activates the non-canonical NF-κB pathway, while CTAR2 is responsible for canonical NF-κB activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | EBV infection |
| + |
N | down-regulates activity
|
NfKb-p65/p50 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260340 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17108024 |
The data presented here indicate that N protein inhibits interferon production, while ORF 3b and ORF 6 proteins are able to inhibit both interferon production and interferon signaling. IRF-3 activation is inhibited in cells that express ORF 3b, ORF 6, or N protein, and NF-κB is inhibited in cells expressing N protein. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV CYTOKINE STORM, SARS-CoV FIBROSIS, SARS-CoV INFLAMMATORY RESPONSE, SARS-CoV INNATE RESPONSE TO dsRNA, SARS-CoV STRESS GRANULES |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
HSD11B2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253877 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15659537 |
Overexpression of p50 inhibited HSD11B2 promoter activity and overexpression of Egr-1 inhibited transactivation of the HSD11B2 promoter by p65/p50. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
Interferon-type-I |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260329 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 20610653 |
Type 1 IFNs are induced in a cell type-specific manner through Toll-like receptor and RIG-I-like receptor pathways, both of which activate interferon regulatory factors (IRFs) and nuclear factor _B (NF-_B) transcription factors. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | COVID-19 Causal Network, EBV infection, Innate Immune Response, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE, SARS-CoV INNATE RESPONSE TO dsRNA |
| + |
TGFB1 | up-regulates
|
NfKb-p65/p50 |
0.387 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-179179 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18586026 |
These data show that tgf-beta-induced nf-kappab activation is through tak1/mek-mediated aktactivation, which is essential for tgf-beta to support of osteoclast survival |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CXCL8 |
0.646 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260974 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19185596 |
S protein is a ligand for human TLR2. S protein utilizes toll-like receptor 2(TLR 2) to increase IL-8 production.Our results show that SARS S protein in a soluble form increased IL-8 production through hTLR2 ligand interaction. we have provided evidence that S protein induces IL-8 in PBMC in vitro and in THP-1 cells. The ability of S protein to increase IL-8 mRNA was mediated by activation of NF-κB possibly via TLR2 ligand and could be inhibited by the NF-κB inhibitor TPCK. The ability to detect elevated NF-κB transcription factor activity in the nucleus in response to S protein suggests that this most likely occurs by the mechanism of induction. Moreover increased secretion of IL-8 and IL-6 cytokines indicated that levels of proinflammatory mediators could be enhanced by S protein interaction with monocyte macrophages and could stimulate NK, neutrophil and monocyte migration to the site of infection. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
IL6 |
0.635 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255357 |
|
|
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, Multiple sclerosis, SARS-CoV CYTOKINE STORM |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
IL1RN |
0.334 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254794 |
|
|
Homo sapiens |
Neutrophil, Monocyte |
| pmid |
sentence |
| 20032313 |
The interleukin 1 receptor antagonist (IL-1ra) is an important negative regulator of the inflammatory response, whose genetic deficiency has been recently shown to cause a severe autoinflammatory syndrome in humans. In this study we characterized the molecular mechanisms whereby interleukin 10 (IL-10) potentiates IL-1ra transcription in LPS-stimulated monocytes and neutrophils. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | IL1 Signaling , SARS-CoV CYTOKINE STORM |
| + |
NLRX1 | up-regulates activity
relocalization
|
NfKb-p65/p50 |
0.272 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260399 |
|
|
Homo sapiens |
HEK-293T Cell |
| pmid |
sentence |
| 18219313 |
NLRX1 synergistically potentiated ROS production induced by tumour necrosis factor alpha, Shigella infection and double-stranded RNA, resulting in amplified NF-kappaB-dependent and JUN amino-terminal kinases-dependent signalling. We observed that NLRX1-positive cells showed increased p65 translocation as early as 15 min after infection, an effect that was maintained over time. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
KDM2A | down-regulates
demethylation
|
NfKb-p65/p50 |
0.462 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217415 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20080798 |
Fbxl11 and nsd1 have opposite effects on nf-kb; both bind to p65 subunit after activation of nf-kb. / nsd1 activates nf-kb and reverses the inhibitory effect of fbxl11 / these data confirm that fbxl11 and nsd1 constitute an enzyme pair that methylates and demethylates p65 on k218 and 221 in response to cytokine stimulation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MEN1 | down-regulates
binding
|
NfKb-p65/p50 |
0.424 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217406 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11526476 |
Menin represses p65-mediated transcriptional activation on nf-kappab sites in a dose-dependent and specific manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
MMP13 |
0.311 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254800 |
|
|
Homo sapiens |
Chondrocyte Cell Line |
| pmid |
sentence |
| 12734180 |
The suppressive effect of IGF-1 and OP-1 on MMP-13 expression was due in part to down-regulation of the expression of pro-inflammatory cytokines and the activity of their intermediate molecules, including NF-kappaB and AP-1 factors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
miR-155 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255920 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 18619954 |
We found that directed expression of MRFs in the neural tube of chicken embryos induced ectopic expression of miR-1 and miR-206. Conversely, the lack of Myf5 but not of MyoD resulted in a loss of miR-1 and miR-206 expression. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML |
| + |
NfKb-p65/p50 | up-regulates
transcriptional regulation
|
CCL2 |
0.579 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254509 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 20086235 |
Both NF-κBs bind to a conserved DNA motif (80) that is found in numerous IL-1–responsive genes, in particular the ones encoding IκBα (81), IL-6 (82), IL-8 (18, 83,84), monocyte chemoattractant protein 1 (MCP1) (28), and cyclooxygenase 2 (COX2) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Inflammosome Activation, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
BIRC3 |
0.67 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-64103 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9916987 |
The iaps have been shown to be induced by nf-kappab or v-rel in multiple cell lines and conversely, hiap1 and hiap2 have been shown to activate nf-kappab possibly forming a positive feed-back loop. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | IL1 Signaling |
| + |
SLC44A2 | up-regulates
|
NfKb-p65/p50 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260390 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12761501 |
Large-scale identification and characterization of human genes that activate NF-kappaB and MAPK signaling pathways |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
NOS2 |
0.453 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255353 |
|
|
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 |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
KLK3 |
0.265 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253667 |
|
|
Homo sapiens |
LNCaP Cell |
| pmid |
sentence |
| 11909978 |
NF-kappa B activates prostate-specific antigen expression and is upregulated in androgen-independent prostate cancer. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TSC22D3 | down-regulates activity
binding
|
NfKb-p65/p50 |
0.359 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253299 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 11468175 |
GILZ inhibits NF-kappaB nuclear translocation and DNA binding due to a direct protein-to-protein interaction of GILZ with the NF-kappaB subunits. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates
binding
|
SP1 |
0.559 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216334 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10671503 |
Rela (p65) nf-kappab subunit interacts with the zinc finger dna-binding domain of sp1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML |
| + |
RPS6KA5 | up-regulates
phosphorylation
|
NfKb-p65/p50 |
0.618 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217424 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12628924 |
Transcriptional activation of the nf-kappab p65 subunit by mitogen- and stress-activated protein kinase-1 (msk1)mutational analysis of p65 revealed ser276 as a target for phosphorylation and transactivation in response to tnf. Moreover, we identified msk1 as a nuclear kinase for p65, since msk1 associates with p65 in a stimulus-dependent way and phosphorylates p65 at ser276. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PPARG | down-regulates quantity by repression
|
NfKb-p65/p50 |
0.613 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249555 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 17681149 |
Transcriptional repression of inflammatory response genes occurs by negative interference of PPARg with the nuclear factor kB (NF-kB), signal transducer and activator of transcription (STAT), and activating protein 1 (AP-1) signaling pathways |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization |
| + |
TNFRSF11A | up-regulates activity
|
NfKb-p65/p50 |
0.26 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253047 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10075662 |
RANK activates NF-κB by interacting with TRAF6 via a novel TRAF6 interaction motif and TRAF6 potentially activates NIK, leading to NF-κB activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NFKB1 | form complex
binding
|
NfKb-p65/p50 |
0.709 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-55375 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9450761 |
Here we report the crystal structure at 2.9 a resolution of the p50/p65 heterodimer bound to the kappab dna |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Glucocorticoid receptor Signaling |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
GAP43 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266770 |
|
|
Rattus norvegicus |
|
| pmid |
sentence |
| 26865625 |
In this study, we demonstrated for the first time that growth-associated protein 43 (GAP43), a well known growth cone protein that promotes axonal regeneration, can be induced in rat brain astrocytes by the proinflammatory endotoxin lipopolysaccharide via both nuclear factor-κB and signal transducer and activator of transcription 3-mediated transcriptional activation. |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
NLRP3 inflammasome |
0.365 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260328 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 28531279 |
The activation of NLRP3 inflammasomes in macrophages requires two stimuli. The first signal, called priming, is provided by an inflammatory stimulus such as TLRs and TNF-α receptor (TNFR) that leads to NF-κB-mediated NLRP3 expression and post-translational modifications of NLRP3 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
MMP9 |
0.421 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254798 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15536164 |
Biglycan, NGAL, and MMP-9 are transcriptionally up-regulated by NF-kappaB, a transcription factor that is activated in FAP nerves and SG. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates
binding
|
CITED1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216331 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9660950 |
The transcriptional coactivator cpb/p300 associates with nf-kappa b p65 through two sites, an n-terminal domain that interacts with the c-terminal region of unphosphorylated p65, and a second domain that only interacts with p65 phosphorylated on serine 276. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
B2M |
0.358 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254658 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12480693 |
The nuclear factor kappa B (NF-kappa B) subunits p50 and p65 bind to the kappa B box and p65 transactivates beta(2)m. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity
transcriptional regulation
|
HES1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253063 |
|
|
Homo sapiens |
U2-OS Cell |
| pmid |
sentence |
| 24300895 |
These data indicate that basal NFκB activity at the conserved +26/+34 site of the HES1 gene promotes its expression, and that glucocorticoids can silence HES1 by inhibiting this activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
USP6 | up-regulates
|
NfKb-p65/p50 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-164949 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20418905 |
These data confirm that tre17 activates nfkappab in a usp-dependent manner |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
SOCS3 |
0.392 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249566 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19643666 |
Expression of SOCS1 and SOCS3 is regulated primarily by activation of STAT1 and STAT3, respectively, although their expression can be mediated through other signaling cascades, including the mitogen activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappaB) pathways. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NOD2 | up-regulates
|
NfKb-p65/p50 |
0.372 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252412 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18079694 |
Nod1 and Nod2 stimulation activates NF-kappaB through RICK, a caspase-recruitment domain-containing kinase. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
DHX9 | up-regulates activity
binding
|
NfKb-p65/p50 |
0.459 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260947 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 30137501 |
A DNA-sensing-independent Role of a Nuclear RNA Helicase, DHX9, in Stimulation of NF-κB-mediated Innate Immunity Against DNA Virus Infection. Taken together, our results show a critical role of nuclear DHX9 (as a transcription coactivator) in the stimulation of NF-κB-mediated innate immunity against DNA virus infection, independently of DHX9's DNA-sensing function. DHX9 interacts with NF-κB p65 and RNAPII in the nucleus during DNA virus infection |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | down-regulates
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255693 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22021368 |
Once genetic mutation of AML1 occurs in hematopoietic cells, aberrant activation of NF-κB signaling exerts antiapoptotic and proliferation-promoting effects via activation of BCL-XL or JUNB. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML, COVID-19 Causal Network, EBV infection, Fibrosis, FLT3-ITD signaling, Inhibition of Apoptosis, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV FIBROSIS, SARS-CoV STRESS GRANULES, TNF-alpha Signaling |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
GADD45B |
0.293 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-111963 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11713530 |
Here we report that nf-kappab complexes downregulate the c-jun amino-terminal kinase (jnk) cascade, thus establishing a link between the nf-kappab and the jnk pathways. This link involves the transcriptional upregulation of gadd45beta/myd118, which downregulates jnk induced by the tnf receptor (tnf-r). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NFKBIE | down-regulates
binding
|
NfKb-p65/p50 |
0.586 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217361 |
|
|
Homo sapiens |
Leukemia Cell |
| pmid |
sentence |
| 12835716 |
Nf-kb is normally sequestered in the cell cytoplasm by binding to ikbx, ikbb, ikbe |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CFI |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254786 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10630630 |
The production of CFI by Hep G2 cells was enhanced in a dose- and time-dependent fashion by 12-O-tetradecanoyl-1,2-phorbol 13-acetate (TPA), a potent PKC activator. The enhancement of the activity of transfected chimeric CAT constructs by TPA was abrogated by calphostin C and by pyrrolidine dithiocarbamate (an inhibitor of NF-kappaB and AP-1 transactivation). These results indicate that TPA regulation of CFI gene requires PKC signalling and is mediated by via a TPA response element (TRE) in the CFI promoter region located at -136/-130 and involves the transactivation of AP-1 and NF-kappaB transcription factors |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
ABCB1 |
0.262 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254654 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19763573 |
PSC833, cyclosporine analogue, downregulates MDR1 expression by activating JNK/c-Jun/AP-1 and suppressing NF-kappaB. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
|
CCND1 |
0.487 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255358 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20219869 |
Importantly, NF-kB can promote the expression and stability of cyclin D1 in muscle (4, 35, 39, 132), leading to increased cell proliferation and inhibition of differentiation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Skeletal Muscle |
| Pathways: | Acute Myeloid Leukemia |
| + |
NfKb-p65/p50 | up-regulates
|
M1_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249519 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30060484 |
The bacterial endotoxin LPS is a known agonist of TLR2 that activates the expression of proinflammatory cytokines and the phosphorylation of MAPKs and NFκB [49]. In addition, the activation of the MAPK and NFκB signaling cascades drive inflammation and macrophage polarization. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization, Multiple sclerosis |
| + |
nitric oxide | up-regulates
|
NfKb-p65/p50 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255350 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20219869 |
Similarly, exposure of cells to oxidative stress, in particular, nitric oxide (NO) or peroxynitrite (ONOO), can activate NF-kB and cause its translocation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Skeletal Muscle |
| Pathways: | Multiple sclerosis |
| + |
NfKb-p65/p50 | up-regulates
binding
|
JUN |
0.578 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216337 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18174238 |
Chromatin immunoprecipitation (chip) analysis confirmed the serum-induced recruitment of jund to the promoter in vivo and showed that the presence of jund was dependent on the presence of p65 and p50, indicating a protein-protein-dependent mechanism of jund recruitment |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, Glucocorticoid receptor Signaling, SARS-CoV CYTOKINE STORM, TNF-alpha Signaling |
| + |
IL1R1 | up-regulates activity
|
NfKb-p65/p50 |
0.524 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249512 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9625767 |
Il-1 binding to its receptor triggers a cascade of signaling events, including activation of the stress-activated mitogen-activated protein (map) kinases, c-jun nh2-terminal kinase (jnk) and p38 map kinase, as well as transcription factor nuclear factor kappab (nf-kappab) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | IL1 Signaling , SARS-CoV CYTOKINE STORM |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CD40 |
0.571 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254785 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19164127 |
We found that upon TLR7 and TLR8 activation, JNK and NF-kappaB positively regulated the expression of CCR7, CD86, CD83, and CD40 and the production of IL-6 and IL-12p40. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CD83 |
0.26 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254781 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19164127 |
We found that upon TLR7 and TLR8 activation, JNK and NF-kappaB positively regulated the expression of CCR7, CD86, CD83, and CD40 and the production of IL-6 and IL-12p40. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MFGE8 | down-regulates activity
|
NfKb-p65/p50 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260652 |
|
|
Rattus norvegicus |
Macrophage |
| pmid |
sentence |
| 19020771 |
In our current study, we have shown that after LPS-stimulation, MFG-E8-mediated apoptotic cell phagocytosis suppresses various ERK1/2, p38, JNK, and NFκB activation, resulting in a lower TNF-α release. We also explored whether MFG-E8 helps to suppress the proinflammatory pathway within RPMs. We hence incubated the macrophages with apoptotic cells and stimulated them with LPS and examined the activation of MAP kinase and NFkB pathways after the exogenous addition of recombinant MFG-E8 (rMFG-E8). While apoptotic cells alone had no effect on these pathways, the addition of rMFG-E8 to apoptotic cells prior to phagocytosis and LPS stimulation had a marked suppressive effect on all of the investigated pathways, particularly on the p38 and NFκB pathways that play a key role in the cytokine response of macrophages |
|
| Publications: |
1 |
Organism: |
Rattus Norvegicus |
| + |
TLR4 | up-regulates activity
|
NfKb-p65/p50 |
0.576 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249517 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 7635431 |
The activation of NF-kB is triggered by different stimuli, eg., lipopolysaccharides (LPSs), muramyl peptides, viruses,e inflammatory cytokines tumor necrosis factor-alpha(TNF-a) and interleukin (IL)-1b, irradiation, and reactive xygen intermediates (H2O2). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | FLT3-ITD signaling, Macrophage polarization |
| + |
NfKb-p65/p50 | up-regulates quantity
transcriptional regulation
|
miR-155 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255802 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26055960 |
Our results suggest that activating mutation of FLT3 in AML can lead, to increased expression of miR-155, which then causes down-regulation of SPI1 and CEBPB and consequently causes block of myeloid differentiation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML |
| + |
SCF-betaTRCP | up-regulates activity
ubiquitination
|
NfKb-p65/p50 |
0.509 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235305 |
|
|
Chlorocebus aethiops |
|
| pmid |
sentence |
| 11295495 |
The scf-betatrcp complex is responsible for the ubiquitination of p100 and p105 following their phosphorylation by ikk. |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| Pathways: | NF-KB Canonical |
| + |
NfKb-p65/p50 | up-regulates
|
Interferon_Production |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-216322 |
|
|
Mus musculus |
MEF Cell |
| pmid |
sentence |
| 20610653 |
Type 1 IFNs are induced in a cell type-specific manner through Toll-like receptor and RIG-I-like receptor pathways, both of which activate interferon regulatory factors (IRFs) and nuclear factor _B (NF-_B) transcription factors. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | B-cell activation, EBV infection, Toll like receptors |
| + |
Angiotensin 1-7 | down-regulates activity
|
NfKb-p65/p50 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260447 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24168260 |
We hypothesized that the ACE2/Ang-(1-7)/Mas axis protects against pulmonary fibrosis by inhibiting the MAPK/NF-κB pathway.In summary, our study demonstrate that exogenous Ang-(1-7) and ACE2 overexpression protect against BLM- or AngII-induced pulmonary fibrosis by down-regulating the MAPK/NF-κB pathway. However, constant infusion of Ang-(1-7) paradoxically initiates an inflammatory response in the lungs. The antifibrotic effects of Ang-(1-7) noted here make the heptapeptide a strong candidate for a therapeutic target in humans with pulmonary fibrosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
STAT1 | down-regulates
binding
|
NfKb-p65/p50 |
0.451 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217418 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16481475 |
Acetylated stat1 is able to interact with nf-kappab p65. As a consequence, p65 dna binding, nuclear localization, and expression of anti-apoptotic nf-kappab target genes decrease. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | EBV infection, SARS-CoV CYTOKINE STORM |
| + |
NfKb-p65/p50 | down-regulates
|
Cell_death |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256654 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22021368 |
Once genetic mutation of AML1 occurs in hematopoietic cells, aberrant activation of NF-κB signaling exerts antiapoptotic and proliferation-promoting effects via activation of BCL-XL or JUNB. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CCL2 |
0.579 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255356 |
|
|
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, Inflammosome Activation, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE |
| + |
PPARGC1A | down-regulates quantity by repression
transcriptional regulation
|
NfKb-p65/p50 |
0.365 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217978 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 20404331 |
In mouse muscles, overexpression of PGC-1beta (like PGC-1alpha) inhibited denervation atrophy, ubiquitin ligase induction, and transcription by NFkappaB |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Tissue: |
Skeletal Muscle |
3.0
NfKb-p65/p50
CPX-5828