| + |
ERG | down-regulates quantity by repression 
transcriptional regulation
|
CXCL8 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253912 |
|
|
Homo sapiens |
HUVEC Cell |
| pmid |
sentence |
| 19359602 |
ERG can inhibit the activity of the IL-8 promoter in a dose dependent manner. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL8 | up-regulates 
binding
|
CXCR2 |
0.856 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-107983 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11350788 |
Il-8 activates both the cxcr1 and the cxcr2 on microvascular endothelial cells, using different signal transduction cascades. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ELF4 | up-regulates quantity by expression 
transcriptional regulation
|
CXCL8 |
0.243 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-119204 |
|
|
Homo sapiens |
Neutrophil, T-lymphocyte |
| pmid |
sentence |
| 14625302 |
Myeloid elf1-like factor is a potent activator of interleukin-8 expression in hematopoietic cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL8 | up-regulates
|
Angiogenesis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252288 |
|
|
|
|
| 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 |
| + |
AP1 | up-regulates quantity by expression
transcriptional regulation
|
CXCL8 |
0.563 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261029 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32446778 |
The up-regulation of the CXCL8 gene expression, could be due to a direct effect of the virus at the cellular level. Indeed, intestinal and lung cells lines infected by SARS-CoV, promptly increase their secretion of CXCL8 [88]. This observation would fit with the notion that the expression of CXCL8 is dependent on the tran-scription factor Activator protein 1 (AP-1), which was shown to bestrongly up-regulated by SARS-CoV |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
S | up-regulates quantity
|
CXCL8 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260279 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 17412287 |
The ability of S-protein to induce TNF-a |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
CXCL8 | up-regulates
binding
|
CXCR1 |
0.773 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-107920 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11350788 |
Il-8 activates both the cxcr1 and the cxcr2 on microvascular endothelial cells, using different signal transduction cascades. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL8 | up-regulates
|
Inflammation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260257 |
|
|
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: | SARS-CoV CYTOKINE STORM |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CXCL8 |
0.634 |
| 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 |
| + |
CRP | up-regulates quantity by expression
transcriptional regulation
|
CXCL8 |
0.492 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252143 |
|
|
Homo sapiens |
Retinal Pigment Epithelium Cell |
| pmid |
sentence |
| 26961257 |
In this study, we provide mechanistic insight into how CRP contributes to the development of AMD. In particular, we show that monomeric CRP (mCRP) but not the pentameric form (pCRP) upregulates IL-8 and CCL2 levels in retinal pigment epithelial cells. Further, we show that complement factor H (FH) binds mCRP to dampen its proinflammatory activity. FH from AMD patients carrying the “risk” His402 polymorphism displays impaired binding to mCRP, and therefore proinflammatory effects of mCRP remain unrestrained. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CXCL8 | up-regulates
|
ARDS |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261030 |
|
|
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 |
3.0
CXCL8
- 
- 