| + |
HIF1A | up-regulates quantity by expression 
transcriptional regulation
|
CCL2 |
0.414 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251719 |
|
|
Homo sapiens |
Perivascular Astrocyte |
| pmid |
sentence |
| 17474992 |
These findings suggest that both MCP-1 and MCP-5 are HIF-1 target genes and that HIF-1α is involved in transcriptional induction of these two chemokines in astrocytes by hypoxia. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CCL2 | up-regulates activity
binding
|
CCR2 |
0.783 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255113 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20219869 |
The investigators showed that myoblasts constitutively express receptors for CCL2 (CCR2), CCL3 (CCR1 and CCR5), and CCL4 (CCR5), and that stimulation with either CCL2 or CCL4 was sufficient to promote myoblast proliferation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
NfKb-p65/p50 | up-regulates 
transcriptional regulation
|
CCL2 |
0.567 |
| 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 |
| + |
IFNAR | up-regulates quantity by expression
|
CCL2 |
0.322 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260851 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 32283152 |
The rapid replication of SARS-CoV in BALB/c mice induces the delayed release of IFN-α/β, which is accompanied by the influx of many pathogenic inflammatory mononuclear macrophages. The accumulated mononuclear macrophages receive activating signals through the IFN-α/β receptors on their surface and produce more monocyte chemoattractants (such as CCL2, CCL7, and CCL12), resulting in the further accumulation of mononuclear macrophages. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | COVID-19 Causal Network, Inflammosome Activation, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE |
| + |
CCL2 | up-regulates activity
binding
|
CCR4 |
0.479 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-237555 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17160712 |
CCR2 and CCR4 are two cell surface receptors that bind CCL2 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CCL2 | up-regulates
|
Inflammation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261317 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32446778 |
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 inflammatory response. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Inflammosome Activation, SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE |
| + |
CCL2 | up-regulates
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277709 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 33505964 |
Exosomes from tumor cells package assorted proteins and chemokines with immunomodulatory capability, including CSF-1, CCL2, and TGF-β, to promote M2-like characterization of TAMs |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CCL2 | up-regulates
|
Macrophage_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260849 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 32283152 |
The rapid replication of SARS-CoV in BALB/c mice induces the delayed release of IFN-α/β, which is accompanied by the influx of many pathogenic inflammatory mononuclear macrophages. The accumulated mononuclear macrophages receive activating signals through the IFN-α/β receptors on their surface and produce more monocyte chemoattractants (such as CCL2, CCL7, and CCL12), resulting in the further accumulation of mononuclear macrophages. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
Macrophage_activation | up-regulates quantity
|
CCL2 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260962 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 32283152 |
The rapid replication of SARS-CoV in BALB/c mice induces the delayed release of IFN-α/β, which is accompanied by the influx of many pathogenic inflammatory mononuclear macrophages. The accumulated mononuclear macrophages receive activating signals through the IFN-α/β receptors on their surface and produce more monocyte chemoattractants (such as CCL2, CCL7, and CCL12), resulting in the further accumulation of mononuclear macrophages. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
CCL2 | up-regulates
|
ARDS |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261032 |
|
|
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 |
| + |
AP1 | up-regulates activity
transcriptional regulation
|
CCL2 |
0.601 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260764 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21561061 |
3b Potentiates AP-1-Dependent MCP-1 Promoter Activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM |
| + |
PRDM1 | down-regulates quantity by repression 
transcriptional regulation
|
CCL2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-271679 |
|
|
|
|
| pmid |
sentence |
| 19915049 |
Blimp-1 binds to the proinflammatory cytokine/chemokine genes, Il-6 and Ccl2, and negatively regulates their expression. |
|
| Publications: |
1 |
| + |
CCL2 | up-regulates
|
Immune_response |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261027 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32283152 |
High levels of expression of IL-1B, IFN-γ, IP-10, and monocyte chemoattractant protein 1 (MCP-1) have been detected in patients with COVID-19. These inflammatory cytokines may activate the T-helper type 1 (Th1) cell response. Th1 activation is a key event in the activation of specific immunity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Inflammosome Activation, SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE |
| + |
NfKb-p65/p50 | up-regulates quantity by expression
transcriptional regulation
|
CCL2 |
0.567 |
| 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 |
| + |
CRP | up-regulates quantity by expression
transcriptional regulation
|
CCL2 |
0.454 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252144 |
|
|
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 |
3.0
CCL2
- 
- 