| + |
KDM6B | down-regulates 
|
M1_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249563 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22378047 |
IL-4-induced c-Myc activity controls a subset of M2-associated genes. IL-4 also induces the M2-polarizing JMJD3-IRF4 axis to inhibit IRF5-mediated M1 polarization. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization |
| + |
M1_polarization | up-regulates 
|
IFNG |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263827 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 32454942 |
Macrophages and microglia show a high plasticity and have been arbitrarily classified into “M1” (proinflammatory) and “M2” (prorepair, anti-inflammatory) phenotypes depending on their activation state, although it is now widely accepted that this classification is hugely oversimplified, particularly for microglia, and only partially reflects the real situation. According to the M1/M2 model, M1 polarized cells are characterized by the release of proinflammatory mediators, such as TNF, IL-1β, and IFNγ |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization, Multiple sclerosis |
| + |
M1_polarization | up-regulates
|
IL1B |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263825 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 32454942 |
Macrophages and microglia show a high plasticity and have been arbitrarily classified into “M1” (proinflammatory) and “M2” (prorepair, anti-inflammatory) phenotypes depending on their activation state, although it is now widely accepted that this classification is hugely oversimplified, particularly for microglia, and only partially reflects the real situation. According to the M1/M2 model, M1 polarized cells are characterized by the release of proinflammatory mediators, such as TNF, IL-1β, and IFNγ |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
IRF4 | down-regulates
|
M1_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249561 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22378047 |
IL-4-induced c-Myc activity controls a subset of M2-associated genes. IL-4 also induces the M2-polarizing JMJD3-IRF4 axis to inhibit IRF5-mediated M1 polarization. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization |
| + |
SLC11A1 | up-regulates
|
M1_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254037 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11909746 |
Functional studies in Nramp1 transfected macrophages have demonstrated that the Nramp1 protein plays a vital role in early macrophage activation [10,29,30]. Nramp1 is constitutively expressed in macrophage cell lines of the myeloid lineage (isolated peritoneal, splenic, and liver resident macrophages), and can be induced by treatment of macrophages with IFN-γ, or IFN-γ plus lipopolysaccharide (LPS) |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAT5A | up-regulates
|
M1_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249510 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22025054 |
The activation of receptors for both GM-CSF and IFN-g stimulates the Jak kinaseSTAT transcription factor pathway, and an ISRE in the Irf5 promoter can bind STAT1 and STAT2, which suggests a possible mechanism for IRF5 expression induced by GM-CSF and IFN-g. Consequently, high expression of IRF5 results in polarization of the macrophage phenotype toward M1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
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 |
| + |
IRF5 | up-regulates
|
M1_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249562 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22378047 |
IL-4-induced c-Myc activity controls a subset of M2-associated genes. IL-4 also induces the M2-polarizing JMJD3-IRF4 axis to inhibit IRF5-mediated M1 polarization. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
nitric oxide | up-regulates
|
M1_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255556 |
|
|
|
|
| pmid |
sentence |
| 24669294 |
While investigating the factors that regulate macrophage arginine metabolism, Mills and colleagues found that macrophages activated in mouse strains with Th1 and Th2 backgrounds differed qualitatively in their ability to respond to the classic stimuli IFN-γ or lipopolysaccharide (LPS) or both and defined an important metabolic difference in the pathway: M1 macrophages made the toxic nitric oxide (NO), whereas M2 macrophages made the trophic polyamines |
|
| Publications: |
1 |
| Pathways: | Multiple sclerosis |
| + |
M1_polarization | up-regulates
|
TNF |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263826 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 32454942 |
Macrophages and microglia show a high plasticity and have been arbitrarily classified into “M1” (proinflammatory) and “M2” (prorepair, anti-inflammatory) phenotypes depending on their activation state, although it is now widely accepted that this classification is hugely oversimplified, particularly for microglia, and only partially reflects the real situation. According to the M1/M2 model, M1 polarized cells are characterized by the release of proinflammatory mediators, such as TNF, IL-1β, and IFNγ |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
STAT1 | up-regulates
|
M1_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249496 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19029990 |
STAT1 binds as a homodimer to cis elements known as gammaactivated sequences in the promoters of the genes encoding NOS2, the MHC class II transactivator (CIITA) and IL-12, among others. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
M1_polarization