| + |
SMAD3/SMAD4 | up-regulates 
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249551 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22703233 |
Our results establish a novel biological role for TGFbeta signaling in controlling expression of genes characteristic for alternatively activated macrophages. We speculate that lack of TbetaRII signaling reduces the anti-inflammatory M2 phenotype of macrophages because of reduced expression of these products. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253587 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27418133 |
The SMAD2/3 and PI3K/AKT signaling pathways were crucial for TGF-?-induced SNAIL overexpression in THP-1 cells. These findings suggest that TGF-? skews macrophage polarization towards a M2-like phenotype via SNAIL up-regulation, and blockade of TGF-?/SNAIL signaling restores the production of pro-inflammatory cytokines |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
KDM6B | up-regulates
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249564 |
|
|
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 |
| + |
L-ornithine | up-regulates activity
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256076 |
|
|
|
|
| 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 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256075 |
|
|
|
|
| pmid |
sentence |
| 25386178 |
In general, M2 type macrophages act as anti-inflammatory cells via diversion of arginine away from NOS or via the synthesis of downstream products derived from the ornithine that is generated via arginase |
|
| Publications: |
2 |
| + |
STAT6 | up-regulates
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249541 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22025054 |
IL-4R signals through a JAKSTAT6 pathway, and many of the genes associated with mouse M2 macrophages are regulated by STAT6, including arginase 1 (Arg1), macrophage mannose receptor 1 (Mrc1; also known as Cd206), resistin-like-? (Retnla; also known as Fizz1) and chitinase 3-like 3 (Chi3l3; also known as Ym1). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization |
| + |
MAPK14 | up-regulates
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255447 |
|
|
|
|
| pmid |
sentence |
| 22933625 |
The IL-10-mediated shift in macrophage phenotype in injured muscle may be amplified by activation of mitogen-activated protein kinase (MAPK), especially p38 MAPK, through signaling that is antagonized by MAPK phosphatase-1 (MKP-1). |
|
| Publications: |
1 |
| + |
SMAD2/SMAD4 | up-regulates
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249550 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22703233 |
Our results establish a novel biological role for TGFbeta signaling in controlling expression of genes characteristic for alternatively activated macrophages. We speculate that lack of TbetaRII signaling reduces the anti-inflammatory M2 phenotype of macrophages because of reduced expression of these products. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253588 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 27418133 |
The SMAD2/3 and PI3K/AKT signaling pathways were crucial for TGF-?-induced SNAIL overexpression in THP-1 cells. These findings suggest that TGF-? skews macrophage polarization towards a M2-like phenotype via SNAIL up-regulation, and blockade of TGF-?/SNAIL signaling restores the production of pro-inflammatory cytokines |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
STAT3 | up-regulates
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249547 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10347215 |
The data presented this far show that the JAK-STAT signaling pathway and specifically Stat3 and Jak1 are required for induction of IL-10-dependent anti-inflammatory and developmental responses in macrophages. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization, Multiple sclerosis |
| + |
M2_polarization | up-regulates quantity by expression
|
IL10 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255448 |
|
|
|
|
| pmid |
sentence |
| 22933625 |
P38 activation contributes to the macrophage phenotype switch in injured muscle, which could elevate production of IL-10 (63), creating positive feedback for the phenotype switch |
|
| Publications: |
1 |
| Pathways: | Macrophage polarization, Multiple sclerosis |
| + |
IRF4 | up-regulates
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249543 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20729857 |
We found Irf4 to be one of the direct targets of Jmjd3-mediated demethylation. Finally, we found that Irf4 is a transcription factor crucial for the induction of M2 macrophage responses. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249559 |
|
|
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: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization |
| + |
CSF1 | up-regulates
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277708 |
|
|
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
|
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 |
| + |
IL33 | up-regulates 
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277712 |
|
|
Homo sapiens |
M2 Macrophage |
| pmid |
sentence |
| 36660926 |
IL-33 secreted by pericytes and CAFs promotes M2 polarization and induced MMP9 expression in M2 TAMs facilitating metastasis development via the IL-33-ST2-NF-κB-MMP9-laminin pathway in a mouse model of pancreatic cancer |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
M2_polarization | up-regulates
|
TGFb |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263824 |
|
|
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. M2 polarized cells express a variety of anti-inflammatory mediators, such as IL-4, IL-10, and transforming growth factor-β (TGF-β), and contribute to immunoregulation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
M2_polarization | up-regulates
|
IL4 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263822 |
|
|
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. M2 polarized cells express a variety of anti-inflammatory mediators, such as IL-4, IL-10, and transforming growth factor-β (TGF-β), and contribute to immunoregulation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization, Multiple sclerosis |
| + |
FCGR1A | up-regulates
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249524 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24445665 |
Although crosslinking of activating FcgammaRs on monocytes and macrophages induces the production of several pro-inflammatory cytokines and chemokines, immune complex-mediated signalling via activating FcgammaRs together with Toll-like receptor (TLR) triggering induces a specific M2 activation state in macrophages macrophages in this state were termed M2b or regulatory macrophages. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
M2_polarization | up-regulates
|
IL10 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263823 |
|
|
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. M2 polarized cells express a variety of anti-inflammatory mediators, such as IL-4, IL-10, and transforming growth factor-β (TGF-β), and contribute to immunoregulation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization, Multiple sclerosis |
| + |
PPARG | up-regulates
|
M2_polarization |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249542 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17681149 |
This mechanism is mainly operative in native monocytes that, in the presence of an appropriate M2 stimulus such as IL-4, can be primed by PPARg ligands to an enhanced M2 phenotype. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Macrophage polarization |
3.0
M2_polarization