| + |
TGFb | up-regulates activity 
binding
|
TGFBR2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256179 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 22703233 |
TGFbeta signals are transmitted via a cell surface receptor complex consisting of the TGFbeta type I receptor (TbetaRI) and TGFbeta type II receptor (TbetaRII). To initiate signal transduction, TGFbeta binds to TbetaRII, which in turn recruits TbetaRI, leading to the formation of a tetrameric receptor complex. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256178 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22326956 |
TGF-beta signaling mediates a wide range of biological activities in development and disease. TGF-beta ligands signal through heterodimeric type I and type II receptors (TGF-beta receptor type I [TbetaRI, also known as ALK5 and TGFBR1] and TbetaRII) that are members of the serine/threonine kinase family. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, Hepatocellular Tumor, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV FIBROSIS, Thyroid cancer, TGFb in cancer |
| + |
TGFb | up-regulates quantity by expression 
transcriptional regulation
|
SMAD3/SMAD4 |
0.629 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260428 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30017632 |
Transforming growth factor-β1 (TGF-β1) is considered as a crucial mediator in tissue fibrosis and causes tissue scarring largely by activating its downstream small mother against decapentaplegic (Smad) signaling. Different TGF-β signalings play different roles in fibrogenesis. TGF-β1 directly activates Smad signaling which triggers pro-fibrotic gene overexpression. Excessive studies have demonstrated that dysregulation of TGF-β1/Smad pathway was an important pathogenic mechanism in tissue fibrosis. Smad2 and Smad3 are the two major downstream regulator that promote TGF-β1-mediated tissue fibrosis, while Smad7 serves as a negative feedback regulator of TGF-β1/Smad pathway thereby protects against TGF-β1-mediated fibrosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, Hepatocellular Tumor, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV FIBROSIS, TGFb in cancer |
| + |
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 |
| + |
TGFb | up-regulates
|
Angiogenesis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270216 |
|
|
|
|
| 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 |
| Pathways: | Pancreatic ductal adenocarcinoma (PDA) |
| + |
TGFb | up-regulates quantity by expression
transcriptional regulation
|
SNAI1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-265251 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 29305973 |
Epithelial-mesenchymal transition (EMT) takes place, namely fibrosis, development and cancer. the process of EMT is integral to a number of physiological and disease states. TGF-β1 is a major effector of this process that activates various key transcription factors such as Snai1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TGFb | up-regulates
|
SMAD3 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-97123 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12524424 |
Because tgf-beta inhibits adipogenesis by signaling through smad3, we examined physical and functional interactions of smad3 and smad4 with c/ebpbeta, c/ebpdelta, and ppargamma2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, Hepatocellular Tumor, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV FIBROSIS, TGFb in cancer |
3.0
TGFb