| + |
SMAD4 | form complex 
binding
|
SMAD2/SMAD4 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235178 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11274206 |
the receptor-regulated Smad, such as Smad2, forms a heterocomplex with the co-mediator Smad, Smad4 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer |
| + |
SKI | down-regulates activity 
binding
|
SMAD2/SMAD4 |
0.767 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253300 |
|
|
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 12793438 |
The ski and snon protein family associate with and repress the activity of smad2, smad3, and smad4, three members of the tgf-fl signaling pathway |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
SMAD2/SMAD4 | up-regulates quantity by expression 
transcriptional regulation
|
NANOG |
0.534 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242044 |
|
|
Homo sapiens |
Esophageal Squamous Cell Carcinoma Cell |
| pmid |
sentence |
| 18682241 |
We also find that SMADs bind with the NANOG promoter and that SMAD2/3 activity enhances NANOG promoter activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-242049 |
|
|
Homo sapiens |
Embryonic Stem Cell |
| pmid |
sentence |
| 19279133 |
Here, we show that Smad2/3, the downstream effectors of Activin/Nodal signalling, bind and directly control the activity of the Nanog gene in hESCs. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
SMAD2/SMAD4 | up-regulates 
|
Fibrosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260440 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30017632 |
Smad4 interacted withSmad2/3 and participated in the transcription of downstream pro-fi-brotic target genes |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
SMAD2 | form complex
binding
|
SMAD2/SMAD4 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235188 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11274206 |
the receptor-regulated Smad, such as Smad2, forms a heterocomplex with the co-mediator Smad, Smad4 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Hepatocellular Tumor, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer |
| + |
SMAD2/SMAD4 | up-regulates activity
binding
|
SP1 |
0.58 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256288 |
|
|
Homo sapiens |
HaCaT Cell |
| pmid |
sentence |
| 11013220 |
TGF-β induces the formation and nuclear translocation of a trimeric Smad complex, which in this case is likely to consist of one monomer each of Smad2, Smad3 and Smad4. Smad2 and Smad4 associate directly with Sp1 and co-activate the transcriptional activity of Sp1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMAD2/SMAD4 | up-regulates
|
M2_polarization |
0.7 |
| 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 |
|
| 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. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
SKIL | down-regulates activity
binding
|
SMAD2/SMAD4 |
0.836 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253302 |
|
|
Homo sapiens |
Melanoma Cell |
| pmid |
sentence |
| 12793438 |
The ski and snon protein family associate with and repress the activity of smad2, smad3, and smad4, three members of the tgf-fl signaling pathway |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
SMAD2/SMAD4 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2B |
0.586 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256287 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11013220 |
Our data demonstrate the physical interactions and functional cooperativity of Sp1 with a complex of Smad2, Smad3 and Smad4 in the induction of the p15Ink4B gene. These findings explain the tumor suppressor roles of Smad2 and Smad4 in growth arrest signaling by TGF-β. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer |
| + |
SMAD2/SMAD4 | down-regulates quantity by repression 
transcriptional regulation
|
MYC |
0.649 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256291 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11689553 |
To identify this pathway, we analyzed TGF-β-responsive elements in the human c-myc promoter and found that Smad proteins directly bound to an element in the c-myc promoter and suppressed c-myc promoter activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Hepatocellular Tumor |
| + |
SMAD2/SMAD4 | up-regulates activity
binding
|
AP1 |
0.528 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256180 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22926518 |
The activated TGFβ type I receptor kinase propagates the signal within the cell through phosphorylation of the receptor-regulated (R-)Smad proteins Smad2 and Smad3 at their extreme carboxyl-terminal serine residues.1, 2 The activated R-Smads then form heteromeric complexes with the common-partner (Co-)Smad, Smad4, and accumulate in the nucleus, where they can bind DNA and regulate gene expression. The Smads control gene expression in a cell type-specific manner by interacting with other proteins, such as AP-1, AP-2 and Ets transcription factors and specific co-activators and co-repressors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Hepatocellular Tumor, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer |
3.0
SMAD2/SMAD4
CPX-3208