| + |
USP2 | up-regulates activity 
deubiquitination
|
TGFBR1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-273605 |
Lys502 |
LSQQEGIkM |
in vitro |
|
| pmid |
sentence |
| 29490279 |
Here, we report the role of USP2a in promoting metastasis by facilitating TGF-β-triggered signaling. USP2a interacts with TGFBR1 and TGFBR2 upon TGF-β stimulation and removes K33-linked polyubiquitin chains from Lys502 of TGFBR1, promoting the recruitment of SMAD2/3. Simultaneously, TGFBR2 phosphorylates Ser207/Ser225 of USP2a, leading to the disassociation of SMAD2/3 from TGFBR1. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
TGFBR1 |
phosphorylation
|
TP63 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-199781 |
Ser160 |
SSTFDALsPSPAIPS |
Homo sapiens |
|
| pmid |
sentence |
| 23166821 |
We show that phosphorylation of _np63_ at s66/68 in response to ultraviolet (uv) irradiation is mediated by alk5 |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-199785 |
Ser68 |
FLEQPICsVQPIDLN |
Homo sapiens |
|
| pmid |
sentence |
| 23166821 |
We show that phosphorylation of _np63_ at s66/68 in response to ultraviolet (uv) irradiation is mediated by alk5 |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
TGFBR2 | up-regulates activity
phosphorylation
|
TGFBR1 |
0.718 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-246728 |
Ser172 |
SLDRPFIsEGTTLKD |
Homo sapiens |
|
| pmid |
sentence |
| 8576253 |
Recent studies have revealed that upon TGF-beta binding several serine and threonine residues in the GS domain of TGF-beta type I receptor (T beta R-I) are phosphorylated by TGF-beta type II receptor (T beta R-II) and that the phosphorylation of GS domain is essential for TGF-beta signalingThese observations indicate that serine 172 and threonine 176 of T beta R-I are dispensable for extracellular matrix protein production but essential to the growth inhibition by TGF-beta |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-246732 |
Thr176 |
PFISEGTtLKDLIYD |
Homo sapiens |
|
| pmid |
sentence |
| 8576253 |
Recent studies have revealed that upon TGF-beta binding several serine and threonine residues in the GS domain of TGF-beta type I receptor (T beta R-I) are phosphorylated by TGF-beta type II receptor (T beta R-II) and that the phosphorylation of GS domain is essential for TGF-beta signalingThese observations indicate that serine 172 and threonine 176 of T beta R-I are dispensable for extracellular matrix protein production but essential to the growth inhibition by TGF-beta |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255961 |
Thr176 |
PFISEGTtLKDLIYD |
in vitro |
|
| pmid |
sentence |
| 8576253 |
From our present data, it is not easy to deduce the mechanistic significance of serine 172 and threonine 176 of TβR-I in TGF-β signaling. Although it was reported that TGF-β-induced phosphorylation of these residues was not detected in vivo(22), it is still possible that TβR-II may phosphorylate these residues as minor phosphorylation site(s). |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255962 |
Thr200 |
LPLLVQRtIARTIVL |
in vitro |
|
| pmid |
sentence |
| 8576253 |
From our present data, it is not easy to deduce the mechanistic significance of serine 172 and threonine 176 of TβR-I in TGF-β signaling. Although it was reported that TGF-β-induced phosphorylation of these residues was not detected in vivo(22), it is still possible that TβR-II may phosphorylate these residues as minor phosphorylation site(s). |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-32744 |
Thr200 |
LPLLVQRtIARTIVL |
Neovison vison |
|
| pmid |
sentence |
| 7774578 |
The tgf-beta type ii receptor (t beta r-ii) is a transmembrane serine/threonine kinase that, upon ligand binding, recruits and phosphorylates a second transmembrane kinase, t beta r-i, as a requirement for signal transduction. In contrast to the relatively innocuous nature of single site mutations in the ttsgsgsg sequence, mutation of thr200 or 204 to valine causes marked losses in ligand-induced phosphorylation and signaling. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-32748 |
Thr204 |
VQRTIARtIVLQESI |
Neovison vison |
|
| pmid |
sentence |
| 7774578 |
The TGF-beta type II receptor (T beta R-II) is a transmembrane serine/threonine kinase that, upon ligand binding, recruits and phosphorylates a second transmembrane kinase, T beta R-I, as a requirement for signal transduction. In contrast to the relatively innocuous nature of single site mutations in the ttsgsgsg sequence, mutation of thr200 or 204 to valine causes marked losses in ligand-induced phosphorylation and signaling. |
|
| Publications: |
6 |
Organism: |
Homo Sapiens, In Vitro, Neovison Vison |
| Pathways: | COVID-19 Causal Network, Fibrosis, Hepatocellular Tumor, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV FIBROSIS, Thyroid cancer, TGF-beta Signaling, TGFb in cancer |
| + |
TGFBR1 | down-regulates 
phosphorylation
|
EEF1A1 |
0.346 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-167943 |
Ser300 |
EMHHEALsEALPGDN |
Homo sapiens |
|
| pmid |
sentence |
| 20832312 |
Phosphorylation of eEF1A1 at Ser300 by T_R-I results in inhibition of mRNA translation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TGFBR1 | up-regulates activity
phosphorylation
|
SMAD3 |
0.812 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235385 |
Ser423 |
SPSIRCSsVS |
Mus musculus |
Mv1Lu Cell, C2C12 Cell |
| pmid |
sentence |
| 19458083 |
A major event leading to smad3 activation is the tgf-beta-induced, tbetari-mediated phosphorylation at two c-terminal serine residues, ser-423 and ser-425, which triggers dissociation of smad3 from its receptors to form a complex with smad4 and accumulate in the nucleus |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235380 |
Ser425 |
SIRCSSVs |
Mus musculus |
Mv1Lu Cell, C2C12 Cell |
| pmid |
sentence |
| 19458083 |
A major event leading to Smad3 activation is the TGF-beta-induced, TbetaRI-mediated phosphorylation at two C-terminal serine residues, Ser-423 and Ser-425, which triggers dissociation of Smad3 from its receptors to form a complex with Smad4 and accumulate in the nucleus |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254361 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19701891 |
The binding of TGF‐β1 to its receptor complex activates the intracellular kinase domain of TGF‐βRII, which leads to the phosphorylation and activation of Smad2, Smad3 and Smad4 as well as non‐Smad proteins (Smad‐independent pathway) |
|
| Publications: |
3 |
Organism: |
Mus Musculus, Homo Sapiens |
| Pathways: | Adipogenesis, COVID-19 Causal Network, Colorectal Carcinoma, Fibrosis, Cell cycle: G1/S phase transition, Hepatocellular Tumor, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV FIBROSIS, TGF-beta Signaling, Thyroid Hormone Metabolism, TGFb in cancer |
| + |
TGFBR1 | up-regulates activity
phosphorylation
|
SMAD2 |
0.825 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236107 |
Ser465 |
SPSVRCSsMS |
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 9346908 |
Recently, it was demonstrated that Smad2 interacts transiently with and is a direct substrate of the transforming growth factor-_ (TGF-_) type I receptor, T_RI. Phosphorylation sites on smad2 were localized to a carboxyl-terminal fragment containing three serine residues at positions 464, 465, and 467. In this report, we show that T_RI specifically phosphorylates Smad2 on serines 465 and 467.These results indicate that receptor-dependent phosphorylation of Smad2 on serines 465 and 467 is required in mammalian cells to permit association with Smad4 and to propagate TGF-_ signals. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-235995 |
Ser467 |
SVRCSSMs |
Chlorocebus aethiops |
|
| pmid |
sentence |
| 9346908 |
Recently, it was demonstrated that Smad2 interacts transiently with and is a direct substrate of the transforming growth factor-beta (TGF-beta) type I receptor, TbetaRI. Phosphorylation sites on Smad2 were localized to a carboxyl-terminal fragment containing three serine residues at positions 464, 465, and 467. These results indicate that receptor-dependent phosphorylation of Smad2 on serines 465 and 467 is required in mammalian cells to permit association with Smad4 and to propagate TGF-_ signals. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249549 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 10973958 |
The pathway restricted (r)Smads (e.g. Smad1, 2, 3, and 5) are serine/threonine kinase activated proteins that interact in an unphosphorylated state with a TGF-b superfamily receptor. Upon ligand binding they are phosphorylated by the receptor and released. |
|
| Publications: |
3 |
Organism: |
Chlorocebus Aethiops, Homo Sapiens |
| Pathways: | Hepatocellular Tumor, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer |
| + |
PPP2R5A | up-regulates
binding
|
TGFBR1 |
0.262 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-60743 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9774674 |
In this report, we show that another wd-40 repeat protein, the balpha subunit of protein phosphatase 2a, associates with the cytoplasmic domain of type i tgf-beta receptors..[..] Furthermore, balpha enhances the growth inhibition activity of tgf-beta in a receptor-dependent manner |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TGFBR1 | up-regulates activity
binding
|
TRAF6 |
0.43 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236119 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18758450 |
Here we report that the ubiquitin ligase (e3) traf6 interacts with a consensus motif present in tbetari. The tbetari-traf6 interaction is required for tgf-beta-induced autoubiquitylation of traf6 and subsequent activation of the tak1-p38/jnk pathway, which leads to apoptosis. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-241918 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 18922473 |
We report here that TRAF6 is specifically required for the Smad-independent activation of JNK and p38 and its carboxyl TRAF homology domain physically interacts with TGF-² receptors |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Tissue: |
HEK-293T Cell |
| Pathways: | COVID-19 Causal Network, P38 Signaling, SARS-CoV MAPK PERTURBATION, TGF-beta Signaling |
| + |
SMAD6 | down-regulates activity
binding
|
TGFBR1 |
0.739 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-64079 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9892110 |
SMAD6 functions as a negative regulator of the TGFB and BMP signaling pathways by interacting with other SMADs and/or TBRI. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-167160 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20663871 |
The inhibitory Smads (I-Smads), i.e. Smad6 and Smad7, are negative regulators of transforming growth factor-_ (TGF-_) family signaling. I-Smads inhibit TGF-_ family signaling principally through physical interaction with type I receptors (activin receptor-like kinases), so as to compete with receptor-regulated Smads (R-Smads) for activation. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
TGFBR1 | up-regulates activity
|
RHOA |
0.638 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-227499 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19726546 |
Thus, TGF-_1 rapidly stimulates activity of both RhoA and Rac1 and this activation requires ALK5/T_RI kinase activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PPP1CC | down-regulates
dephosphorylation
|
TGFBR1 |
0.465 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-121277 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14718519 |
We found smad7 interacts with growth arrest and dna damage protein, gadd34, a regulatory subunit of the protein phosphatase 1 (pp1) holoenzyme, which subsequently recruits catalytic subunit of pp1 (pp1c) to dephosphorylate t?RI. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network |
| + |
PPP2R2A | up-regulates
binding
|
TGFBR1 |
0.532 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-227517 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9774674 |
In this report, we show that another WD-40 repeat protein, the B_ subunit of protein phosphatase 2A, associates with the cytoplasmic domain of type I TGF-_ receptors. [...] We therefore conclude that B_ specifically and directly associates with the type I receptor cytoplasmic domain in vitro. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
UCHL5 | up-regulates quantity by stabilization
binding
|
TGFBR1 |
0.502 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-150135 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17052192 |
Smad7 can act as an adaptor able to recruit uch37 to the type i tgf-beta receptor. Consequently, uch37 dramatically up-regulates tgf-beta-dependent gene expression by de-ubiquitinating and stabilizing the type i tgf-beta receptor. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TGFBR1 | up-regulates activity
|
RAC1 |
0.281 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-227496 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19726546 |
Thus, TGF-_1 rapidly stimulates activity of both RhoA and Rac1 and this activation requires ALK5/T_RI kinase activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMURF2 | down-regulates quantity by destabilization
polyubiquitination
|
TGFBR1 |
0.708 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272938 |
|
|
Chlorocebus aethiops |
COS-1 Cell |
| pmid |
sentence |
| 11163210 |
Smad7 Recruits Smurf2 to the TGFβ Receptor Complex. Here, we identify Smurf2, a C2-WW-HECT domain ubiquitin ligase and show that Smurf2 associates constitutively with Smad7. Smurf2 is nuclear, but binding to Smad7 induces export and recruitment to the activated TGF beta receptor, where it causes degradation of receptors and Smad7 via proteasomal and lysosomal pathways. |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
TGFBR1 | up-regulates activity
binding
|
ZFYVE9 |
0.629 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-62868 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9865696 |
Sara functions to recruit smad2 to the tgfbeta receptor by controlling the subcellular localization of smad2 and by interacting with the tgfbeta receptor complex |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
TGFBR1 | up-regulates
phosphorylation
|
SHC1 |
0.545 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-227503 |
|
|
Mus musculus |
Swiss-3T3 Cell |
| pmid |
sentence |
| 17673906 |
We now report that upon TGF-_ stimulation, T_RI phosphorylates ShcA on serine and, to a lesser degree, on tyrosine to activate Erk MAP kinases. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Thyroid cancer |
| + |
6-[2-tert-butyl-5-(6-methyl-2-pyridinyl)-1H-imidazol-4-yl]quinoxaline | down-regulates
chemical inhibition
|
TGFBR1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206715 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TGFBR1 | up-regulates
binding
|
PIK3R1 |
0.382 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-227525 |
|
|
Homo sapiens |
Respiratory Smooth Muscle |
| pmid |
sentence |
| 9435577 |
These studies revealed that PI 3-kinase is associated in vivo with both TGF-_ receptor subtypes and that TGF-_1 stimulation enhances PI 3-kinase activity associated with type I TGF-_ receptor in hASM cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
452342-67-5 | down-regulates
chemical inhibition
|
TGFBR1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-193018 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-159863 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18075500 |
Gw788388 is a new tgf-beta type i receptor inhibitor with a much improved pharmacokinetic profile compared with sb431542. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Tissue: |
Kidney |
| + |
SB 431542 | down-regulates
chemical inhibition
|
TGFBR1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206706 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TGFBR1 | up-regulates activity
binding
|
VPS39 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261375 |
|
|
Chlorocebus aethiops |
|
| pmid |
sentence |
| 12941698 |
TLP interacts with TGF-β and activin receptors in vivo. Endogenous TLP associates with both active and kinase-deficient TGF-beta and activin type II receptors, but interacts with the common-mediator Smad4 only in the presence of TGF-beta/activin signaling. |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
SMURF1 | down-regulates quantity by destabilization
polyubiquitination
|
TGFBR1 |
0.692 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272943 |
|
|
Chlorocebus aethiops |
COS-7 Cell |
| pmid |
sentence |
| 11278251 |
Here we show that Smurf1, an E3 ubiquitin ligase for bone morphogenetic protein-specific Smads, also interacts with Smad7 and induces Smad7 ubiquitination and translocation into the cytoplasm. In addition, Smurf1 associates with TbetaR-I via Smad7, with subsequent enhancement of turnover of TbetaR-I and Smad7. |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
TGFBR1 | up-regulates
binding
|
PI3K |
0.349 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252730 |
|
|
Homo sapiens |
Respiratory Smooth Muscle |
| pmid |
sentence |
| 9435577 |
These studies revealed that PI 3-kinase is associated in vivo with both TGF-_ receptor subtypes and that TGF-_1 stimulation enhances PI 3-kinase activity associated with type I TGF-_ receptor in hASM cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA), Thyroid Hormone Metabolism |
| + |
TGFB1 | up-regulates activity
binding
|
TGFBR1 |
0.845 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249548 |
|
|
Homo sapiens |
|
| 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-255960 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22326956 |
In Tgfbr2fl/fl control MEPM cells, radioactive TGF-β2 ligands (12.5 kDa) bind to TβRI (53 kDa), TβRII (70 kDa), and TβRIII (100–200 kDa, highly glycosylated molecule) and form the ligand-receptor complexes of TβRI::TGF-β2 (65.5 kDa), TβRII::TGF-β2 (82.5 kDa), and TβRIII::TGF-β2 (112.5–212.5 kDa) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-196022 |
|
|
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: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | Adipogenesis, COVID-19 Causal Network, Colorectal Carcinoma, Cell cycle: G1/S phase transition, P38 Signaling, SARS-CoV MAPK PERTURBATION, Thyroid cancer, TGF-beta Signaling, Thyroid Hormone Metabolism, TGFb in cancer |
| + |
WWP1 | down-regulates
ubiquitination
|
TGFBR1 |
0.53 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-126581 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15221015 |
Similar to smurfs, wwp1 associated with smad7 and induced its nuclear export, and enhanced binding of smad7 to tgf-beta type i receptor to cause ubiquitination and degradation of the receptor. Consistent with these results, wwp1 inhibited phosphorylation of smad2 induced by tgf-beta. Wwp1 thus negatively regulates tgf-beta signaling in cooperation with smad7 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMURF2 | down-regulates activity
ubiquitination
|
TGFBR1 |
0.708 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-153423 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17317136 |
Recruitment of ww and hect domain e3-ubiquitin ligases smurf1 and 2 to induce type i receptor ubiquitination and subsequent receptor degradation; |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-104999 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11163210 |
Smurf2 is nuclear, but binding to Smad7 induces export and recruitment to the activated TGF beta receptor, where it causes degradation of receptors and Smad7 via proteasomal and lysosomal pathways. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
DACT2 | down-regulates
binding
|
TGFBR1 |
0.394 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-151750 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17197390 |
Here, we provide evidence that unlike dpr1 that modulates wnt signaling, mdpr2 negatively regulates tgf-? Signaling and promotes tgf-? Receptor degradation in lysosomes. these results suggest that mdpr2 interferes with tgf-? By directly binding to and targeting the receptors for lysosomal inhibitor-sensitive degradation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TGFBR1 | up-regulates
binding
|
PIK3R2 |
0.343 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-227531 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9435577 |
These studies revealed that PI 3-kinase is associated in vivo with both TGF-_ receptor subtypes and that TGF-_1 stimulation enhances PI 3-kinase activity associated with type I TGF-_ receptor in hASM cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMAD7 | down-regulates activity
binding
|
TGFBR1 |
0.789 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260438 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30017632 |
Smad7 inhibits both transforming growth factor β (TGF-β)- and BMP-induced Smad signaling. Smad7 can use both surfaces in its interaction with the ALK-2, -3, and -4 receptors, but only the basic groove is used in the interaction between Smad7 and the TGF-β type I receptor (TβRI, also known as ALK-5). |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-64088 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9892110 |
SMAD7 functions as an antagonist to TGFB by binding to the TBRI and thus inhibiting activation of SMAD2 and SMAD3. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-167163 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20663871 |
The inhibitory Smads (I-Smads), i.e. Smad6 and Smad7, are negative regulators of transforming growth factor-_ (TGF-_) family signaling. I-Smads inhibit TGF-_ family signaling principally through physical interaction with type I receptors (activin receptor-like kinases), so as to compete with receptor-regulated Smads (R-Smads) for activation. |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS, TGF-beta Signaling |
| + |
TGFB2 | up-regulates
binding
|
TGFBR1 |
0.744 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-196025 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22326956 |
Tgf-? Signaling mediates a wide range of biological activities in development and disease. Tgf-? Ligands signal through heterodimeric type i and type ii receptors (tgf-? Receptor type i [t?RI, also known as alk5 and tgfbr1] and t?RII) that are members of the serine/threonine kinase family. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
TGFBR1 | up-regulates 
|
ERK1/2 |
0.314 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255033 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26194464 |
TbRI phosphorylates not only the C-termini of R-Smads but also activates various protein kinases including mitogen-activated protein kinases (MAPKs): extracellular signal regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 MAPK (p38), which then phosphorylate the variable linker regions of R-Smad |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Adipogenesis, COVID-19 Causal Network, Colorectal Carcinoma, Hepatocellular Tumor, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV MAPK PERTURBATION, Thyroid cancer |
| + |
SMURF | down-regulates activity
ubiquitination
|
TGFBR1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253264 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17317136 |
Recruitment of ww and hect domain e3-ubiquitin ligases smurf1 and 2 to induce type i receptor ubiquitination and subsequent receptor degradation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
FKBP1A | down-regulates activity
binding
|
TGFBR1 |
0.852 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-236142 |
|
|
Homo sapiens |
Mv1Lu Cell |
| pmid |
sentence |
| 8756725 |
Blocking fkbp12/type i receptor interaction with fk506 nonfunctional derivatives enhances the ligand activity, indicating that fkbp12 binding is inhibitory to the signaling pathways of the tgf beta family ligands |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
TGFBR1 | up-regulates
phosphorylation
|
SPTBN1 |
0.518 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-97626 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12543979 |
This suggests that, upon stimulation with tgf-beta1, phosphorylation of elf could induce a conformational change that reduces its affinity for ankyrin and tropomyosin and facilitates an association with smad3 and smad4 instead. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
TGFBR1 | up-regulates quantity by expression
transcriptional regulation
|
SERPINE1 |
0.436 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260590 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 28520219 |
The transforming growth factor-β pathway is the major driver of fibrotic response. Plasminogen activator inhibitor-1 (PAI-1) is a crucial downstream target of this pathway. Transforming growth factor-β positively regulates PAI-1 gene expression via two main pathways including Smad-mediated canonical and non-canonical pathways. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, SARS-CoV FIBROSIS |
| + |
TGFB1 | up-regulates
binding
|
TGFBR1 |
0.845 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255031 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26194464 |
TGF-b ligands bind to TGF-b type II receptor (TbRII), which transphosphorylates and activates TGF-b type I receptor (TbRI). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Adipogenesis, COVID-19 Causal Network, Colorectal Carcinoma, Cell cycle: G1/S phase transition, P38 Signaling, SARS-CoV MAPK PERTURBATION, Thyroid cancer, TGF-beta Signaling, Thyroid Hormone Metabolism, TGFb in cancer |
| + |
SB 505124 | down-regulates
chemical inhibition
|
TGFBR1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-122910 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14978253 |
Sb-505124 is a selective inhibitor of transforming growth factor-beta type i receptors alk4, alk5, and alk7. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-206742 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
SMURF1 | down-regulates activity
ubiquitination
|
TGFBR1 |
0.692 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-153414 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17317136 |
Recruitment of WW and HECT domain E3-ubiquitin ligases Smurf1 and 2 to induce type I receptor ubiquitination and subsequent receptor degradation; |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATP6V1H | up-regulates activity
binding
|
TGFBR1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266886 |
|
|
Mus musculus |
Bone Marrow Stromal Cell |
| pmid |
sentence |
| 29782852 |
ATP6V1H interacts with TGF-β receptor I and AP-2 complex to regulate the proliferation and differentiation of BMSCs. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
HSP90AA1 | up-regulates
binding
|
TGFBR1 |
0.416 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-179268 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18591668 |
The data in fig. 5 suggest that hsp90 specifically interacts with t?RI And t?RII In vitro and in vivo. Coupled with our data showing that loss of hsp90 function decreases t?R Levels and blocks tgf?-Induced smad2/3 activation and transcription, this result suggests that hsp90 controls tgf? Signaling as an essential component for stabilizing t?Rs. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
LY-2157299 | down-regulates
chemical inhibition
|
TGFBR1 |
0.8 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-159354 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18039567 |
Ly2157299, a new type i receptor tgf-beta kinase antagonist, was |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-193775 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| Other |
|
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
TGFBR2 | up-regulates
phosphorylation
|
TGFBR1 |
0.718 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255032 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26194464 |
TGF-b ligands bind to TGF-b type II receptor (TbRII), which transphosphorylates and activates TGF-b type I receptor (TbRI). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Fibrosis, Hepatocellular Tumor, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV FIBROSIS, Thyroid cancer, TGF-beta Signaling, TGFb in cancer |
3.0
TGFBR1
- 
- 