Product: TGFBR1 Antibody
Catalog: AF5347
Source: Rabbit
Application: WB, IHC, IF/ICC, ELISA(peptide)
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Sheep, Rabbit, Dog, Xenopus
Mol.Wt.: 56 kD.; 56kD(Calculated).
Uniprot: P36897
RRID: AB_2837832

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IF/ICC 1:100-1:500, IHC 1:50-1:200, ELISA(peptide) 1:20000-1:40000
*The optimal dilutions should be determined by the end user.
Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Sheep(100%), Rabbit(100%), Dog(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
TGFBR1 Antibody detects endogenous levels of total TGFBR1.
RRID:
AB_2837832
Cite Format: Affinity Biosciences Cat# AF5347, RRID:AB_2837832.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

AAT 5; AAT5; Activin A receptor type II like kinase 53kDa; Activin A receptor type II like kinase, 53kD; Activin A receptor type II like protein kinase of 53kD; activin A receptor type II-like kinase, 53kDa; activin A receptor type II-like protein kinase of 53kD; Activin receptor like kinase 5; Activin receptor-like kinase 5; ACVRLK 4; ACVRLK4; ALK 5; ALK-5; ALK5; LDS1A; LDS2A; MSSE; Serine/threonine protein kinase receptor R4; Serine/threonine-protein kinase receptor R4; SKR 4; SKR4; TbetaR I; TbetaR-I; TGF beta receptor type 1; TGF beta receptor type I; TGF beta type I receptor; TGF-beta receptor type I; TGF-beta receptor type-1; TGF-beta type I receptor; TGFBR 1; TGFBR1; TGFBR1 protein; TGFR 1; TGFR-1; TGFR1; TGFR1_HUMAN; Transforming growth factor beta receptor 1; Transforming growth factor beta receptor I (activin A receptor type II like kinase, 53kD); Transforming growth factor beta receptor I; transforming growth factor, beta receptor 1; transforming growth factor, beta receptor I (activin A receptor type II-like kinase, 53kD); Transforming growth factor-beta receptor type I;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
P36897 TGFR1_HUMAN:

Found in all tissues examined, most abundant in placenta and least abundant in brain and heart. Expressed in a variety of cancer cell lines (PubMed:25893292).

Description:
On ligand binding, forms a receptor complex consisting of two type II and two type I transmembrane serine/threonine kinases. Type II receptors phosphorylate and activate type I receptors which autophosphorylate, then bind and activate SMAD transcriptional regulators. Receptor for TGF-beta.
Sequence:
MEAAVAAPRPRLLLLVLAAAAAAAAALLPGATALQCFCHLCTKDNFTCVTDGLCFVSVTETTDKVIHNSMCIAEIDLIPRDRPFVCAPSSKTGSVTTTYCCNQDHCNKIELPTTVKSSPGLGPVELAAVIAGPVCFVCISLMLMVYICHNRTVIHHRVPNEEDPSLDRPFISEGTTLKDLIYDMTTSGSGSGLPLLVQRTIARTIVLQESIGKGRFGEVWRGKWRGEEVAVKIFSSREERSWFREAEIYQTVMLRHENILGFIAADNKDNGTWTQLWLVSDYHEHGSLFDYLNRYTVTVEGMIKLALSTASGLAHLHMEIVGTQGKPAIAHRDLKSKNILVKKNGTCCIADLGLAVRHDSATDTIDIAPNHRVGTKRYMAPEVLDDSINMKHFESFKRADIYAMGLVFWEIARRCSIGGIHEDYQLPYYDLVPSDPSVEEMRKVVCEQKLRPNIPNRWQSCEALRVMAKIMRECWYANGAARLTALRIKKTLSQLSQQEGIKM

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Bovine
100
Sheep
100
Dog
100
Xenopus
100
Rabbit
100
Horse
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P36897 As Substrate

Site PTM Type Enzyme
Ubiquitination
S165 Phosphorylation P37173 (TGFBR2)
S172 Phosphorylation P37173 (TGFBR2)
T176 Phosphorylation P37173 (TGFBR2)
K178 Ubiquitination
T185 Phosphorylation P37173 (TGFBR2)
T186 Phosphorylation P37173 (TGFBR2)
S187 Phosphorylation P37173 (TGFBR2)
S189 Phosphorylation P37173 (TGFBR2)
S191 Phosphorylation P37173 (TGFBR2)
T200 Phosphorylation P17252 (PRKCA)
T204 Phosphorylation
S210 Phosphorylation
T298 Phosphorylation
K337 Ubiquitination
K391 Ubiquitination
K449 Ubiquitination
K490 Ubiquitination
K502 Ubiquitination

PTMs - P36897 As Enzyme

Substrate Site Source
P17813 (ENG) S646 Uniprot
P17813 (ENG) S649 Uniprot
P68104 (EEF1A1) S300 Uniprot
P84022 (SMAD3) S422 Uniprot
P84022 (SMAD3) S423 Uniprot
P84022 (SMAD3) S425 Uniprot
Q03167 (TGFBR3) S831 Uniprot
Q15796 (SMAD2) S464 Uniprot
Q15796 (SMAD2) S465 Uniprot
Q15796 (SMAD2) S467 Uniprot
Q15797-1 (SMAD1) S462 Uniprot
Q15797-1 (SMAD1) S463 Uniprot
Q15797-1 (SMAD1) S465 Uniprot
Q96FW1 (OTUB1) S18 Uniprot
Q9H3D4-2 (TP63) S66 Uniprot
Q9H3D4 (TP63) S68 Uniprot
Q9H3D4 (TP63) S160 Uniprot

Research Backgrounds

Function:

Transmembrane serine/threonine kinase forming with the TGF-beta type II serine/threonine kinase receptor, TGFBR2, the non-promiscuous receptor for the TGF-beta cytokines TGFB1, TGFB2 and TGFB3. Transduces the TGFB1, TGFB2 and TGFB3 signal from the cell surface to the cytoplasm and is thus regulating a plethora of physiological and pathological processes including cell cycle arrest in epithelial and hematopoietic cells, control of mesenchymal cell proliferation and differentiation, wound healing, extracellular matrix production, immunosuppression and carcinogenesis. The formation of the receptor complex composed of 2 TGFBR1 and 2 TGFBR2 molecules symmetrically bound to the cytokine dimer results in the phosphorylation and the activation of TGFBR1 by the constitutively active TGFBR2. Activated TGFBR1 phosphorylates SMAD2 which dissociates from the receptor and interacts with SMAD4. The SMAD2-SMAD4 complex is subsequently translocated to the nucleus where it modulates the transcription of the TGF-beta-regulated genes. This constitutes the canonical SMAD-dependent TGF-beta signaling cascade. Also involved in non-canonical, SMAD-independent TGF-beta signaling pathways. For instance, TGFBR1 induces TRAF6 autoubiquitination which in turn results in MAP3K7 ubiquitination and activation to trigger apoptosis. Also regulates epithelial to mesenchymal transition through a SMAD-independent signaling pathway through PARD6A phosphorylation and activation.

PTMs:

Phosphorylated at basal levels in the absence of ligand. Activated upon phosphorylation by TGFBR2, mainly in the GS domain. Phosphorylation in the GS domain abrogates FKBP1A-binding.

N-Glycosylated.

Ubiquitinated; undergoes ubiquitination catalyzed by several E3 ubiquitin ligases including SMURF1, SMURF2 and NEDD4L2. Results in the proteasomal and/or lysosomal degradation of the receptor thereby negatively regulating its activity. Deubiquitinated by USP15, leading to stabilization of the protein and enhanced TGF-beta signal. Its ubiquitination and proteasome-mediated degradation is negatively regulated by SDCBP.

Subcellular Location:

Cell membrane>Single-pass type I membrane protein. Cell junction>Tight junction. Cell surface. Membrane raft.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Found in all tissues examined, most abundant in placenta and least abundant in brain and heart. Expressed in a variety of cancer cell lines.

Subunit Structure:

Homodimer; in the endoplasmic reticulum but also at the cell membrane. Heterohexamer; TGFB1, TGFB2 and TGFB3 homodimeric ligands assemble a functional receptor composed of two TGFBR1 and TGFBR2 heterodimers to form a ligand-receptor heterohexamer. The respective affinity of TGBRB1 and TGFBR2 for the ligands may modulate the kinetics of assembly of the receptor and may explain the different biological activities of TGFB1, TGFB2 and TGFB3. Interacts with CD109; inhibits TGF-beta receptor activation in keratinocytes. Interacts with RBPMS. Interacts (unphosphorylated) with FKBP1A; prevents TGFBR1 phosphorylation by TGFBR2 and stabilizes it in the inactive conformation. Interacts with SMAD2, SMAD3 and ZFYVE9; ZFYVE9 recruits SMAD2 and SMAD3 to the TGF-beta receptor. Interacts with TRAF6 and MAP3K7; induces MAP3K7 activation by TRAF6. Interacts with PARD6A; involved in TGF-beta induced epithelial to mesenchymal transition. Interacts with SMAD7, NEDD4L, SMURF1 and SMURF2; SMAD7 recruits NEDD4L, SMURF1 and SMURF2 to the TGF-beta receptor. Interacts with USP15 and VPS39. Interacts with SDCBP (via C-terminus) Interacts with CAV1 and this interaction is impaired in the presence of SDCBP. Interacts with APPL1; interaction is TGF beta dependent; mediates trafficking of the TGFBR1 from the endosomes to the nucleus via microtubules in a TRAF6-dependent manner.

Family&Domains:

Belongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family. TGFB receptor subfamily.

Research Fields

· Cellular Processes > Transport and catabolism > Endocytosis.   (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Adherens junction.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Environmental Information Processing > Signal transduction > FoxO signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TGF-beta signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Apelin signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Hippo signaling pathway.   (View pathway)

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Colorectal cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Pancreatic cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Gastric cancer.   (View pathway)

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

References

1). Liu H et al. Enhancer of zeste homolog 2 modulates oxidative stress-mediated pyroptosis in vitro and in a mouse kidney ischemia-reperfusion injury model. FASEB J 2020 Jan;34(1):835-852 (PubMed: 31914694) [IF=4.966]

Application: WB    Species: human    Sample: HK-2 cells

FIGURE 7|EZH2 regulated Nox4 expression via the ALK5/Smad2/Smad3 pathway. D-G, HK-2 cells were transfected with an siRNA against EZH2 or a negative control siRNA (si-NC) for 48 h before being exposed to H/R. D-F, Western blot analysis for the protein expression of ALK5, Smad2, Smad3, p-Smad2, and Smad3 in the indicated groups and quantitative analysis of ALK5, p-Smad2, and p-Smad3, n = 3.

2). Feng F et al. TIPE2 suppresses malignancy of pancreatic cancer through inhibiting TGFβ1 mediated signaling pathway. Front Oncol 2021 Jun 23;11:680985. (PubMed: 34249724) [IF=4.848]

3). Li Y et al. Transforming Growth Factor-β3 Chitosan Sponge (TGF-β3/CS) Facilitates Osteogenic Differentiation of Human Periodontal Ligament Stem Cells. Int J Mol Sci 2019 Oct 9;20(20):4982. (PubMed: 31600954) [IF=4.556]

Application: WB    Species: human    Sample: hPDLSCs

Figure 6. |Mechanism of TGF-β3 in osteogenic differentiation of hPDLSCs based on this study. (A)Schematic representation of the mechanism of TGF-β3 in osteogenic differentiation of hPDLSCs. (B)After osteogenic induction of hPDLSCs with various concentrations of TGF-β3 for 7 and 14 d,expression of osteogenic pathway proteins was detected by (B) western blotting and analyzed by grayscale scanning for (C) TGF-βRI, (D) TGF-βRII, (E) t-p38, (F) Pp38, and (G) Runx2 (n = 3). ns means no significant differences, p >0.05 vs. control; *** p < 0.001 vs. control. Abbreviations: TGF-βRI,transforming growth factor-β receptor I; TGF-βRII, transforming growth factor-β receptor II; t-p38,total p38; Pp38, phosphorylated p38; Runx2, runt-related transcription factor 2.

4). Chen G et al. Myricetin suppresses the proliferation and migration of vascular smooth muscle cells and inhibits neointimal hyperplasia via suppressing TGFBR1 signaling pathways. Phytomedicine 2021 Nov;92:153719. (PubMed: 34500301) [IF=4.268]

5). Rana MN et al. PDE9 Inhibitor PF-04447943 Attenuates DSS-Induced Colitis by Suppressing Oxidative Stress, Inflammation, and Regulating T-Cell Polarization. Front Pharmacol 2021 Apr 8;12:643215. (PubMed: 33967779) [IF=4.225]

6). Chen S et al. miR-96-5p regulated TGF-β/SMAD signaling pathway and suppressed endometrial cell viability and migration via targeting TGFBR1. Cell Cycle 2020 Jul;19(14):1740-1753. (PubMed: 32635855) [IF=3.699]

Application: WB    Species: human    Sample: endometrial

Figure 1.| Down-regulation of miR-96-5p and up-regulation of TGFBR1 in ectopic endometrial tissue.(e) Western blot showed protein expression of TGFBR1 and SMAD3 was upregulated in ectopic endometrial tissue (*, P < 0.05).

7). Tan Z et al. Taohong siwu decoction attenuates myocardial fibrosis by inhibiting fibrosis proliferation and collagen deposition via TGFBR1 signaling pathway. J Ethnopharmacol 2021 Jan 16;270:113838. (PubMed: 33460756) [IF=3.690]

Application: WB    Species: mice    Sample: cardiac fibroblasts

Fig. 6. THSWD suppresses expression of collagen and activation of the TGFBR1 signaling pathway. (A, B) CFs were incubated without or with TGF-β1 (10 ng/ml) and THSWD (15, 30 and 60 μg/ml) for 24 h, and the expression levels of collagen I, collagen III, collagen V, phospho-TGFBR1, TGFBR1, phospho-Smad2, Smad2, phospho-Smad3 and Smad3 were tested by western blotting. (C–E) Expression levels of collagen I, collagen III and collagen V were normalized with GAPDH (n = 3). (F–H) Expression levels of phospho-TGFBR1, phospho-Smad2, and phospho-Smad3 were normalized to that of TGFBR1, Smad2 and Smad3 proteins, respectively (n = 3). Data were shown as mean ± SD. #P < 0.05, vs. control group. *P < 0.05, **P < 0.01, vs. model group.

Application: IHC    Species: mice    Sample: heart tissues

Fig. 4. IHC analysis of TGFBR1 signaling pathway related-protein expression in heart tissues. (A) IHC showed inhibition of TGFBR1, Smad3, collagen I, collagen III and α-SMA in THSWD-treated mouse heart tissues compared with the model group. (B–F) Quantitative analysis for IHC staining of TGFBR1, Smad3, collagen I, collagen III and α-SMA. Data were shown as mean ± SD. **P < 0.01, vs. model group.

8). Li Y et al. Corilagin alleviates hypertrophic scars via inhibiting the transforming growth factor (TGF)-β/Smad signal pathway. Life Sci 2021 Apr 13;119483. (PubMed: 33862115) [IF=3.647]

Application: WB    Species: Human    Sample: Hypertrophic scar tissue

Fig. 5. Corilagin inhibited the protein levels of TGF-β1, TGFβRI and blocked the phosphorylation of Smad2 and Smad3, as well as affect the protein levels of MMPs and TIMPs. A. Western blot results showed the protein levels of TGF-β1, TGFβRI, and TGFβRII in HSFs incubated with corilagin for 3 days, GAPDH served as control. n = 3. B. Protein levels of phosphorylated and total Smad2 and Smad3 examined by western blot assay after HSFs were treated with corilagin for 3 days. GAPDH served as control. n = 3. C. Immunofluorescence staining of Smad2/3 in HSFs after treating with corilagin (0 μM) + TGF-β1 (0 ng/mL), corilagin (0 μM) + TGF-β1 (5 ng/mL) and corilagin (25 μM) + TGF-β1 (5 ng/mL) for 12 h. Smad2/3 is shown by green fluorescence and nuclei were stained with DAPI, which emits blue fluorescence. Scale bars = 50 μm. D. Protein levels of Smad7 examined by western blot assay after HSFs were treated with corilagin for 3 days. GAPDH served as control. n = 3. E. Protein levels of MMP2, MMP9, MMP13 and TIMP1 in HSFs after treatment with corilagin for 3 days. GAPDH served as control. n = 3. Data are show as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

9). Liu S et al. Sphingomyelin synthase 1 regulates the epithelial‑to‑mesenchymal transition mediated by the TGF‑β/Smad pathway in MDA‑MB‑231 cells. Mol Med Rep 2018 Dec 4 (PubMed: 30535436)

Application: IF/ICC    Species: human    Sample: MDA?MB?231 cells

Figure 3. |Overexpression of SMS1 inhibits TGF?β1?induced EMT. (A) Expression of SMS1 and of (B) E?cadherin and Vimentin were measured by western blotting in MDA?MB?231 cells. (C) Immunofluorescence staining of E?cadherin and of (D) Vimentin by a fluorescence microscope in MDA?MB?231 cells. Magnification, x20. Data are presented as the mean ± standard deviation (n=3). *P<0.05, **P<0.01 vs. the control group; #P<0.05 vs. the TGF?β1 group. SMS, sphingomyelin synthase 1; TGF, transforming growth factor.

Application: WB    Species: human    Sample: MDA?MB?231 cells

Figure 4.| Overexpression of SMS1 regulates TGF?β1?induced EMT via TGF?β type I receptors. (A)?Expression of TβRI and (B)?phosphorylation of Smad2 and Smad2 were measured by western blotting in MDA?MB?231 cells.

10). Wu Y et al. Hydroxypropyl‑β‑cyclodextrin attenuates the epithelial‑to‑mesenchymal transition via endoplasmic reticulum stress in MDA‑MB‑231 breast cancer cells. Mol Med Rep 2020 Jan;21(1):249-257. (PubMed: 31746388)

Application: WB    Species: human    Sample: MDA‑MB‑231 cells

Figure 2.| HP‑β‑CD can inhibit the TGF‑β/Smad signaling pathway by decreasing the expression of TGF‑β type I receptors while activating ER stress. MDA‑MB‑231 cells were treated with 5 mmol/l HP‑β‑CD then with or without 10 ng/ml TGF‑β1 for 48 h. Western blotting was used to measure (A) the relative expression of TGF‑β/Smad pathway‑related proteins (p‑Smad2 and Smad2) and (B) expression of TβRI.

Application: IF/ICC    Species: human    Sample: MDA‑MB‑231 cells

Figure 2. | HP‑β‑CD can inhibit the TGF‑β/Smad signaling pathway by decreasing the expression of TGF‑β type I receptors while activating ER stress. MDA‑MB‑231 cells were treated with 5 mmol/l HP‑β‑CD then with or without 10 ng/ml TGF‑β1 for 48 h. Western blotting was used to measure (A) the relative expression of TGF‑β/Smad pathway‑related proteins (p‑Smad2 and Smad2) and (B) expression of TβRI. (C) Confocal microscope image for immunofluorescence staining of TβRI.

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