TGFBR1 Antibody | Affinity Biosciences

製品:	TGFBR1 Antibody
カタログ:	AF5347
タンパク質の説明:	Rabbit polyclonal antibody to TGFBR1
アプリケーション:	WB IHC IF/ICC
反応性:	Human, Mouse, Rat
予測:	Pig, Bovine, Sheep, Rabbit, Dog, Xenopus
分子量:	56 kDa.; 56kD(Calculated).
ユニプロット:	P36897
RRID:	AB_2837832

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サイズ	価格	在庫状況
100ul	$280	在庫あり
200ul	$350	在庫あり

プロトコル

製品説明

ソース:

Rabbit

アプリケーション:

WB 1:500-1:2000, IF/ICC 1:100-1:500, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

反応性:

Human,Mouse,Rat

予測:

Pig(100%), Bovine(100%), Sheep(100%), Rabbit(100%), Dog(100%), Xenopus(100%)

クローナリティ:

Polyclonal

特異性:

TGFBR1 Antibody detects endogenous levels of total TGFBR1.

RRID:

AB_2837832
引用形式: Affinity Biosciences Cat# AF5347, RRID:AB_2837832.

コンジュゲート:

Unconjugated.

精製:

The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).

保存:

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.

別名:

折りたたみ／展開

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;

免疫原

免疫原:

Uniprot:

P36897(TGFR1_HUMAN) >>Visit HPA database.

遺伝子(ID):

TGFBR1(7046)

発現特異性:

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).

タンパク質の説明:

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.

タンパク質配列:

P36897 TGFR1_HUMAN:
Protein BLAST With
NCBI/
ExPASy/
Uniprot

MEAAVAAPRPRLLLLVLAAAAAAAAALLPGATALQCFCHLCTKDNFTCVTDGLCFVSVTETTDKVIHNSMCIAEIDLIPRDRPFVCAPSSKTGSVTTTYCCNQDHCNKIELPTTVKSSPGLGPVELAAVIAGPVCFVCISLMLMVYICHNRTVIHHRVPNEEDPSLDRPFISEGTTLKDLIYDMTTSGSGSGLPLLVQRTIARTIVLQESIGKGRFGEVWRGKWRGEEVAVKIFSSREERSWFREAEIYQTVMLRHENILGFIAADNKDNGTWTQLWLVSDYHEHGSLFDYLNRYTVTVEGMIKLALSTASGLAHLHMEIVGTQGKPAIAHRDLKSKNILVKKNGTCCIADLGLAVRHDSATDTIDIAPNHRVGTKRYMAPEVLDDSINMKHFESFKRADIYAMGLVFWEIARRCSIGGIHEDYQLPYYDLVPSDPSVEEMRKVVCEQKLRPNIPNRWQSCEALRVMAKIMRECWYANGAARLTALRIKKTLSQLSQQEGIKM

種類予測

種類予測:

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

Zebrafish

Chicken

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P36897 基板として

P36897

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

PTMs - P36897 酵素として

P36897

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

研究背景

P36897_TGFR1_HUMAN

機能:

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.

細胞の位置付け:

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

組織特異性:

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

サブユニット構造:

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.

タンパク質ファミリー:

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

研究領域

· 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.

参考文献

1). Double-Layer Nanofibrous Sponge Tube via Electrospun Fiber and Yarn for Promoting Urethral Regeneration. Advanced Fiber Materials, 2023 [IF=16.1]

2). Beauvericin suppresses the proliferation and pulmonary metastasis of osteosarcoma by selectively inhibiting TGFBR2 pathway. International Journal of Biological Sciences, 2023 (PubMed: 37781043) [IF=9.2]

Application: WB Species: Mouse Sample: OS cells

Figure 2 BEA inhibits the TGF-β/Smad2/3 signaling pathway in OS cells. (A) KEGG pathway enrichment analysis in BEA-treated and untreated 143B cells. (B) The effect of BEA on the TGF-β1-induced phosphorylation of Smad2/3, TGFBR1, and TGFBR2 in OS cells was evaluated by Western blotting. (C) Cellular immunofluorescence assay was performed to assess the nuclear translocation of p-Smad2/3 in OS cells treated with BEA. Scale bar: 20 μm. (D) The transcriptional activity of Smad2/3 in OS cells treated as indicated was determined by a Smad2/3 luciferase reporter assay. (E) 143B and U2OS cells were treated with BEA (2 μM) for 24 h and total RNA was harvested and analyzed by qPCR. Quantification of the mRNA levels of COL1A1, COL3A1, COL6A1, COL10A1, MMP2, LOX, LOXL2 in OS cells.

3). Loss of Smooth Muscle Tenascin-X Inhibits Vascular Remodeling Through Increased TGF-β Signaling. Arteriosclerosis, thrombosis, and vascular biology, 2024 (PubMed: 38934115) [IF=8.7]

Application: IHC Species: Mouse Sample:

Figure 5. TGF-β (transforming growth factor-β) signaling is responsible for the effect of smooth muscle TN-X (tenascin-X) deficiency after carotid artery ligation. A, Experimental design of carotid artery ligation combined with control IgG or anti-TGF-β antibody treatment. B, Representative images of carotid arteries from SMC-Tnxb-KO mice after treatment with control IgG or anti-TGF-β antibodies and carotid artery ligation stained with elastic stain. The bar diagram shows the neointima areas in sections at the indicated distances from the ligation site (n=6 animals per group). C through F, Comparative analysis of control, SMC-Tnxb-KO, and SMC-Tnxb/Tgfbr1/Tgfbr2-KO mice 7 days after carotid artery ligation. Shown are representative images of the immunostained vessels (C), the αSMA (α-smooth muscle actin) staining intensity normalized to carotid media area (D), and the percentage of phospho-SMAD2 (SMAD family member 2)–positive area in carotid media area (E). F, The bar diagrams show levels of Myh11, Acta2, and Tagln mRNA in the media of ligated carotid arteries as analyzed by quantitative real-time polymerase chain reaction (n=6 animals per group; at least 3 sections were analyzed per animal). G and H, Representative images of carotid arteries from control, SMC-Tnxb-KO, or SMC-Tnxb/Tgfbr1/Tgfbr2-KO mice 4 weeks after ligation. Shown are representative images of the unligated and ligated carotid arteries. The bar diagram shows the statistical analysis of the neointima area at different distances from the ligation site (n=6 animals per group). Bar lengths: 100 µm (B and G) and 50 µm (C). Shown are mean±SEM values (unpaired Student t test [B and F], 1-way ANOVA and Bonferroni post hoc test [D, E, and H]).

4). Ethyl ferulate suppresses post-myocardial infarction myocardial fibrosis by inhibiting transforming growth factor receptor 1. Phytomedicine, 2023 (PubMed: 37801895) [IF=7.9]

5). Myricetin suppresses the proliferation and migration of vascular smooth muscle cells and inhibits neointimal hyperplasia via suppressing TGFBR1 signaling pathways. PHYTOMEDICINE, 2021 (PubMed: 34500301) [IF=7.9]

Application: WB Species: Sample: VSMCs

Fig. 5.| Adenovirus-mediated TGFBR1 overexpression partially reverses the suppressive impact of myricetin on the activation of TGFBR1 signaling. (A) Forty-eight hours post-infection with negative control Ad-GFP or Ad-TGFBR1, VSMCs were treated with myricetin (60 μM) for 24 h, and western blotting was used to assess pTGFBR1, TGFBR1 and its downstream molecules p-samd3, Smad3, p-Smad2 and Smad2 expression.

Application: WB Species: Human Sample: VSMCs

Fig. 4. Myricetin suppresses TGFBR1 signaling pathway activation. (A) Western blotting was used to assess p-TGFBR1, TGFBR1 and its downstream molecules psamd3, Smad3, p-Smad2 and Smad2 expression in cells treated with different doses of myricetin for 24 h. (B-G) The densitometry analysis and quantitative results of (A) (n = 3). Results are shown as mean ± standard deviation (SD). * p < 0.05, ** p < 0.01 compared with the control group.

6). Caffeic acid mitigates myocardial fibrosis and improves heart function in post-myocardial infarction by inhibiting transforming growth factor-β receptor 1 signaling pathways. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2024 (PubMed: 38906025) [IF=7.5]

7). miR-770–5p inhibits the activation of pulmonary fibroblasts and silica-induced pulmonary fibrosis through targeting TGFBR1. ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY, 2021 (PubMed: 34082245) [IF=6.8]

Application: IF/ICC Species: Human Sample: MRC-5 cells

Fig. 4. TGFBR1 was a direct target of miR-770–5p. (A) The position of the miR-770–5p target site in the TGFBR1 3’ UTR; Binding sequences between miR-770–5p and 3’UTR of TGFBR1 were highlighted. (B-C) The dual-luciferase reporter assay was performed to identify the binding between TGFBR1 mRNA and miR-770–5p in MRC-5 and HEK293T cells. Luciferase activities were calculated as the ratio of firefly/renilla activities and normalized to the TGFBR1-WT + miR-NC group. (D) qRTPCR analysis of TGFBR1 mRNA expression in MRC-5 cells in MRC-5 transfected with 30 nM of miR-NC or miR-770–5p mimic before treated with 5 ng/mL of TGF-β1 for 48 h. (E) Immunofluorescence analysis of TGFBR1 in MRC-5 cells transfected with 30 nM of miR-NC or miR-770–5p mimic before treated with 5 ng/mL of TGF-β1 for 48 h; Red represents TGFBR1 staining; Blue represents nuclear DNA staining by DAPI; Bars = 25 µm. (F) Western blot analysis of TGFBR1 expression in MRC-5 transfected with 30 nM of miR-NC or miR-770–5p mimic before treated with 5 ng/mL of TGF-β1 for 48 h. (G) qRT-PCR analysis of TGFBR1 mRNA expression in lung tissues of mice exposed to silica. (H) qRT-PCR analysis of TGFBR1 mRNA expression in lung tissues of silicosis patients. All the data are expressed as the means ± SD of at least 3 independent experiments. *P < 0.05 vs. the control/normal group; #P < 0.05 vs. The TGF-β1 plus miR-NC group.

8). 20(S)-ginsenoside Rg3 exerts anti-fibrotic effect after myocardial infarction by alleviation of fibroblasts proliferation and collagen deposition through TGFBR1 signaling pathways. Journal of Ginseng Research, 2023 [IF=6.3]

Application: WB Species: Mouse Sample: CFs

Fig. 6. TGFBR1 overexpression partly abolishes Rg3's inhibition on CFs growth, collagen synthesis, together with Smads activation. (A) CFs were infected with recombinant adenovirus for 48 h, and later stimulated by TGF-β1 (10 ng/ml) and Rg3 (20 μM), and Edu assay was performed to detect CFs proliferation (magnification, 200 × ). Red and blue fluorescence indicate proliferating cells as well as nuclei, separately. (B) Edu-positive cell proportion. (C) Expression of proliferation and collagen-related proteins in CFs following Ad-TGFBR1 or control adenovirus transfection. (D) Protein expression of TGFBR1 signaling in CFs after transfection. Relative PCNA (E), CDK6 (F), Cyclin D1 (G), collagen I (H), collagen III (I), p-TGFBR1 (J), p-Smad2 (K), and p-Smad3 (L) expression. Data are represented by mean ± SD for at least 3 groups. ∗p < 0.05, ∗∗p < 0.01. n.s, not significant.

9). Corilagin alleviates hypertrophic scars via inhibiting the transforming growth factor (TGF)-β/Smad signal pathway. LIFE SCIENCES, 2021 (PubMed: 33862115) [IF=6.1]

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.)

Application: WB Species: human Sample: HSFs

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.

10). LncRNAH19 acts as a ceRNA of let-7 g to facilitate endothelial-to-mesenchymal transition in hypoxic pulmonary hypertension via regulating TGF-β signalling pathway. Respiratory research, 2024 (PubMed: 38987833) [IF=5.8]

Application: WB Species: Rat Sample:

Fig. 6 H19 deficiency regulated EndMT of PAECs via the let-7 g/TGFβ signalling. (A) The expression level of let-7 g in PAECs ;(B) Immunofluorescence double staining of CD31 and α-SMA in RPAECs treated with let-7 g mimic; (C) Immunofluorescence double staining of CD31 and α-SMA in RPAECs treated with let-7 g inhibitor; (D) the potential binding sites of let-7 g to TGFβR1 predicted by Targetscan 7.0 and quantification of the fluorescence intensity in HEK293T cells; (E-F) After transfection of let-7 g mimic or inhibitor, the expression level of TGFβR1 protein in HPAECs; (G) Transfection of after transfection of TGFβR1-Si, the expression levels of CD31, Vimentin and α-SMA were detected by Western blot

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TGFBR1 Antibody - #AF5347

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