TGFBR1 Antibody - #AF5347

>>买2送1 进行中>>
>>满百送 进行中>>
>>赠送JD卡 进行中>>
>>3倍积分 进行中>>
(28)   (51)  
产品: TGFBR1 抗体
货号: AF5347
描述: Rabbit polyclonal antibody to TGFBR1
应用: WB IHC IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Bovine, Sheep, Rabbit, Dog, Xenopus
分子量: 56 kDa.; 56kD(Calculated).
蛋白号: P36897
RRID: AB_2837832

浏览相似产品>>

   规格 价格 库存
 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

货期: 当天发货

联系销售
相关下载
MS Report
HPLC Report
MSDS
说明书
COA
实验方案
WB Handbook
IHC Protocol
IF/ICC Protocol

产品描述

来源:
Rabbit
应用:
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: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human,Mouse,Rat
预测:
Pig(100%), Bovine(100%), Sheep(100%), Rabbit(100%), Dog(100%), Xenopus(100%)
克隆:
Polyclonal
特异性:
TGFBR1 Antibody detects endogenous levels of total TGFBR1.
RRID:
AB_2837832
引用格式: Affinity Biosciences Cat# AF5347, RRID:AB_2837832.
偶联:
Unconjugated.
纯化:
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.
别名:

展开/折叠

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;

抗原和靶标

免疫原:
Uniprot:

P36897(TGFR1_HUMAN) >>Visit HPA database.

基因/基因ID:
TGFBR1(7046)
表达:
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).

描述:
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.
序列:
MEAAVAAPRPRLLLLVLAAAAAAAAALLPGATALQCFCHLCTKDNFTCVTDGLCFVSVTETTDKVIHNSMCIAEIDLIPRDRPFVCAPSSKTGSVTTTYCCNQDHCNKIELPTTVKSSPGLGPVELAAVIAGPVCFVCISLMLMVYICHNRTVIHHRVPNEEDPSLDRPFISEGTTLKDLIYDMTTSGSGSGLPLLVQRTIARTIVLQESIGKGRFGEVWRGKWRGEEVAVKIFSSREERSWFREAEIYQTVMLRHENILGFIAADNKDNGTWTQLWLVSDYHEHGSLFDYLNRYTVTVEGMIKLALSTASGLAHLHMEIVGTQGKPAIAHRDLKSKNILVKKNGTCCIADLGLAVRHDSATDTIDIAPNHRVGTKRYMAPEVLDDSINMKHFESFKRADIYAMGLVFWEIARRCSIGGIHEDYQLPYYDLVPSDPSVEEMRKVVCEQKLRPNIPNRWQSCEALRVMAKIMRECWYANGAARLTALRIKKTLSQLSQQEGIKM

种属预测

种属预测:

score>80的预测可信度较高，可尝试用于WB检测。*预测模型主要基于免疫原序列比对，结果仅作参考，不作为质保凭据。

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

翻译修饰 - P36897 作为底物

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

翻译修饰 - P36897 作为激酶

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

功能:

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.

翻译修饰:

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.

细胞定位:

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
组织特异性:

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

亚基结构:

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.

蛋白家族:

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

研究领域

· 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.

文献引用

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

限制条款

产品的规格、报价、验证数据请以官网为准，官网链接：www.affbiotech.com | www.affbiotech.cn（简体中文）| www.affbiotech.jp（日本語）

产品的数据信息为Affinity所有，未经授权不得收集Affinity官网数据或资料用于商业用途，对抄袭产品数据的行为我们将保留诉诸法律的权利。

产品相关数据会因产品批次、产品检测情况随时调整，如您已订购该产品，请以订购时随货说明书为准，否则请以官网内容为准，官网内容有改动时恕不另行通知。

Affinity保证所销售产品均经过严格质量检测。如您购买的商品在规定时间内出现问题需要售后时，请您在Affinity官方渠道提交售后申请。

产品仅供科学研究使用。不用于诊断和治疗。 

产品未经授权不得转售。

Affinity Biosciences将不会对在使用我们的产品时可能发生的专利侵权或其他侵权行为负责。Affinity Biosciences, Affinity Biosciences标志和所有其他商标所有权归Affinity Biosciences LTD.