产品: Smad3 抗体
货号: AF6362
描述: Rabbit polyclonal antibody to Smad3
应用: WB IHC IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
分子量: 58kDa; 48kD(Calculated).
蛋白号: P84022
RRID: AB_2835210

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

产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*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%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
克隆:
Polyclonal
特异性:
Smad3 Antibody detects endogenous levels of total Smad3.
RRID:
AB_2835210
引用格式: Affinity Biosciences Cat# AF6362, RRID:AB_2835210.
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

DKFZP586N0721; DKFZp686J10186; hMAD 3; hMAD-3; hSMAD3; HSPC193; HST17436; JV15 2; JV15-2; JV152; LDS1C; LDS3; MAD (mothers against decapentaplegic Drosophila) homolog 3; MAD homolog 3; Mad homolog JV15 2; Mad protein homolog; MAD, mothers against decapentaplegic homolog 3; Mad3; MADH 3; MADH3; MGC60396; Mothers against decapentaplegic homolog 3; Mothers against DPP homolog 3; SMA and MAD related protein 3; SMAD 3; SMAD; SMAD family member 3; SMAD, mothers against DPP homolog 3; Smad3; SMAD3_HUMAN;

抗原和靶标

免疫原:
Uniprot:
基因/基因ID:
描述:
Smad3 transcription factor phosphorylated and activated by TGF-beta-type receptors. A receptor-regulated Smad (R-smad). Binds directly to consensus DNA-binding elements in the promoters of target genes. In mouse required for establishemnt of the mucosal immune response and proper development of skeleton.
序列:
MSSILPFTPPIVKRLLGWKKGEQNGQEEKWCEKAVKSLVKKLKKTGQLDELEKAITTQNVNTKCITIPRSLDGRLQVSHRKGLPHVIYCRLWRWPDLHSHHELRAMELCEFAFNMKKDEVCVNPYHYQRVETPVLPPVLVPRHTEIPAEFPPLDDYSHSIPENTNFPAGIEPQSNIPETPPPGYLSEDGETSDHQMNHSMDAGSPNLSPNPMSPAHNNLDLQPVTYCEPAFWCSISYYELNQRVGETFHASQPSMTVDGFTDPSNSERFCLGLLSNVNRNAAVELTRRHIGRGVRLYYIGGEVFAECLSDSAIFVQSPNCNQRYGWHPATVCKIPPGCNLKIFNNQEFAALLAQSVNQGFEAVYQLTRMCTIRMSFVKGWGAEYRRQTVTSTPCWIELHLNGPLQWLDKVLTQMGSPSIRCSSVS

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

翻译修饰 - P84022 作为底物

Site PTM Type Enzyme
Ubiquitination
S2 Acetylation
S3 Phosphorylation
T8 Phosphorylation P11802 (CDK4) , P24941 (CDK2)
K13 Ubiquitination
K19 Acetylation
K29 Acetylation
K33 Ubiquitination
K36 Sumoylation
S37 Phosphorylation
K63 Ubiquitination
T66 Phosphorylation P49841 (GSK3B)
S78 Phosphorylation
K81 Ubiquitination
Y88 Phosphorylation
Y125 Phosphorylation
T132 Phosphorylation
T179 Phosphorylation P49336 (CDK8) , P28482 (MAPK1) , P24941 (CDK2) , P50750 (CDK9) , P11802 (CDK4) , P31749 (AKT1)
S204 Phosphorylation P28482 (MAPK1) , Q14680 (MELK) , Q16539 (MAPK14) , P27361 (MAPK3) , P11802 (CDK4)
S208 Phosphorylation P49336 (CDK8) , P11802 (CDK4) , P28482 (MAPK1) , Q16539 (MAPK14) , P50750 (CDK9)
S213 Phosphorylation P50750 (CDK9) , P49336 (CDK8) , P11802 (CDK4) , P28482 (MAPK1) , P24941 (CDK2)
S275 Phosphorylation
S309 Phosphorylation
K378 Acetylation
T388 Phosphorylation
T412 Phosphorylation
S416 Phosphorylation
S418 Phosphorylation P78368 (CSNK1G2)
S422 Phosphorylation P36897 (TGFBR1)
S423 Phosphorylation P36897 (TGFBR1)
S425 Phosphorylation P36897 (TGFBR1)

研究背景

功能:

Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD3/SMAD4 complex, activates transcription. Also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. Has an inhibitory effect on wound healing probably by modulating both growth and migration of primary keratinocytes and by altering the TGF-mediated chemotaxis of monocytes. This effect on wound healing appears to be hormone-sensitive. Regulator of chondrogenesis and osteogenesis and inhibits early healing of bone fractures. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.

翻译修饰:

Phosphorylated on serine and threonine residues. Enhanced phosphorylation in the linker region on Thr-179, Ser-204 and Ser-208 on EGF and TGF-beta treatment. Ser-208 is the main site of MAPK-mediated phosphorylation. CDK-mediated phosphorylation occurs in a cell-cycle dependent manner and inhibits both the transcriptional activity and antiproliferative functions of SMAD3. This phosphorylation is inhibited by flavopiridol. Maximum phosphorylation at the G(1)/S junction. Also phosphorylated on serine residues in the C-terminal SXS motif by TGFBR1 and ACVR1. TGFBR1-mediated phosphorylation at these C-terminal sites is required for interaction with SMAD4, nuclear location and transactivational activity, and appears to be a prerequisite for the TGF-beta mediated phosphorylation in the linker region. Dephosphorylated in the C-terminal SXS motif by PPM1A. This dephosphorylation disrupts the interaction with SMAD4, promotes nuclear export and terminates TGF-beta-mediated signaling. Phosphorylation at Ser-418 by CSNK1G2/CK1 promotes ligand-dependent ubiquitination and subsequent proteasome degradation, thus inhibiting SMAD3-mediated TGF-beta responses. Phosphorylated by PDPK1.

Acetylation in the nucleus by EP300 in the MH2 domain regulates positively its transcriptional activity and is enhanced by TGF-beta.

Poly-ADP-ribosylated by PARP1 and PARP2. ADP-ribosylation negatively regulates SMAD3 transcriptional responses during the course of TGF-beta signaling.

Ubiquitinated. Monoubiquitinated, leading to prevent DNA-binding. Deubiquitination by USP15 alleviates inhibition and promotes activation of TGF-beta target genes. Ubiquitinated by RNF111, leading to its degradation: only SMAD3 proteins that are 'in use' are targeted by RNF111, RNF111 playing a key role in activating SMAD3 and regulating its turnover (By similarity). Undergoes STUB1-mediated ubiquitination and degradation.

细胞定位:

Cytoplasm. Nucleus.
Note: Cytoplasmic and nuclear in the absence of TGF-beta. On TGF-beta stimulation, migrates to the nucleus when complexed with SMAD4 (PubMed:15799969). Through the action of the phosphatase PPM1A, released from the SMAD2/SMAD4 complex, and exported out of the nucleus by interaction with RANBP1 (PubMed:16751101, PubMed:19289081). Co-localizes with LEMD3 at the nucleus inner membrane (PubMed:15601644). MAPK-mediated phosphorylation appears to have no effect on nuclear import (PubMed:19218245). PDPK1 prevents its nuclear translocation in response to TGF-beta (PubMed:17327236).

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

Monomer; in the absence of TGF-beta. Homooligomer; in the presence of TGF-beta. Heterotrimer; forms a heterotrimer in the presence of TGF-beta consisting of two molecules of C-terminally phosphorylated SMAD2 or SMAD3 and one of SMAD4 to form the transcriptionally active SMAD2/SMAD3-SMAD4 complex. Interacts with TGFBR1. Part of a complex consisting of AIP1, ACVR2A, ACVR1B and SMAD3. Interacts with AIP1, TGFB1I1, TTRAP, FOXL2, PML, PRDM16, HGS, WWP1 and SNW1. Interacts (via MH2 domain) with CITED2 (via C-terminus). Interacts with NEDD4L; the interaction requires TGF-beta stimulation. Interacts (via MH2 domain) with ZFYVE9. Interacts with HDAC1, TGIF and TGIF2, RUNX3, CREBBP, SKOR1, SKOR2, SNON, ATF2, SMURF2 and TGFB1I1. Interacts with DACH1; the interaction inhibits the TGF-beta signaling. Forms a complex with SMAD2 and TRIM33 upon addition of TGF-beta. Found in a complex with SMAD3, RAN and XPO4. Interacts in the complex directly with XPO4. Interacts (via MH2 domain) with LEMD3; the interaction represses SMAD3 transcriptional activity through preventing the formation of the heteromeric complex with SMAD4 and translocation to the nucleus. Interacts with RBPMS. Interacts (via MH2 domain) with MECOM. Interacts with WWTR1 (via its coiled-coil domain). Interacts (via the linker region) with EP300 (C-terminal); the interaction promotes SMAD3 acetylation and is enhanced by TGF-beta phosphorylation in the C-terminal of SMAD3. This interaction can be blocked by competitive binding of adenovirus oncoprotein E1A to the same C-terminal site on EP300, which then results in partially inhibited SMAD3/SMAD4 transcriptional activity. Interacts with SKI; the interaction represses SMAD3 transcriptional activity. Component of the multimeric complex SMAD3/SMAD4/JUN/FOS which forms at the AP1 promoter site; required for synergistic transcriptional activity in response to TGF-beta. Interacts (via an N-terminal domain) with JUN (via its basic DNA binding and leucine zipper domains); this interaction is essential for DNA binding and cooperative transcriptional activity in response to TGF-beta. Interacts with PPM1A; the interaction dephosphorylates SMAD3 in the C-terminal SXS motif leading to disruption of the SMAD2/3-SMAD4 complex, nuclear export and termination of TGF-beta signaling. Interacts (dephosphorylated form via the MH1 and MH2 domains) with RANBP3 (via its C-terminal R domain); the interaction results in the export of dephosphorylated SMAD3 out of the nucleus and termination of the TGF-beta signaling. Interacts with MEN1. Interacts with IL1F7. Interaction with CSNK1G2. Interacts with PDPK1 (via PH domain). Interacts with DAB2; the interactions are enhanced upon TGF-beta stimulation. Interacts with USP15. Interacts with PPP5C; the interaction decreases SMAD3 phosphorylation and protein levels. Interacts with LDLRAD4 (via the SMAD interaction motif). Interacts with PMEPA1. Interacts with ZC3H3 (By similarity). Interacts with ZNF451. Identified in a complex that contains at least ZNF451, SMAD2, SMAD3 and SMAD4. Interacts with ZFHX3. Interacts weakly with ZNF8. Interacts (when phosphorylated) with RNF111; RNF111 acts as an enhancer of the transcriptional responses by mediating ubiquitination and degradation of SMAD3 inhibitors (By similarity). Interacts with STUB1, HSPA1A, HSPA1B, HSP90AA1 and HSP90AB1. Interacts (via MH2 domain) with ZMIZ1 (via SP-RING-type domain); in the TGF-beta signaling pathway increases the activity of the SMAD3/SMAD4 transcriptional complex.

蛋白家族:

The MH1 domain is required for DNA binding. Also binds zinc ions which are necessary for the DNA binding.

The MH2 domain is required for both homomeric and heteromeric interactions and for transcriptional regulation. Sufficient for nuclear import.

The linker region is required for the TGFbeta-mediated transcriptional activity and acts synergistically with the MH2 domain.

Belongs to the dwarfin/SMAD family.

研究领域

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

· 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)

· Cellular Processes > Cellular community - eukaryotes > Signaling pathways regulating pluripotency of stem cells.   (View pathway)

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

· Environmental Information Processing > Signal transduction > Wnt 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)

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

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

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

文献引用

1). Myricetin suppresses the proliferation and migration of vascular smooth muscle cells and inhibits neointimal hyperplasia via suppressing TGFBR1 signaling pathways. PHYTOMEDICINE (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.

2). 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 [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.

3). Myricetin ameliorates bleomycin-induced pulmonary fibrosis in mice by inhibiting TGF-β signaling via targeting HSP90β. BIOCHEMICAL PHARMACOLOGY (PubMed: 32535102) [IF=5.8]

4). Regorafenib-Attenuated, Bleomycin-Induced Pulmonary Fibrosis by Inhibiting the TGF-β1 Signaling Pathway. International Journal of Molecular Sciences (PubMed: 33671452) [IF=5.6]

Application: WB    Species: Mouse    Sample: Mlg cells

Figure 3. Regorafenib down-regulates TGF-β1/Smad and TGF-β1/non-Smad signals in pulmonary fibroblasts. (A) CAGAmouse embryonic fibroblast (NIH-3T3) cells were exposed to TGF-β1 (5 ng/mL) or a series concentration (0–32 µM) in serum-free medium for 18 h; (B) Mlg cells were treated with TGF-β1 (5 ng/mL) and/or RG (2 µM, 4 µM) for 30 min, and Western blot was used to detect Smad3, Smad2, and their phosphorylation expression levels. Densitometric analysis are shown beside; (C) Mlg cells were incubated with RG (2 µM, 4 µM) and/or TGF-β1 (5 ng/mL) for 12 h to analyze the Erk1/2 and Akt and their phosphorylation levels by Western blotting. Densitometric analysis are shown beside; (D) BLM-PPF cells were incubated with RG (2 µM, 4 µM) for 12 h to analyze Erk1/2 and Akt and their phosphorylation levels by Western blotting. Densitometric analysis are shown beside. β-tubulin or GAPDH were used as a loading control. Data in (A–D) are means ± standard error of mean (SEM); ### p < 0.001, * p < 0.05, ** p < 0.01, *** p < 0.001 (one-way ANOVA), NS: not significant.

5). Adipose Mesenchymal Stromal Cell-Derived Exosomes Carrying MiR-122-5p Antagonize the Inhibitory Effect of Dihydrotestosterone on Hair Follicles by Targeting the TGF-β1/SMAD3 Signaling Pathway. International Journal of Molecular Sciences (PubMed: 36982775) [IF=5.6]

Application: WB    Species: Mouse    Sample:

Figure 4 miR-122-5p targets and negatively regulates SMAD3. (A) Binding site prediction of miR-122-5p in SMAD3 3′-UTR. (B) Luciferase analysis showing miR-122-5p targeting SMAD3. (C) The expression of miR-122-5p in Exo-miR-122-5p and Exo-in-miR-122-5p. (D) Protein expression of SMAD3 and p-SMAD3 in DPCs treated with Exo-miR-122-5p and Exo-in-miR-122-5p.

6). Exosome‑encapsulated miR‑26a attenuates aldosterone‑induced tubulointerstitial fibrosis by inhibiting the CTGF/SMAD3 signaling pathway. International Journal of Molecular Medicine (PubMed: 36524378) [IF=5.4]

Application: WB    Species: Mice    Sample: kidneys

Figure 6 miR-26a/CTGF inhibits SMAD3 activation. (A) Western blot analysis of SMAD3 and p-SMAD3 protein expression levels in the kidneys of mice in the sham, ALD, ALD + Exo-NC and ALD + Exo-miR-26a groups. (B) Western blot analysis of SMAD3 and p-SMAD3 protein expression levels in mTECs co-transfected with oe-CTGF or oe-NC and miR-26a mimic or NC mimic for 6 h, and then treated with ALD (1×10−6 M) for 48 h. (C) Western blot analysis of SMAD3 and p-SMAD3 protein levels in mTECs co-transfected with si-CTGF or si-NC and miR-26a inhibitor or NC inhibitor for 6 h, and then treated with ALD (1×10−6 M) for 48 h. Data are presented as mean ± SD; Data are presented as the mean ± SD; *P<0.05, **P<0.01, ***P<0.001; #P<0.05, ##P<0.01. ALD, aldosterone; CTGF, connective tissue growth factor; Exo, exosome encapsulated; miR, microRNA; mTEC, mouse tubular epithelial cells; NC, negative control; p-phosphorylated.

7). Taohong siwu decoction attenuates myocardial fibrosis by inhibiting fibrosis proliferation and collagen deposition via TGFBR1 signaling pathway. Journal of Ethnopharmacology (PubMed: 33460756) [IF=5.4]

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). Mesenchymal stem cells ameliorate silica‐induced pulmonary fibrosis by inhibition of inflammation and epithelial‐mesenchymal transition. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE (PubMed: 34076355) [IF=5.3]

Application: WB    Species: rat    Sample: lung

FIGURE 5|BMSCs blocked the activation of TGF-β/Smad pathway. (D) Western blot results of TGF-β1, Smad2, p-Smad2, Smad3, p-Smad3 and Smad7 protein expression levels. n = 3 rats per group.

9). High-dose vitamin D3 c ameliorates renal fibrosis by vitamin D receptor activation and inhibiting TGF-β1/Smad3 signaling pathway in 5/6 nephrectomized rats. European Journal of Pharmacology (PubMed: 34147475) [IF=5.0]

Application: IHC    Species: Rat    Sample: kidney tissues

Fig. 6. Vitamin D3 activated the vitamin D receptor and inhibited the activation of the TGF-β1/Smad3 signaling pathway. Renal expression of (A) Vitamin D receptor, (B) TGF-β1, and (C) Smad3 mRNA was determined by RT-qPCR. (D) Protein expression levels of the vitamin D receptor and TGF-β1 analyzed by Western blot; (E, F) Vitamin D receptor and TGF-β1 protein expression relative to GADPH protein expression; (G) p-Smad3 protein expression visualized in renal sections using immunohistochemistry (scale bar: 100 μm); (H) average optical density (AOD) analysis of p-Smad3. Data expressed as mean ± S.E.M. (n = 3–7), *P < 0.05 vs sham group; **P < 0.01 vs sham group; ***P < 0.001 vs sham group; #P < 0.05 vs 5/6 Nx group; ##P < 0.01 vs 5/6 Nx group; ###P < 0.001 vs 5/6 Nx group; ns, no significance.

10). Enhancer of zeste homolog 2 modulates oxidative stress-mediated pyroptosis in vitro and in a mouse kidney ischemia-reperfusion injury model. FASEB JOURNAL (PubMed: 31914694) [IF=4.8]

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.

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.