Smad7 Antibody - #AF5147

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製品: Smad7 Antibody
カタログ: AF5147
タンパク質の説明: Rabbit polyclonal antibody to Smad7
アプリケーション: WB IHC
反応性: Human, Mouse, Rat
予測: Pig, Bovine, Rabbit, Dog
分子量: 46 kDa; 46kD(Calculated).
ユニプロット: O15105
RRID: AB_2837633

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MS Report
HPLC Report
MSDS
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WB Handbook
IHC Protocol
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製品説明

ソース:
Rabbit
アプリケーション:
WB 1:500-1:2000, 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(94%), Rabbit(100%), Dog(87%)
クローナリティ:
Polyclonal
特異性:
Smad7 Antibody detects endogenous levels of total Smad7.
RRID:
AB_2837633
引用形式: Affinity Biosciences Cat# AF5147, RRID:AB_2837633.
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

CRCS3; FLJ16482; hSMAD 7; hSMAD7; MAD (mothers against decapentaplegic Drosophila) homolog 7; MAD; Mad homolog 7; MAD homolog 8; MAD mothers against decapentaplegic homolog 7; MADH 7; MADH 8; MADH6; MADH8; Mothers Against Decapentaplegic Drosophila Homolog of 6; Mothers Against Decapentaplegic Drosophila Homolog of 7; Mothers against decapentaplegic homolog 7; Mothers against decapentaplegic homolog 8; Mothers against DPP homolog 7; Mothers against DPP homolog 8; SMA- AND MAD-RELATED PROTEIN 7; SMAD 7; SMAD; SMAD family member 7; SMAD, mothers against DPP homolog 7 (Drosophila); SMAD, mothers against DPP homolog 7; SMAD6; Smad7; SMAD7_HUMAN;

免疫原

免疫原:
Uniprot:

O15105(SMAD7_HUMAN) >>Visit HPA database.

遺伝子(ID):
SMAD7(4092)
発現特異性:
O15105 SMAD7_HUMAN:

Ubiquitous with higher expression in the lung and vascular endothelium.

タンパク質の説明:
Antagonist of signaling by TGF-beta (transforming growth factor) type 1 receptor superfamily members; has been shown to inhibit TGF-beta (Transforming growth factor) and activin signaling by associating with their receptors thus preventing SMAD2 access. Functions as an adapter to recruit SMURF2 to the TGF-beta receptor complex. Also acts by recruiting the PPP1R15A-PP1 complex to TGFBR1, which promotes its dephosphorylation.
タンパク質配列:
MFRTKRSALVRRLWRSRAPGGEDEEEGAGGGGGGGELRGEGATDSRAHGAGGGGPGRAGCCLGKAVRGAKGHHHPHPPAAGAGAAGGAEADLKALTHSVLKKLKERQLELLLQAVESRGGTRTACLLLPGRLDCRLGPGAPAGAQPAQPPSSYSLPLLLCKVFRWPDLRHSSEVKRLCCCESYGKINPELVCCNPHHLSRLCELESPPPPYSRYPMDFLKPTADCPDAVPSSAETGGTNYLAPGGLSDSQLLLEPGDRSHWCVVAYWEEKTRVGRLYCVQEPSLDIFYDLPQGNGFCLGQLNSDNKSQLVQKVRSKIGCGIQLTREVDGVWVYNRSSYPIFIKSATLDNPDSRTLLVHKVFPGFSIKAFDYEKAYSLQRPNDHEFMQQPWTGFTVQISFVKGWGQCYTRQFISSCPCWLEVIFNSR

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
Rabbit
100
Pig
100
Bovine
94
Dog
87
Chicken
50
Zebrafish
33
Horse
0
Sheep
0
Xenopus
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - O15105 基板として

Site PTM Type Enzyme
K64 Acetylation
K64 Ubiquitination
K70 Acetylation
K70 Methylation
K70 Ubiquitination
T96 Phosphorylation Q14680 (MELK)
K101 Ubiquitination
S117 Phosphorylation
T121 Phosphorylation
S249 Phosphorylation
T354 Phosphorylation

研究背景

機能:

Antagonist of signaling by TGF-beta (transforming growth factor) type 1 receptor superfamily members; has been shown to inhibit TGF-beta (Transforming growth factor) and activin signaling by associating with their receptors thus preventing SMAD2 access. Functions as an adapter to recruit SMURF2 to the TGF-beta receptor complex. Also acts by recruiting the PPP1R15A-PP1 complex to TGFBR1, which promotes its dephosphorylation. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.

PTMs:

Phosphorylation on Ser-249 does not affect its stability, nuclear localization or inhibitory function in TGFB signaling; however it affects its ability to regulate transcription (By similarity). Phosphorylated by PDPK1.

Ubiquitinated by WWP1 (By similarity). Polyubiquitinated by RNF111, which is enhanced by AXIN1 and promotes proteasomal degradation. In response to TGF-beta, ubiquitinated by SMURF1; which promotes its degradation.

Acetylation prevents ubiquitination and degradation mediated by SMURF1.

細胞の位置付け:

Nucleus. Cytoplasm.
Note: Interaction with NEDD4L or RNF111 induces translocation from the nucleus to the cytoplasm (PubMed:16601693). TGF-beta stimulates its translocation from the nucleus to the cytoplasm. PDPK1 inhibits its translocation from the nucleus to the cytoplasm 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
組織特異性:

Ubiquitous with higher expression in the lung and vascular endothelium.

サブユニット構造:

Interacts with WWP1 (By similarity). Interacts with COPS5. Interacts with NEDD4L. Interacts with STAMBP. Interacts with RNF111, AXIN1 and AXIN2. Interacts with PPP1R15A. Interacts (via MH2 domain) with EP300. Interacts with ACVR1B, SMURF1, SMURF2 and TGFBR1; SMAD7 recruits SMURF1 and SMURF2 to the TGF-beta receptor and regulates its degradation. Interacts with PDPK1 (via PH domain).

タンパク質ファミリー:

Belongs to the dwarfin/SMAD family.

研究領域

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

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

参考文献

1). FOXO3 regulates Smad3 and Smad7 through SPON1 circular RNA to inhibit idiopathic pulmonary fibrosis. International Journal of Biological Sciences, 2023 (PubMed: 37416778) [IF=9.2]
2). 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. 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.
3). Green tea peptides ameliorate diabetic nephropathy by inhibiting the TGF-β/Smad signaling pathway in mice. Food & Function, 2022 (PubMed: 35234233) [IF=6.1]
4). miR‐448‐3p alleviates diabetic vascular dysfunction by inhibiting endothelial–mesenchymal transition through DPP‐4 dysregulation. JOURNAL OF CELLULAR PHYSIOLOGY, 2020 (PubMed: 32542696) [IF=5.6]

Application: WB    Species: Human    Sample: aortic endothelial cells

FIGURE 3 High glucose treatment reduced miR‐448‐3p expression, increased DPP‐4 expression, activated TGF‐β/Smad pathway, and promoted EndMT in aortic endothelial cells. (a) Relative mRNA expression levels of miR‐448‐3p and DPP‐4 in high glucose‐treated aortic endothelial cells. (b) The protein levels of DPP‐4, CD31, VE‐cadherin, α‐SMA, and vimentin in each group. (c) Relative protein levels of TGF‐β1, Smad2, p‐Smad2 (S465/S467), Smad3, p‐Smad3 (S423/S425), and Smad7 in all the groups. Data were expressed as means ± standard deviation (SD), n = 3. *p < .05 compared with the OC group. DPP‐4, dipeptidyl peptidase‐4; EndMT, endothelial–mesenchymal transition; HG, high glucose; miR, microRNA; mRNA, messenger RNA; TGF‐β, transforming growth factor‐β; α‐SMA, α‐smooth muscle actin
5). Molecular mechanism of Gan-song Yin inhibiting the proliferation of renal tubular epithelial cells by regulating miR-21-5p in adipocyte exosomes. Journal of ethnopharmacology, 2024 (PubMed: 38043753) [IF=5.4]

Application: WB    Species: Mouse    Sample: TCMK-1 cells

Fig. 4. Mechanism of GSY on TCMK-1. A. Viability of TCMK-1 cells treated with different concentrations of GSY. B. TCMK-1 cell viability in each experimental group. C. Changes in TCMK-1 cell cycle level after GSY intervention. D. Changes in apoptosis level of TCMK-1 cells after GSY intervention. E. Expression of TGF-β1, SMAD2, SMAD3, SMAD7, p-SMAD2, p-SMAD3 and p-SMAD7 proteins in TCMK-1 cells after GSY intervention. F. Gene expression levels of TGF-β1, SMAD2, SMAD3 and SMAD7 in TCMK-1 cells after GSY intervention. *p < 0.05; **p < 0.01; ***p < 0.001. NC: Negative control; MOD: Model (60 mmol/L glucose). All experiments were repeated three times.
6). miR‑29b suppresses proliferation and induces apoptosis of hepatocellular carcinoma ascites H22 cells via regulating TGF‑β1 and p53 signaling pathway. INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 2021 (PubMed: 34184070) [IF=5.4]

Application: WB    Species: Mice    Sample: H22 cells

Figure 4 Effect of miR-29b on the TGF-β1 signaling pathway in H22 cells. (A and B) Western blot analysis of TGF-β1, p-Smad3 and Smad7. (C-E) Protein intensities of TGF-β1, p-Smad3 and Smad7. Values represent the means ± SD (n=3). (F-H) mRNA levels of TGF-β1, Smad3 and Smad7. Values represent the means ± SD (n=5). #P<0.05 and ##P<0.01 vs. control mimic; *P<0.05 and **P<0.01 vs. control inhibitor. miR, microRNA; TGF, transforming growth factor; SD, standard deviation; p-, phosphorylated.
7). Mesenchymal stem cells ameliorate silica‐induced pulmonary fibrosis by inhibition of inflammation and epithelial‐mesenchymal transition. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 2021 (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.
8). SIRT1 activation ameliorates rhesus monkey liver fibrosis by inhibiting the TGF-β/smad signaling pathway. Chemico-biological interactions, 2024 (PubMed: 38555046) [IF=5.1]
9). TFPI2 suppresses the interaction of TGF-β2 pathway regulators to promote endothelial-mesenchymal transition in diabetic nephropathy. Journal of Biological Chemistry, 2022 (PubMed: 35157852) [IF=4.8]

Application: WB    Species: Human    Sample: hRGECs

Figure 9 TFPI2 promotes TGF-β/Smad signaling activation. Human renal glomerular endothelial cells (hRGECs) were infected with adenovirus encoding shRNA targeting TFPI2 (TFPI2 shRNA) or overexpressing TFPI2 (TFPI2 OE), followed by stimulation of 5 ng/ml TGF-β2 for 48 h. A, the expression of SMAD7, TGFBR1, TGFBR2, SMAD2/3, and phospho-SMAD2/3 (p-SMAD2/3) was determined by Western blot. Semiquantitative analysis of (B) SMAD7, (C) TGFBR1, and (D) TGFBR2, as well as (E and F) the ratio of p-SMAD2/3 to SMAD2/3. G and H, immunofluorescent staining of SMAD2/3 in hRGECs. Yellow arrows indicated nuclear translocation of SMAD2/3. Data are shown as the mean ± SD (n = 3). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. TGF-β, transforming growth factor beta; TFP12, tissue factor pathway inhibitor 2.
10). Microvesicles-delivering Smad7 have advantages over microvesicles in suppressing fibroblast differentiation in a model of Peyronie's disease. BMC biotechnology, 2024 (PubMed: 38849776) [IF=3.5]
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