E-cadherin Antibody - #AF0131

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产品: E-cadherin 抗体
货号: AF0131
描述: Rabbit polyclonal antibody to E-cadherin
应用: WB IHC IF/ICC
文献验证: WB, IHC, IF/ICC
反应: Human, Mouse, Rat, Monkey
预测: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
蛋白号: P12830
RRID: AB_2833315

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   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

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说明书
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实验方案
WB Handbook
IHC Protocol
IF/ICC Protocol

产品描述

来源:
Rabbit
应用:
WB 1:500-1:3000, 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, Monkey
克隆:
Polyclonal
特异性:
E-cadherin Antibody detects endogenous levels of total E-cadherin.
RRID:
AB_2833315
引用格式: Affinity Biosciences Cat# AF0131, RRID:AB_2833315.
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

Arc 1; CADH1_HUMAN; Cadherin 1; cadherin 1 type 1 E-cadherin; Cadherin1; CAM 120/80; CD 324; CD324; CD324 antigen; cdh1; CDHE; E-Cad/CTF3; E-cadherin; ECAD; Epithelial cadherin; epithelial calcium dependant adhesion protein; LCAM; Liver cell adhesion molecule; UVO; Uvomorulin;

抗原和靶标

免疫原:

A synthesized peptide derived from human E-cadherin, corresponding to a region within C-terminal amino acids.

基因/基因ID:
CDH1(999)
描述:
CDH1 a single-pass type I membrane protein, and calcium dependent cell adhesion proteins. It is a ligand for integrin alpha-E/beta-7, and it colocalizes with DLG7 at sites of cell-cell contact in intestinal epithelial cells. Anchored to actin microfilaments through association with alpha-, beta- and gamma-catenin. Sequential proteolysis induced by apoptosis or calcium influx, results in translocation from sites of cell-cell contact to the cytoplasm. Involved in mechanisms regulating cell-cell adhesions, mobility and proliferation of epithelial cells. Defects in CDH1 are involved in dysfunction of the cell-cell adhesion system, triggering cancer invasion (gastric, breast, ovary, endometrium and thyroid) and metastasis.

研究领域

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

· Environmental Information Processing > Signal transduction > Rap1 signaling pathway.   (View pathway)

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

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

· Environmental Information Processing > Signaling molecules and interaction > Cell adhesion molecules (CAMs).   (View pathway)

· Human Diseases > Infectious diseases: Bacterial > Bacterial invasion of epithelial cells.

· Human Diseases > Infectious diseases: Bacterial > Pathogenic Escherichia coli infection.

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

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

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

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

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

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

文献引用

1). Genomic and Transcriptomic Characterization of Natural Killer T Cell Lymphoma. CANCER CELL, 2020 (PubMed: 32183952) [IF=48.8]

Application: IF/ICC    Species: human    Sample: NK-92 cells

Figure 6. Biological Function of MGA and BRDT. (D) Immunofluorescence images of E-cadherin (green), fibronectin (red), or vimentin (red) in NK-92 cells transfected with MGA shRNAs or scramble. Cells were counterstained with DAPI (blue). (G) Immunofluorescence images of E-cadherin (green), fibronectin (red), or vimentin (red) in NK-92 cells transfected with pCMV6-BRDT (upper panel) or vector control (lower panel). Cells were counterstained with DAPI (blue).
2). CircGPR137B/miR-4739/FTO feedback loop suppresses tumorigenesis and metastasis of hepatocellular carcinoma. Molecular Cancer, 2022 (PubMed: 35858900) [IF=37.3]

Application: WB    Species: Human    Sample: HepG2 and Hep3B cells

Fig. 6 FTO is regulated by circGPR137B/miR-4739 axis in HCC. A Schematic representation of the binding sites between miR-4739 and FTO 3’UTR. B Comparison of the luciferase activity of WT or Mut FTO 3’UTR after treatment with miR-4739 mimics in HepG2 and Hep3B cells. C, D RT-qPCR and western blot analysis of the expression of FTO, p21, p27, cleaved caspase-3/− 9, N-cadherin, E-cadherin and vimentin after the transfection with circGPR137B lentiviruses and (or) miR-4739 mimics in HepG2 and Hep3B cells. E, F, G MTT, colony formation and transwell analysis of the cell proliferation, colony number and cell invasion after the transfection with FTO plasmids and (or) miR-4739 mimics in HepG2 and Hep3B cells. Data are the means ± SEM of three experiments. *P < 0.05, **P < 0.01, ***P < 0.001
3). Adaptive Antioxidant Nanomedicines Inhibit Ferroptosis in Renal Tubular Epithelial Cells to Alleviate Diabetic Kidney Disease.. Advanced Science, 2025 (PubMed: 40619591) [IF=14.1]

Application: WB    Species: Mouse    Sample: kidney

Figure 7 AAN inhibits inflammation and fibrosis in DKD. A-B) F4/80 immunohistochemical staining images (A) and F4/80 positive cells rate (B) of mice in different groups, Scale bar: 50 µm. C-E) Enzyme-linked immunosorbent assays of TNF-α (C), IL-6 (D) and IL-1β (E) in renal tissue homogenates of mice in different groups. F) Western blot analysis of INOS and COX-2 expression levels in LPS-induced HK-2 cells treated with different concentrations of AAN. G-H) Representative images of Masson-stained in kidney of different mice (G), and Collagen fiber area statistics (H), Scale bar: 50 µm. I-N) Western blot analysis of fibrosis-related protein expression levels in kidney (I), and quantitative analysis of α-SMA (J), Vimentin (K), E-cadherin (L), Collagen I (M) and Fibronectin (N). O) Representative images of Collagen I-stained in kidney of different mice, Scale bar: 50 µm. Data represent means ± S.D. from three independent replicates. ###P < 0.001 vs Control group; *P < 0.05, **P < 0.01, ***P < 0.001 vs HG group. ns means P > 0.05.
4). Engineering supramolecular dynamics of self-assembly and turnover of oncogenic microRNAs to drive their synergistic destruction in tumor models. Biomaterials, 2024 (PubMed: 38733658) [IF=12.8]

Application: WB    Species: Human    Sample: MCF-7 cells

Fig. 6. Biological activity of “Crab” aRNases in tumor cells. (A, B) Kinetics of miR-21 downregulation in MCF-7 cells by Crab-p-21, Crab-α-21 and Crab-β-21 aRNases and ON-21 oligonucleotide (A), and miR-17 downregulation in MCF-7 cells by Crab-α-17 aRNase and ON-17 oligonucleotide (B). Stem-loop PCR data of miR-21 and miR-17 levels are shown. The inhibitory effect of specific “Crab” aRNases was compared to the control non-targeted Crab-α-Scr conjugate. The expression of miRNAs was normalized to U6. Data represent the mean ± s.e. of three independent experiments. *, ** and *** statistically significant differences from control Crab-α-Scr conjugate with p≤0.05, p≤0.01 and p≤0.001. (C-E) Western-blot analysis of PDCD4 (C), E2F1 (D) and E-cadherin (E) protein level 72 h after transfection of MCF-7 cells by Crab-α-21, Crab-p-21 (C) and Crab-α-17 (D, E). Protein levels were normalized to the level of GAPDH. Data represent the mean ± s.e. of three independent experiments. *, ** and *** statistically significant differences with p≤0.05, p≤0.01 and p≤0.001. (F-H) Real-time analysis of the growth rate of MCF-7 cells after transfection with Crab-α-21 (F), Crab-β-21, Crab-p-21 (G) and Crab-α-17 (H) aRNases. (I) Real-time analysis of the growth rate of A-549 cells after transfection with Crab-α-21 and Crab-β-21. Control − tumor cells without treatment. LF – tumor cells treated with Lipofectamine™ 2000 only. Cell transfection was performed using Lipofectamine™ 2000 with aRNase concentration of 1 μM.
5). Psychologic Stress Drives Progression of Malignant Tumors via DRD2/HIF1α Signaling. CANCER RESEARCH, 2021 (PubMed: 34321238) [IF=12.5]

Application: IF/ICC    Species: mouse    Sample: tumor cells

Fig. 2. |DRD2 overexpression promotes the metastasis, invasion, tube formation, and cloning formation of tumor cells.K and L, Effect of DRD2 on the expression of E-cadherin and vimentin detected by IF. Each experiment was performed in triplicate. Results are shown as means ± SD, *, P < 0.05; **, P < 0.01.

Application: IHC    Species: mouse    Sample: tumor cells

Fig. 6. |TFP inhibits EMT of melanoma cells.D–F, IHC analysis of E-cadherin, vimentin, HIF1α, VEGFA, and Twist1 in melanoma tumor tissues of mice under stress stimulation. Representative images and staining scores are shown. Scale bar, 100 μm.

Application: WB    Species: mouse    Sample: dopamine-treated melanoma cells

Fig. 6. |TFP inhibits EMT of melanoma cells.C, Effect of TFP on the EMT markers (E-cadherin and vimentin) in dopamine-treated melanoma cells.
6). Twist1 Regulates Vimentin through Cul2 Circular RNA to Promote EMT in Hepatocellular Carcinoma. CANCER RESEARCH, 2018 (PubMed: 29844124) [IF=12.5]

Application: IF/ICC    Species: human    Sample: PLC cells

Figure 3. |Twist1 up-regulates Vimentin expression through increased circ-10720,which adsorbs miRNA.(F) Representative immunofluorescence images of Ecadherin and Vimentin in PLC cells transfected with Twist1 alone or co-transfected with circ-10720 siRNA.
7). YY1 complex promotes Quaking expression via super-enhancer binding during EMT of hepatocellular carcinoma. CANCER RESEARCH, 2019 (PubMed: 30760518) [IF=12.5]

Application: WB    Species: human    Sample: PLC-PRF-5 cells

Fig. 3 | YY1 and p65 promote EMT, migration, and invasion by targeting QKI. (a) Expression of E-cadherin and Vimentin transfected with YY1, p65, and QKI or co-transfected with QKI siRNA. (b) Morphological changes in PLC-PRF-5 cells transfected with YY1, p65, and QKI or co-transfected with QKI siRNA observed with SEM. (c) Representative immunofluorescence images of E-cadherin and Vimentin of PLC-PRF-5 cells treated in the same manner as in the wound-healing assay.

Application: IHC    Species: mouse    Sample: tumor tissues

Fig. 5| QKI expression is required for the YY1 complex to promote the metastasis and malignancy of HCC. (a) Comparison of PLC-PRF-5 and Hep3B tumor growth in mice were measured starting 6 days after implantation. All of the groups were euthanized on day 24. (b) Metastatic lung nodules were counted in each group. (c) QKI, p65, YY1, E-cadherin, and Vimentin expression levels in the tumor tissues of p65, YY1, p65+YY1, QKI and p65+YY1+siQKI groups analyzed through IHC staining.

Application: IF/ICC    Species: human    Sample: PLC-PRF-5 cells

Fig. 3| YY1 and p65 promote EMT, migration, and invasion by targeting QKI. (a) Expression of E-cadherin and Vimentin transfected with YY1, p65, and QKI or co-transfected with QKI siRNA. (b) Morphological changes in PLC-PRF-5 cells transfected with YY1, p65, and QKI or co-transfected with QKI siRNA observed with SEM. (c) Representative immunofluorescence images of E-cadherin and Vimentin of PLC-PRF-5 cells treated in the same manner as in the wound-healing assay.
8). Gut Akkermansia muciniphila ameliorates metabolic dysfunction-associated fatty liver disease by regulating the metabolism of L-aspartate via gut-liver axis. Gut Microbes, 2021 (PubMed: 34030573) [IF=12.2]

Application: IHC    Species: Mice    Sample: ileum

Figure 2. A. muciniphila increased markers related to lipid metabolism in liver and gut of HFC mice. HFC induced obese MAFLD (11 weeks of feeding) were administered with saline as the control or A. muciniphila (6 weeks of treatment) to assess liver and ileum parameters: a-c for parameters in the liver and d-f for parameters in the ileum. e-g, representative images of the ileum (Scale bar, for 100 µm). (a) Hepatic mitochondrial copy number determination. (b) Gene expression related to lipid uptake and oxidation in the liver of mice. (c) Protein levels of metabolic regulators mitochondrial complexes, and the LKB1-AMPK axis in the liver of mice. The protein levels were quantified and normalized to the loading control actin (d) Gene expression of lipid uptake and oxidation in the ileum of mice. The gene level or protein level in the HFC group was set as 1, and the relative fold increases were determined by comparison with the HFC control group. (e) Immunohistochemistry analysis of PGC-1α in the ileum of mice. The brown dot indicates the examined protein. Representative images were captured. Scale bar, 100 µm. (f) TG level quantification (indicated by oil red O staining) and oxidative stress-induced cell apoptosis determination (indicated by CHOP examination) in the ileum. Representative images were captured. Scale bar, 100 µm. (g) Immunohistochemistry analysis of E-cadherin and H
9). Stearoyl-CoA desaturase-1 promotes colorectal cancer metastasis in response to glucose by suppressing PTEN. JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH, 2018 (PubMed: 29530061) [IF=11.3]

Application: WB    Species: human    Sample: CRC

Fig. 1| SCD1 is upregulated in human CRC tissues and associated with CRC prognosis. a SCD1 mRNA level in colorectal cancer tissues (CRC) and matched adjacent non-tumor tissues (Control) detected by Real Time-PCR. b Representative Western blot and quantification data of SCD1 and EMT markers (E-cadherin and vimentin) in colorectal cancer tissue and matched adjacent non-tumor tissue.
10). METTL13 Mediates the Translation of Snail in Head and Neck Squamous Cell Carcinoma. International Journal of Oral Science, 2020 (PubMed: 34381012) [IF=10.8]
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