Product: E-cadherin Antibody
Catalog: AF0131
Description: Rabbit polyclonal antibody to E-cadherin
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat, Monkey
Prediction: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 120kDa; 97kD(Calculated).
Uniprot: P12830
RRID: AB_2833315

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Product Info

Source:
Rabbit
Application:
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: 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.

Reactivity:
Human,Mouse,Rat,Monkey
Prediction:
Pig(100%), Zebrafish(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(83%), Xenopus(83%)
Clonality:
Polyclonal
Specificity:
E-cadherin Antibody detects endogenous levels of total E-cadherin.
RRID:
AB_2833315
Cite Format: Affinity Biosciences Cat# AF0131, RRID:AB_2833315.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

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;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
P12830 CADH1_HUMAN:

Non-neural epithelial tissues.

Description:
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.
Sequence:
MGPWSRSLSALLLLLQVSSWLCQEPEPCHPGFDAESYTFTVPRRHLERGRVLGRVNFEDCTGRQRTAYFSLDTRFKVGTDGVITVKRPLRFHNPQIHFLVYAWDSTYRKFSTKVTLNTVGHHHRPPPHQASVSGIQAELLTFPNSSPGLRRQKRDWVIPPISCPENEKGPFPKNLVQIKSNKDKEGKVFYSITGQGADTPPVGVFIIERETGWLKVTEPLDRERIATYTLFSHAVSSNGNAVEDPMEILITVTDQNDNKPEFTQEVFKGSVMEGALPGTSVMEVTATDADDDVNTYNAAIAYTILSQDPELPDKNMFTINRNTGVISVVTTGLDRESFPTYTLVVQAADLQGEGLSTTATAVITVTDTNDNPPIFNPTTYKGQVPENEANVVITTLKVTDADAPNTPAWEAVYTILNDDGGQFVVTTNPVNNDGILKTAKGLDFEAKQQYILHVAVTNVVPFEVSLTTSTATVTVDVLDVNEAPIFVPPEKRVEVSEDFGVGQEITSYTAQEPDTFMEQKITYRIWRDTANWLEINPDTGAISTRAELDREDFEHVKNSTYTALIIATDNGSPVATGTGTLLLILSDVNDNAPIPEPRTIFFCERNPKPQVINIIDADLPPNTSPFTAELTHGASANWTIQYNDPTQESIILKPKMALEVGDYKINLKLMDNQNKDQVTTLEVSVCDCEGAAGVCRKAQPVEAGLQIPAILGILGGILALLILILLLLLFLRRRAVVKEPLLPPEDDTRDNVYYYDEEGGGEEDQDFDLSQLHRGLDARPEVTRNDVAPTLMSVPRYLPRPANPDEIGNFIDENLKAADTDPTAPPYDSLLVFDYEGSGSEAASLSSLNSSESDKDQDYDYLNEWGNRFKKLADMYGGGEDD

Predictions

Predictions:

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
Horse
100
Bovine
100
Sheep
100
Dog
100
Zebrafish
100
Rabbit
100
Xenopus
83
Chicken
83
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P12830 As Substrate

Site PTM Type Enzyme
T66 Phosphorylation
Y68 Phosphorylation
S70 Phosphorylation
T211 Phosphorylation
T217 O-Glycosylation
T330 Phosphorylation
N558 N-Glycosylation
N570 N-Glycosylation
T576 Phosphorylation
T599 Phosphorylation
N622 N-Glycosylation
N637 N-Glycosylation
Y663 Phosphorylation
K738 Ubiquitination
T748 Phosphorylation
Y753 Phosphorylation
Y754 Phosphorylation
Y755 Phosphorylation
S770 Phosphorylation
T790 Phosphorylation Q05655 (PRKCD)
S793 Phosphorylation
Y797 Phosphorylation
S838 Phosphorylation
S840 Phosphorylation
S844 Phosphorylation P48729 (CSNK1A1) , P49674 (CSNK1E) , P48730 (CSNK1D)
S846 Phosphorylation
S847 Phosphorylation P68400 (CSNK2A1)
S850 Phosphorylation P68400 (CSNK2A1)
S851 Phosphorylation
S853 Phosphorylation P68400 (CSNK2A1)
K871 Ubiquitination
Y876 Phosphorylation

Research Backgrounds

Function:

Cadherins are calcium-dependent cell adhesion proteins. They preferentially interact with themselves in a homophilic manner in connecting cells; cadherins may thus contribute to the sorting of heterogeneous cell types. CDH1 is involved in mechanisms regulating cell-cell adhesions, mobility and proliferation of epithelial cells. Has a potent invasive suppressor role. It is a ligand for integrin alpha-E/beta-7.

E-Cad/CTF2 promotes non-amyloidogenic degradation of Abeta precursors. Has a strong inhibitory effect on APP C99 and C83 production.

(Microbial infection) Serves as a receptor for Listeria monocytogenes; internalin A (InlA) binds to this protein and promotes uptake of the bacteria.

PTMs:

During apoptosis or with calcium influx, cleaved by a membrane-bound metalloproteinase (ADAM10), PS1/gamma-secretase and caspase-3. Processing by the metalloproteinase, induced by calcium influx, causes disruption of cell-cell adhesion and the subsequent release of beta-catenin into the cytoplasm. The residual membrane-tethered cleavage product is rapidly degraded via an intracellular proteolytic pathway. Cleavage by caspase-3 releases the cytoplasmic tail resulting in disintegration of the actin microfilament system. The gamma-secretase-mediated cleavage promotes disassembly of adherens junctions. During development of the cochlear organ of Corti, cleavage by ADAM10 at adherens junctions promotes pillar cell separation (By similarity).

N-glycosylation at Asn-637 is essential for expression, folding and trafficking. Addition of bisecting N-acetylglucosamine by MGAT3 modulates its cell membrane location.

Ubiquitinated by a SCF complex containing SKP2, which requires prior phosphorylation by CK1/CSNK1A1. Ubiquitinated by CBLL1/HAKAI, requires prior phosphorylation at Tyr-754.

O-glycosylated. O-manosylated by TMTC1, TMTC2, TMTC3 or TMTC4. Thr-285 and Thr-509 are O-mannosylated by TMTC2 or TMTC4 but not TMTC1 or TMTC3.

Subcellular Location:

Cell junction>Adherens junction. Cell membrane>Single-pass type I membrane protein. Endosome. Golgi apparatus>trans-Golgi network.
Note: Colocalizes with DLGAP5 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. Colocalizes with RAB11A endosomes during its transport from the Golgi apparatus to the plasma membrane.

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

Non-neural epithelial tissues.

Subunit Structure:

Homodimer; disulfide-linked. Component of an E-cadherin/ catenin adhesion complex composed of at least E-cadherin/CDH1, beta-catenin/CTNNB1 or gamma-catenin/JUP, and potentially alpha-catenin/CTNNA1; the complex is located to adherens junctions. Interacts with the TRPV4 and CTNNB1 complex (By similarity). Interacts with CTNND1. The stable association of CTNNA1 is controversial as CTNNA1 was shown not to bind to F-actin when assembled in the complex (By similarity). Alternatively, the CTNNA1-containing complex may be linked to F-actin by other proteins such as LIMA1 (By similarity). Interaction with PSEN1, cleaves CDH1 resulting in the disassociation of cadherin-based adherens junctions (CAJs). Interacts with AJAP1 and DLGAP5. Interacts with TBC1D2. Interacts with LIMA1. Interacts with CAV1. Interacts with PIP5K1C. Interacts with RAB8B (By similarity). Interacts with RAPGEF2 (By similarity). Interacts with DDR1; this stabilizes CDH1 at the cell surface and inhibits its internalization. Interacts with KLRG1. Forms a ternary complex composed of ADAM10, CADH1 and EPHA4; within the complex, CADH1 is cleaved by ADAM10 which disrupts adherens junctions (By similarity).

(Microbial infection) Interacts with L.monocytogenes InlA. The formation of the complex between InlA and cadherin-1 is calcium-dependent.

Family&Domains:

Three calcium ions are usually bound at the interface of each cadherin domain and rigidify the connections, imparting a strong curvature to the full-length ectodomain.

Research Fields

· 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)

References

1). Genomic and Transcriptomic Characterization of Natural Killer T Cell Lymphoma. CANCER CELL, 2020 (PubMed: 32183952) [IF=50.3]

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). METTL13 Mediates the Translation of Snail in Head and Neck Squamous Cell Carcinoma. International Journal of Oral Science, 2020 (PubMed: 34381012) [IF=14.9]

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=14.0]

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). 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

6). 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.

7). Psychologic Stress Drives Progression of Malignant Tumors via DRD2/HIF1α Signaling. CANCER RESEARCH, 2021 (PubMed: 34321238) [IF=11.2]

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.

8). Water-extracted Lonicera japonica polysaccharide attenuates allergic rhinitis by regulating NLRP3-IL-17 signaling axis. Carbohydrate Polymers, 2022 (PubMed: 36184153) [IF=11.2]

9). YY1 complex promotes Quaking expression via super-enhancer binding during EMT of hepatocellular carcinoma. CANCER RESEARCH, 2019 (PubMed: 30760518) [IF=11.2]

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.

10). Twist1 Regulates Vimentin through Cul2 Circular RNA to Promote EMT in Hepatocellular Carcinoma. CANCER RESEARCH, 2018 (PubMed: 29844124) [IF=11.2]

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.

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