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Cow (Bovine) E-cadherin ELISA Kit für Sandwich ELISA - ABIN826143
Sakumoto, Hayashi, Saito, Kanahara, Kizaki, Iga: Comparison of the global gene expression profiles in the bovine endometrium between summer and autumn. in The Journal of reproduction and development 2015
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Human E-cadherin ELISA Kit für Sandwich ELISA - ABIN414360
Calenic, Paun, van Staden, Didilescu, Petre, Dinescu, Greabu: Novel method for proliferation of oral keratinocyte stem cells. in Journal of periodontal research 2014
Human E-cadherin ELISA Kit für Sandwich ELISA - ABIN2683765
Batlle, Sancho, Francí, Domínguez, Monfar, Baulida, García De Herreros: The transcription factor snail is a repressor of E-cadherin gene expression in epithelial tumour cells. in Nature cell biology 2000
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cryo-EM structure of an APC/C-Cdh1 complex with Apc1(WD40) deleted showed that the mutant APC/C is locked into an inactive conformation in which the UbcH10-binding site of the catalytic module is inaccessible. Additionally, an EM density for Apc15 is not visible
FDG (zeige SMUG1 ELISA Kits) uptake on PET was associated with negative E-cadherin expression in patients with lung adenocarcinoma.
Heterozygosity and mutant homozygosity as well as the combination of both TP53 (zeige TP53 ELISA Kits) Arg72Pro and CDH1 rs16260 polymorphisms are responsible to increase the risk of colorectal cancer development in Bangladeshi population.
Combining the targets E-cadherin, epithelial membrane antigen (EMA (zeige ETFA ELISA Kits)), human epidermal growth receptor type 2 (Her2/neu (zeige ERBB2 ELISA Kits)), carcinoembryonic antigen (CEA (zeige CEACAM5 ELISA Kits)) resulted in nearly 100% detection of ductal ovarian metastases, whereas the combination of EMA (zeige ETFA ELISA Kits), Her2/neu (zeige ERBB2 ELISA Kits) and epithelial cell adhesion molecule (EpCAM (zeige EPCAM ELISA Kits)) was most suitable to detect lobular ovarian metastases.
analysis of a novel SMAD (zeige SMAD1 ELISA Kits)-independent pathway linking enhanced activin B (zeige Actbeta ELISA Kits) signaling to reduced E-cadherin expression and increased migration in type II endometrial cancer
Data indicate that CDH11, ICAM1 (zeige ICAM1 ELISA Kits) and CLDN3 (zeige CLDN3 ELISA Kits) were overexpressed in tumors when compared to normal esophagus, normal gastric and non-dysplastic Barrett's.
The combined biomarkers E-cadherin, membranous epidermal growth factor receptor (EGFR (zeige EGFR ELISA Kits)) and vimentin (zeige VIM ELISA Kits) show a stronger prognostic value for and disease-free survival than any of the single biomarkers.
aberrant Notch1 (zeige NOTCH1 ELISA Kits) is linked to hepatocellular carcinoma development, tumor recurrence and invasion, which might be mediated, at least in part, through the Notch1 (zeige NOTCH1 ELISA Kits)-E-Cadherin pathway
Findings unveil a negative role for PKC-delta (zeige PKCd ELISA Kits) in cell-cell adhesion through phosphorylation of E-cadherin.
Amla extract (Emblica officinalis, AE) decreases the gene and protein expression of IGF1R (zeige IGF1R ELISA Kits), a target of miR (zeige MLXIP ELISA Kits)-375, and SNAIL1 (zeige SNAI1 ELISA Kits), a transcription factor that represses E-cadherin expression.
These results provide the first in vivo evidence that Flotillins regulate E-cadherin-mediated cell-cell junctions to allow epiboly progression.
These collective findings indicate that loss of Bit1 (zeige PTRH2 ELISA Kits) expression contributes to the acquisition of malignant phenotype of human lung epithelial cells via Erk (zeige MAPK1 ELISA Kits) activation-induced suppression of E-cadherin expression.
In zebrafish, E-cadherin is expressed in lens epithelium, whereas N-cadherin (zeige CDH2 ELISA Kits) is required for lens fiber growth
These data indicate that emi1 (zeige FBXO5 ELISA Kits) deficiency-induced defects in vivo are due to the dysregulation of an APC/C-Cdh1 molecular axis.
without Chp (zeige CHP ELISA Kits) signaling, E-cadh shifts to intracellular vesicles rather than the adhesive contacts needed for directed cell movement during epiboly
Downregulation of E-cadherin gene may cause omphalocele in the Cd chick model by disrupting CRT (zeige CALR ELISA Kits)-mediated Ca(2 (zeige CA2 ELISA Kits)+) signaling and AJs.
analyzed expression patterns of three zebrafish classical (type I) cadherins (cadherin-1, -2, and -4) in the embryonic zebrafish cranial ganglia and lateral line system
cadherin-1 is detected in the epidermis of the embryonic limb buds and the larval pectoral fins of zebrafish
hab/E-cadherin is necessary for the cell rearrangements that spread the teleost blastoderm over the yolk
Lgl2 (zeige LLGL2 ELISA Kits) and E-cadherin act antagonistically to control the localisation of integrin alpha 6 (zeige ITGA6 ELISA Kits) during the formation of hemidesmosomes in the developing epidermis
E-cadherin mRNA/protein were up-regulated in all flutamide-treated corpus luteum of mid- and late pregnancy.
In pig kidney, strong E-cadherin expression was observed in the basolateral plasma membrane of the tubular epithelial cells. E-cadherin immunolabeling was not detected in glomeruli or blood vessels of pig kidney.
Localisation of NANOG (zeige NANOG ELISA Kits), OCT4 (zeige POU5F1 ELISA Kits), and E-CADHERIN in porcine pre- and peri (zeige PLIN1 ELISA Kits)-implantation embryos.
The epiblast expressed epithelial markers, MUC1 (zeige MUC1 ELISA Kits) and E-CADHERIN, and the pluripotency markers, DNMT3B (zeige DNMT3B ELISA Kits) and CRIPTO (zeige TDGF1 ELISA Kits).
JNK deficient embryos also have increased intercellular adhesion and defects in e-cadherin localization. Conversely, embryos with overactive JNK have epidermal fragility, increased E-cadherin internalization, and increased membrane localized clathrin.
E-cadherin has a role in cranial neural crest migration in Xenopus laevis
the switch from E- to N-cadherin (zeige CDH2 ELISA Kits) during epithelial-mesenchymal transition is essential for acquisition of Contact inhibition of locomotion behavior.
Moderate attenuation of C-cadherin function affects cell adhesion but not gastrulation.
Because paraxial protocadherin and C-cadherin do not directly interact nor form a joint complex with Fz7, Wnt-11 triggers formation of two distinct complexes that act in parallel to reduce cell adhesion by hampering clustering of C-cadherin.
The functional and physical relationships between PAPC, FLRT3, and C-cadherin, was investigated.
PAPC mediates these functions by down-regulating the adhesion activity of C-cadherin.
Results suggest that the basis for cell segregation during morphogenesis does not map exclusively to protein-level differences in E-, N-, or C-cadherin adhesion.
G-protein-coupled receptors control cortical actin assembly by controlling the amount of cadherin expressed on the cell surface.
Two stage cadherin kinetics require multiple extracellular domains but not the cytoplasmic region
Study shows that over time, epithelial tumor cells undergo epithelial state to a mesenchymal-like state changes (including loss of E-cadherin expression) during primary tumor growth and E-cadherin is re-expressed in metastatic tumor cells.
This study reveals a novel role for Cdh1 in craniofacial development through promoting APC (zeige APC ELISA Kits)-dependent non-proteolytic ubiquitination and activation of Gsc (zeige GSC ELISA Kits).
Neutrophil elastase has the capacity to cleave E-cad and interfere with its cell-cell adhesion function in acutely injured lung epithelium.
We describe a mouse model in which inducible deletion of E-cadherin in prostate luminal cells results in their apoptotic cell death by anoikis, in the absence of phenotypic effects in the surrounding stroma
Our results provide a mechanistic explanation for the spontaneous emergence of pluripotent cells from GSC (zeige GSC ELISA Kits) cultures; namely, rare GSCs upregulate CDH1 and initiate MET, processes normally kept in check by ZEB1 (zeige ZEB1 ELISA Kits) and TGF-beta (zeige TGFB1 ELISA Kits) signaling, thereby ensuring germ cells are protected from aberrant acquisition of pluripotency.
PTEN loss in E-cadherin-deficient mouse mammary epithelial cells rescues apoptosis and results in development of classical invasive lobular carcinoma.
Low CDH1 expression is associated with Gastric Tumorigenesis.
These observations highlight the relevance of APC (zeige APC ELISA Kits)/C cofactor Cdh1 activity during G1 to ensure an adequate supply of deoxynucleoside triphosphates to the replisome, prevent replication stress and the resulting chromosomal breaks and, ultimately, suppress tumorigenesis.
Ilk (zeige ILK ELISA Kits) and ELMO2 (zeige ELMO2 ELISA Kits) modulate recycling endosomes in keratinocytes undergoing intercellular adhesion mediated through cell-cell contacts, including E-cadherin-based adherens junctions.
JNK (zeige MAPK8 ELISA Kits) signaling, which is inversely correlated with WNT4 (zeige WNT4 ELISA Kits), plays an important role in perinatal germline cyst breakdown and primordial follicle formation by regulating E-cadherin junctions between oocytes in mouse ovaries.
Transfection of zygotes with 100 and 200 nM E-cadherin siRNA led to a 72 and 38% reduction, respectively, in E-cadherin mRNA relative abundance in Day 7 blastocysts compared with controls.
E-cadherin and beta-catenin (zeige CTNNB1 ELISA Kits) were distributed not only at the cell to cell boundary but throughout the cytoplasm in binucleate trophoblast cells
Results describe the effect of suppression of connexin 43 (zeige GJA1 ELISA Kits) and E-cadherin on the development, mRNA and protein expression of bovine blastocysts cultured in vitro or in vivo.
This gene is a classical cadherin from the cadherin superfamily. The encoded protein is a calcium dependent cell-cell adhesion glycoprotein comprised of five extracellular cadherin repeats, a transmembrane region and a highly conserved cytoplasmic tail. Mutations in this gene are correlated with gastric, breast, colorectal, thyroid and ovarian cancer. Loss of function is thought to contribute to progression in cancer by increasing proliferation, invasion, and/or metastasis. The ectodomain of this protein mediates bacterial adhesion to mammalian cells and the cytoplasmic domain is required for internalization. Identified transcript variants arise from mutation at consensus splice sites.
, cadherin 1, E-cadherin (epithelial)
, calcium-dependent adhesion protein, epithelial
, cell-CAM 120/80
, epithelial cadherin
, cadherin 1, epithelial
, half baked
, cadherin 1, type 1, E-cadherin (epithelial)
, liver cell adhesion molecule
, liver cell adhesion protein
, Epithelial cadherin