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anti-Human E-cadherin Anticorps:
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Human Polyclonal E-cadherin Primary Antibody pour CyTOF, FACS - ABIN4899267
Ihermann-Hella, Lume, Miinalainen, Pirttiniemi, Gui, Peränen, Charron, Saarma, Costantini, Kuure: Mitogen-activated protein kinase (MAPK) pathway regulates branching by remodeling epithelial cell adhesion. dans PLoS genetics 2014
Show all 30 Pubmed References
Human Polyclonal E-cadherin Primary Antibody pour IHC (fro), IHC (p) - ABIN3043808
Duan, Lin, Li, Ding, Qian, Zhang, Ge, Fan, Li: Effects of inhibition of hedgehog signaling on cell growth and migration of uveal melanoma cells. dans Cancer biology & therapy 2014
Show all 30 Pubmed References
Human Polyclonal E-cadherin Primary Antibody pour CyTOF, FACS - ABIN4899263
Gaballah, Costea, Hills, Gollin, Harrison, Partridge: Tissue engineering of oral dysplasia. dans The Journal of pathology 2008
Show all 20 Pubmed References
Human Polyclonal E-cadherin Primary Antibody pour ELISA, ICC - ABIN6261408
Xiang, Deng, Liu, Wan, Feng, Chen, Xiong: MiR-1271 Inhibits Cell Proliferation, Invasion and EMT in Gastric Cancer by Targeting FOXQ1. dans Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 2016
Show all 19 Pubmed References
Human Polyclonal E-cadherin Primary Antibody pour IF, IHC - ABIN6711734
Hu, Yang, Hou, Zhang, Zeng, Zhao, Yu, Tang, Tu, Cui, Liu: LncRNA expression signatures of twist-induced epithelial-to-mesenchymal transition in MCF10A cells. dans Cellular signalling 2014
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Human Polyclonal E-cadherin Primary Antibody pour FACS, IF (cc) - ABIN1387847
Chen, Cheng, Chen, Sue, Liu, Cheng, Hsu, Chen: MicroRNA-328 inhibits renal tubular cell epithelial-to-mesenchymal transition by targeting the CD44 in pressure-induced renal fibrosis. dans PLoS ONE 2014
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Human Monoclonal E-cadherin Primary Antibody pour ELISA, FACS - ABIN4306576
Saulnier, Piscaglia, Puglisi, Barba, Arena, Pani, Alfieri, Gasbarrini: Molecular mechanisms underlying human adipose tissue-derived stromal cells differentiation into a hepatocyte-like phenotype. dans Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver 2010
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Human Monoclonal E-cadherin Primary Antibody pour ICC, IHC (fro) - ABIN335399
Frixen, Behrens, Sachs, Eberle, Voss, Warda, Löchner, Birchmeier: E-cadherin-mediated cell-cell adhesion prevents invasiveness of human carcinoma cells. dans The Journal of cell biology 1991
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Human Monoclonal E-cadherin Primary Antibody pour FACS, ICC - ABIN807921
Armeanu, Bühring, Reuss-Borst, Müller, Klein: E-cadherin is functionally involved in the maturation of the erythroid lineage. dans The Journal of cell biology 1995
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Human Monoclonal E-cadherin Primary Antibody pour FACS, ICC - ABIN457304
Pece, Gutkind: Signaling from E-cadherins to the MAPK pathway by the recruitment and activation of epidermal growth factor receptors upon cell-cell contact formation. dans The Journal of biological chemistry 2001
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The expression of E-cadherin in breast cancer positively correlated with FOXA1 (P = 0.028), whereas negative association was seen between the expression of Twist1 and FOXA1 (P = 0.016).
Calreticulin regulates syncytialization by ensuring appropriate control of both the synthesis and transportation of E-cadherin.
Studied E-cadherin - petidomimetic interactions using nuclear magnetic resonance spectroscopy and molecular docking simulation.
we present a diverse set of data indicating that the loss of E-cadherin enhances IGF1R pathway activity and sensitivity to IGF1R/InsR therapy.
In conditioned media of PIBF-deficient JEG-3 cells, primary lung and ovarian cancer cells MMP9 activity was reduced. PIBF silencing resulted in increased E-cadherin expression, suggesting that by down regulating E-cadherin expression, PIBF might interfere with the cell-cell adhesion mechanisms and by increasing MMP activity induced extracellular matrix degradation, facilitates the invasion of tumor cells.
EGFR-mediated kinase cascade controls the force-dependent recruitment of vinculin to stressed E-cadherin complexes - a key early signature of cadherin-based mechanotransduction.
Reciprocal loop of hypoxia-inducible factor-1alpha and metastasis-associated protein 2 contributes to the progression of pancreatic adenocarcinoma by suppressing E-cadherin transcription and promoting epithelial mesenchymal transformation.
alpha-catenin represents a bona fide tumor suppressor for the development of lobular-type breast cancer and as such provides an alternative event to E-cadherin inactivation, adherens junction dysfunction, and subsequent constitutive actomyosin contraction.
E-cadherin low expression is associated with lobular histology, tumor characteristics and menopausal hormone use, with no evidence of an association with breast cancer specific survival. These data support loss of E-cadherin expression as an important marker of tumor subtypes.
the definition of a specific protocol for CDH1 genetic screening and ongoing coordinated management of patients with Hereditary lobular breast cancer is crucial for the effective surveillance and early detection of lobular breast cancer.
It is a tumor suppressor gene and can be used as a biomarker to assess and evaluate the progression and prognosis of oral dysplastic lesions and oral squamous cell carcinoma.
decreased in Fallopian tube epithelium in tubal pregnancy
findings suggested that NSCLCAT1 potentially has a role in NSCLC and NSCLCAT1-mediated regulation of the Hippo signaling pathway through the transcriptional repression of CDH1
Both at the primary site and metastatic lymph nodes of invasive breast cancer samples, E-cadherin-positive tumors have worse disease-free and overall survival. E-cadherin and vimentin proteins are colocalized within the same tumor cells in a human breast cancer specimen.
E-cadherin expression on multiple myeloma cells activates tumor-promoting properties in plasmacytoid DCs.
restoring the expression of MIST1 reverses the EMT and reduces the tumorigenicity of pancreatic cancer cells partly via the Snail/E-cadherin pathway
E-cadherin and N-cadherin staining scores could be merged into a cadherin (CDH) logistic index, which showed better discrimination than E-cadherin or N-cadherin alone.
CBX7 and PRMT1 contribute to regulate E-cadherin expression through several mechanisms.
Review of the literature revealed a significant enrichment of CDH1 mutations within the extracellular cadherin repeat domains in cleft lip/palate/hereditary diffuse gastric cancer (CLP/HDGC) families in comparison to CDH1 mutations associated with HDGC only.
The frequency of E-cadherin promoter hypermethylation in CT is significantly higher than in AC, indicating that promoter hypermethylation of E-cadherin plays an important role in non-small cell lung cancer carcinogenesis.
These results also suggest the possibility that E- and N-cadherin have heterophilic interactions during early morphogenesis of the embryo; interactions that might help balance the variety of cell affinities needed during embryonic development.
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 expression contributes to the acquisition of malignant phenotype of human lung epithelial cells via Erk activation-induced suppression of E-cadherin expression.
In zebrafish, E-cadherin is expressed in lens epithelium, whereas N-cadherin is required for lens fiber growth
These data indicate that emi1 deficiency-induced defects in vivo are due to the dysregulation of an APC/C-Cdh1 molecular axis.
without Chp 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-mediated Ca(2+) 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 and E-cadherin act antagonistically to control the localisation of integrin alpha 6 during the formation of hemidesmosomes in the developing epidermis
Galpha12/13 regulate epiboly by inhibiting E-cadherin activity and modulating the actin cytoskeleton.
E-cadherin mRNA coinjection demonstrated the specificity of cdh1 morpholino oligonucleotides-induced defects
Results suggest that Wnt11 controls tissue morphogenesis by modulating E-cadherin-mediated cell cohesion through Rab5c, a novel mechanism of Wnt signaling in gastrulation.
E-cadherin/beta-catenin complex plays an important role in mediating the morphological remodeling of porcine trophoblast cells during placental development.
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, OCT4, and E-CADHERIN in porcine pre- and peri-implantation embryos.
The epiblast expressed epithelial markers, MUC1 and E-CADHERIN, and the pluripotency markers, DNMT3B and CRIPTO.
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.
the switch from E- to N-cadherin during epithelial-mesenchymal transition is essential for acquisition of Contact inhibition of locomotion behavior.
E-cadherin plays a salient role in platelet aggregation and clot stability
Study of transgenic mouse model provides insights into invasive lobular carcinoma (ILC) development by uncovering the direct consequences of E-cadherin inactivation in the mouse mammary gland and reveals actomyosin contractility as a critical barrier to ILC development. The discovery of actomyosin regulation as a druggable oncogenic pathway might provide therapeutic opportunities to treat E-cadherin mutated cancers.
Low CDH1 expression is associated with Reduced Checkpoint Blockade Responsiveness in Melanoma.
Cdh1 deletion in the gastric mucosa induces gastric metaplasia.
Deletion of Cdh1 and Pik3ca activation is associated with Immune-Related Invasive Lobular Carcinoma of the Breast.
changes in E-cadherin localisation during later PrE-to-PE transition
findings demonstrate that E-cadherin plays an integral role in the maintenance of exocrine architecture and regulation of homeostatic signaling. The present study provides insights into the involvement of cadherin-mediated cell-cell adhesion in pathogenic conditions such as pancreatitis or pancreatic cancer.
Study using metastatic murine mammary carcinoma cell line 4T1 shows that in sparsely plated 4T1 cells, E-cadherin levels are moderately reduced (~50%), leading to the development of collective migration. Knocking down E-cadherin blocked tether formation in these cells, leading to enhancement of migration rate and, at the same time, to suppression of lung metastases formation in murine mammary carcinoma model.
Cathepsin C regulates neutrophil elastase activation and E-cadherin cleavage in acute pancreatitis.
Studied action of a protective agent (PPBICA) on expression of E-cadherin, inflammation and apoptosis in cisplatin-induced acute kidney injury.
To uncover the molecular changes induced by the concurrent targeting of E-cadherin, p53, and Smad4 loss.
E-cadherin-mediated Mononuclear Phagocytes -epithelium adhesion is associated with the development of Colitis.
E-cadherin deletion leads to loss of cell polarity and disoriented cell division, which subsequently causes dysregulated cell proliferation and strongly predisposes mice for prostate tumorigenesis. We revealed that E-cadherin acts as an anchor to recruit cell polarity protein SCRIB and spindle positioning determinant LGN to the lateral cell membrane, thereby ensuring a proper alignment of the cell division plane.
O-GlcNAcylation of CDH1 is associated with tumorigenicity of colorectal cancer.
Data identify an E-cadherin-dependent mechanical circuit that integrates adhesion, contractile forces and biochemical signaling to drive the polarized organization of junctional tension necessary to build an in vivo epithelial barrier.
Adherens as well as tight junction marker proteins were rapidly and consistently upregulated in both the germinal as well as the functional layer of the oral mucosa. This represents a previously unknown parameter of the epithelial radiation response to clinically relevant fractionation protocols. CONCLUSION: Fractionated irradiation significantly enhanced the expression of all proteins investigated. This study revealed a
E-cadherin expression is reduced in prenatal pancreatic islets of Bmpr1a-deleted mice.
Real-time PCR showed E-cad mRNA decreased in SCC25 while increased in RAW 264.7 of the indirect cell co-culture model, and immunofluoresence (IF) observed the evident switch of E-cad staining from SCC25 to RAW 264.7
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 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 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
, hypothetical protein LOC368517
, cadherin 1, epithelial
, half baked
, cadherin 1, type 1, E-cadherin (epithelial)
, liver cell adhesion molecule
, liver cell adhesion protein
, Epithelial cadherin