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VIM is downregulated and E-cad is upregulated in T1 stage non-small-cell lung cancer, suggesting that a mesenchymal-epithelial transition may take place in the early-stage of tumor development
Reduced membranous expression of E-cadherin and increased cytoplasmic E-cadherin expression predict poor survival in metastatic colorectal cancer.
While no pathogenic somatic mutations were found that could explain the diffuse histology of gastric cancer in DGC and MGC, methylation was the most common somatic inactivation event of the CDH1 gene, and LOH was rare. The previously unreported c.-137C > A variant modify the CDH1 gene expression since it alters the binding sites for transcription factors.
only residual disease and negative E-cadherin immunoexpression were useful independent predictors of unfavourable clinical outcome and shorter overall survival in ovarian serous carcinomas
The CDH1 -160C/A polymorphism was significantly associated with CRC risk.
Results strongly indicate a protective role of allele A of the SNP CHD1 -160C>A against urinary calculi formation in children.
Low E-cadherin immunoexpression among pT3b prostate carcinoma patients indicates those with poorer survival and might benefit from specific therapy.
Silent gonadotroph tumours presented high immunoreactive score (IRS) for N-cadherin and low IRS for the extracellular domain of E-cadherin. A substantial proportion of the tumours presented nuclear staining for the intracellular domain of E-cadherin, accompanied by a reduced membranous expression of the intracellular domain of E-cadherin.
CDH1 germline missense variant segregates with gastric cancer in three unrelated Spanish families.
The authors demonstrate that Ecad interacts with isoform 2 of Dsg via a conserved Leu-175 on the Ecad cis binding interface and facilitates desmosome assembly.
CDH1 -160C/A and Exo1 K589E polymorphisms are associated with increased susceptibility to prostate cancer in Bangladeshi population.
Findings provide evidence that p.L13_L15del variant affects a conserved region of the CDH1 signal peptide core which is essential for E-cadherin synthesis and delivery. Failure in this checkpoint leads to loss of protein expression and function, and ultimately to Hereditary Diffuse Gastric Cancer.
Study identifies an epigenetic regulation of Ecadherin expression by the methylation and acetylation of H3K27 in gastric neoplasm.
Lobular breast cancer (LBC) is a component of the Hereditary Diffuse Gastric Cancer (HDGC) syndrome as a sporadic or familial setting. and novel E-cadherin germline mutations have recently been detected in women affected by LBCs without history for HDGC
Low CDH1 expression is associated with metastasis in breast cancer.
Low CDH1 expression is associated with Hepatocellular Carcinoma.
CDH1 variants are significantly reverse associated with mutation of EGFR tyrosine kinase;CDH1 variants might contribute to pathological development in lung adenocarcinoma
EZH2-mediated epigenetic suppression of EphB3 inhibits gastric cancer proliferation and metastasis by affecting E-cadherin and vimentin expression.
The progression of the endometrioid carcinoma may occur in the setting of various molecular changes, in particular, with decreased expression of E-cadherin and b-catenin and high expression of vimentin, or in the absence of vimentin, utilizing other mechanisms of regulation of proliferative and metastatic potential.
We examined effects of induced mosaic knockdown of molecular regulators of cortical tension (ROCK1) and cell-cell adhesion (CDH1) with CRISPR interference. Mosaic knockdown of ROCK1 or CDH1 resulted in differential patterning within hiPSC colonies due to cellular self-organization, while retaining an epithelial pluripotent phenotype
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.
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
Study found that E-cad is crucial for proper morphogenesis and cell movements during gastrulation indicating that a tight spatio-temporal control of cadherin expression is mandatory for morphogenesis independent of their function in tissue sorting.
NAC1 downregulates the E-cadherin repressor ZEB1 directly via transcriptional repression.
Stretch induced p120 degradation and the endocytosis of E-cadherin, which induced beta-catenin translocation into the nucleus, a key event in lung injury progress and repair.
IGF-II-mediated loss of E-cadherin is central in developing hepatomegaly in mice and abnormal cell growth in the hepatoma cell line
Overall, hypoxia-induced activation of Twist/miR-214/E-cadherin axis is involved in the EMT of TECs, and anti-miR-214 may be an attractive strategy to ameliorate the progression of renal fibrosis.
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.
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 cultures; namely, rare GSCs upregulate CDH1 and initiate MET, processes normally kept in check by ZEB1 and TGF-beta 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.
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