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Human E-cadherin Protein expressed in HEK-293 Cells - ABIN2444102
Eshghi, Gaultney, England, Brûlé, Miras, Sato, Coburn, Bellalou, Moriarty, Haouz, Picardeau: An extracellular Leptospira interrogans leucine-rich repeat protein binds human E- and VE-cadherins. dans Cellular microbiology 2019
Show all 2 Pubmed References
SIRT1 induces the epithelial-mesenchymal transition (EMT) by accelerating E-cadherin degradation via autophagy and facilitates melanoma metastasis.
Six2 facilitates NSCLC cell stemness and attenuates chemotherapeutic sensitivity via suppressing E-cadherin expression.
TRERNA1 promotes cell metastasis and the invasion of HCC via the recruitment of EHMT2 and/or the EHMT2/SNAI1 complex to suppress CDH1.
Study results indicate that CDH1-160 C>A polymorphism does not contribute to the genetic susceptibility of colorectal cancer (CRC) and the polymorphism may not be a direct effect on the progression of the disease in Turkish CRC patients.
Results found that E-CAD expression is epigenetically suppressed by SNAIL2 during the metastasis of colorectal cancer.
We consider that the presence of long-standing diabetes mellitus has a negative impact on the prognosis of pancreatic ductal carcinoma patients which may be relevant to a high frequency of promoter methylation of CDH1
The analysis of chemosensitivity and E-cadherin expression in colorectal cell lines showed that the absence of E-cadherin in HCT116 cells correlated with their higher chemosensitivity, whereas HT29 cells with marked membrane E-cadherin expression were more resistant to all drugs tested
Low CDH1 expression is associated with Multicellular Spheroids in Breast Cancer during Simulated Microgravity.
High CDH1 expression is associated with invasive breast carcinoma.
73.0% of the evaluated tumors showed abnormal E-cadherin expression in IHC.
Upon identification of a homogenous downregulated profile for miR-205-5p in colon adenocarcinoma patients, functional studies demonstrated that experimental upregulation of this sequence is able to significantly raise the levels of E-cadherin through direct inhibition of ZEB1.
Aberrant expression of E-cad may be a promising prognostic signature for HNSCC, especially when it is used with other prognostic markers.
CHIP depletion inhibited cell growth, migration and invasion potential of colorectal cancer cells, accompanied by downregulation of MAPK and AKT signaling activities and upregulation of E-cadherin.
Results found that NRBE3 down-regulates E-cadherin expression by suppressing its transcription which expression is negatively correlated with NRBE3 expression in breast cancer tissues and cell lines.
Ecadherin expression levels were regulated by the manifold, and UPF1, a potential tumor suppressor, may promote the EMT process in Huh7 HCC cells. The findings of the present study suggested that UPF1 expression levels affected the EMT process by targeting Ecadherin, Ncadherin, Vimentin and Twist.
Investigated twist family bHLH transcription factor 1 (Twist), snail family transcriptional repressor 1 (Snail) and E-cadherin in prognosis, recurrence-free survival and overall survival in completely resected N0 NSCLC patients. Found high expression of Twist and Snail and low expression of E-cadherin were associated with unfavourable prognosis.
Study confirmed the association between CDH1 C/T polymorphisms and the risk of developing vitiligo. A relationship was found between CDH1 CC genotype and late age of onset, clinical type, the absence of autoimmune comorbidities and there family history. However, CDH1 TT genotype was found to be increased significantly in patients with autoimmune comorbidities.
CDH1 rs5030625 GAGA genotype is associated with Familial Breast Cancer risk.
the ability of an inflammatory protease, neutrophil elastase, to process the adherens junction protein E-cadherin to generate short peptide fragments with effects on epithelial function, is reported.
Helicobacter pylori plays an important role in the development and progression of gastric carcinoma through silencing of CDH1, RUNX3, p21WAF and p27 expression
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.
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
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.
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