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Human N-Cadherin ELISA Kit for Sandwich ELISA - ABIN414714
Vandyke, Chow, Williams, To, Zannettino: Circulating N-cadherin levels are a negative prognostic indicator in patients with multiple myeloma. in British journal of haematology 2013
Show all 2 Pubmed References
PDGF-A (show PDGFA ELISA Kits)/PDGFRalpha signalling as a tissue-autonomous regulator of contact inhibition of locomotion by controlling N-cadherin upregulation during epithelial-to-mesenchymal transition.
the switch from E- to N-cadherin during epithelial-mesenchymal transition is essential for acquisition of Contact inhibition of locomotion behavior.
Migration of bone marrow-mesenchymal stem cells in response to TGF-beta (show TGFB1 ELISA Kits) was mediated through N-cadherin and noncanonical TGF-beta (show TGFB1 ELISA Kits) signals.
The dependence of migration of the fiber cell apical domains along the Epithelial Fiber Interface for lens morphogenesis on N-cadherin provides new insight into the process of tissue development.
in chicken and mouse embryos, PAPC (show PCDH8 ELISA Kits) expression is tightly regulated by the clock and wavefront system in the posterior PSM (show SH2B1 ELISA Kits) and exhibits a striking complementary pattern to N-cadherin
Loss of N-cadherin in the context of oncogenic K-ras leads to increased pancreatic intraepithelial neoplasia (PanIN) incidence and progression.
Type I collagen was highly expressed in the spinal cord during the scar-forming phase and induced astrocytic scar formation via the integrin-N-cadherin pathway.
cadherin 2 (CDH2) and CDH4 (show CDH4 ELISA Kits) cooperate to regulate radial migration in mouse brain via the protein tyrosine phosphatase 1B (PTP1B (show PTPN1 ELISA Kits)) and alpha- and beta-catenins.
N-cadherin-null enteric neural crest cells do not respond to C3a (show C3 ELISA Kits) co-attraction. C3a (show C3 ELISA Kits) regulates cell migration in a N-cadherin-dependent process.
Study demonstrates a critical role of presynaptic cadherin/catenin/p140Cap (show SRCIN1 ELISA Kits) cell adhesion complexes in stabilizing functional synapses and spines in the developing neocortex.
Knock-down of ZBED6 in insulin (show INS ELISA Kits)-producing cells promotes N-cadherin junctions between beta-cells and neural crest stem cells in vitro.
Knockdown of N-cadherin in 3T3 fibroblasts did not impede gap closure in a soft tissue wound healing model.
In zebrafish, E-cadherin (show CDH1 ELISA Kits) is expressed in lens epithelium, whereas N-cadherin is required for lens fiber growth
Newly synthesized N-cadherin molecules move from the lateral to the basal surface of cardiomyocytes during trabeculation. This localization requires Erbb2 (show ERBB2 ELISA Kits) signaling.
Throughout somitogenesis, Cadherin2 promotes extracellular matrix (ECM (show MMRN1 ELISA Kits)) assembly along tissue boundaries and inhibits ECM (show MMRN1 ELISA Kits) assembly in the tissue mesenchyme.
Cdon (show CDON ELISA Kits) is required to localize N-cadherin to the cell membrane in migratory neural crest cells for directed migration.
shows that a dominant-negative nuclear localization mutant of Sox3 (show SOX3 ELISA Kits) can cause ectopic expression of organizer genes via a mechanism that activates all of these earlier factors, resulting in later axis duplication including major bifurcations of the CNS.
Genetic suppression of N-cadherin function interferes with basal migration of retinal progenitors and subsequent regeneration of HuC (show ELAVL3 ELISA Kits)/D(+) inner retinal neurons.
N-cadherin deficiency in Danio does not prevent the first tooth from starting to develop, but stops its development at the early cytodifferentiation stage and completely inhibits the development of the other first-generation teeth.
N-cadherin regulates motor axon growth and branching without severely affecting the mechanisms that control axonal target selection.
Slit-Robo signaling downregulates N-cadherin activity to allow apical retraction in newly generated retinal ganglion cells.
demonstration of a novel mechanism of cell adhesion, mediated by a complex of Protocadherin-19 (Pcdh19 (show PCDH19 ELISA Kits)) and N-cadherin (Ncad)
Sec8 (show EXOC4 ELISA Kits) regulates N-cadherin expression by controlling Smad3 (show SMAD3 ELISA Kits) and Smad4 (show SMAD4 ELISA Kits) expression through CBP (show CREBBP ELISA Kits), thereby mediating the epithelial-mesenchymal transition.
Results found that the N-glycan at N402 is comprised of beta 1,6 GlcNAc branching and that in glioma, deficient N402 N-glycosylation destabilises N-cadherin and leads to its proteasomal degradation. Destabilisation of N-cadherin inhibits cadherin-mediated cell-cell adhesion and promotes cell migration. Our findings imply that the control of N-cadherin stability by N-glycosylation is important in glioma migration.
In adrenocortical carcinomas, the loss of N-cadherin is a frequent phenomenon while the existence of TERT (show TERT ELISA Kits) promoter mutations is not, and nuclear telomerase expression is present in only a minority of cases.
High CDH2 expression is associated with M2-type acute myeloid leukemia (show BCL11A ELISA Kits).
Results show that mesenchymal N-cadherin-expressing (Ncad+) cells and MCAs invade much more efficiently than E-cadherin (show CDH1 ELISA Kits)-expressing (Ecad (show CDH1 ELISA Kits)+) cells. Data emphasize the role of Ncad in intraperitoneal seeding of EOC and provide the rationale for future studies targeting Ncad in preclinical models of epithelial ovarian cancer metastasis.
Studied the roles of MIRN145 in lung adenocarcinoma (LAC (show LCT ELISA Kits)) and its targeting of N-cadherin. Knockdown of N-cadherin inhibited invasion and migration of LAC (show LCT ELISA Kits) cell lines similar to overexpression of MIRN45.
Genetic mutations in CDH2-encoded N-cadherin may represent a novel pathogenetic basis for arrhythmogenic cardiomyopathy.
Extracellular and intracellular cleavage of N-cadherin might be involved in elevated MMP-9 (show MMP9 ELISA Kits) expression enhancing tumor cell invasion.
Isoform b of DDR1 is responsible for collagen I-induced up-regulation of N-cadherin and tyrosine 513 of DDR1b is necessary.
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. The protein functions during gastrulation and is required for establishment of left-right asymmetry. At certain central nervous system synapses, presynaptic to postsynaptic adhesion is mediated at least in part by this gene product.
cadherin 2, type 1, N-cadherin (neuronal)
, neural cadherin
, cadherin 2 type 1 N-cadherin (neuronal)
, Neural cadherin
, glass onion
, N-cadherin 1
, cadherin 2, N-cadherin (neuronal)
, calcium-dependent adhesion protein, neuronal
, cadherin 2, type 1 preproprotein