Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
Human N-Cadherin Protein expressed in Human Cells - ABIN2003757
LaMora, Voigt: Cranial sensory ganglia neurons require intrinsic N-cadherin function for guidance of afferent fibers to their final targets. in Neuroscience 2009
Show all 5 Pubmed References
Human keratinocyte cells reduce the N-cadherin levels of co-cultured melanoma cells. Cell-to-cell contact is necessary for this keratinocyte-mediated N-cadherin reduction. Keratinocytes reduce intracellular calcium in co-cultured melanoma cells.
The FGFR4-388arg variant promotes lung cancer progression by N-cadherin induction.
This study showed that the significant N-cadherin expression especially in high-grade meningioma group.
Our experiments presented a new mechanism adopted by GDNF supporting glioma development and indicated a possible therapeutic potential via the inhibition of proN-cadherin/FGFR1 interaction.
Twist, E-cadherin, and N-cadherin protein were differently expressed in endometrioid adenocarcinoma tissues and in normal endometrium which indicates their potential function for endometrioid adenocarcinoma development.
In patients with gastric cancer, the strong expression of N-cadherin in lymph nodes correlated with more lymph nodes metastasis, an advanced stage, and poor prognosis
Regulatory networks specifying cortical interneurons from human embryonic stem cells reveal roles for CHD2 in interneuron development
mechanistic experiments revealed that ADAM10-RNAi resulted in an increase in E-cadherin and a decrease in N-cadherin and vimentin expression. Our study implies that high expression of ADAM10 promotes the proliferation and migration of hypopharyngeal squamous cell carcinoma (HSCC). These findings may help to provide a method for treatment of HSCC
A study with nonsyndromic cleft lip with or without cleft palate (NSCL+/-P) cases (N=292) and controls (N=287) established association of a SNP in intron 2 of CDH2 with NSCL+/-P as a risk factor.
Results show that N-cadherin is highly expressed in 70% of patients with glioma. However, N-cadherin, as a representative EMT marker, have limited prognostic value in glioma. Nonetheless, the EMT process in gliomas may be compounded by enhanced N-cadherin expression supported by unfavorable prognostic outcomes.
Findings reveal the importance of CDH2-mediated cell contacts in preserving features of the juvenile nucleus pulposus cell phenotype.
Tumor-promoting role of N-cadherin in thyroid cancer was closely related to the activities of the MAPK/Erk, the phosphatidylinositol-3-kinase (PI3K)/Akt and p16/Rb signaling pathways.
Triple negative breast cancer cells surviving short-term chemotherapy treatment are more invasive than bulk tumor cells. Cell surface pro-N-cadherin expression is associated with the invasive and chemo-resistant behaviors of this tumor cell subset.
Sec8 regulates N-cadherin expression by controlling Smad3 and Smad4 expression through CBP, 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 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.
Results show that mesenchymal N-cadherin-expressing (Ncad+) cells and MCAs invade much more efficiently than E-cadherin-expressing (Ecad+) 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.
Migration of bone marrow-mesenchymal stem cells in response to TGF-beta was mediated through N-cadherin and noncanonical TGF-beta signals.
Studied the roles of MIRN145 in lung adenocarcinoma (LAC) and its targeting of N-cadherin. Knockdown of N-cadherin inhibited invasion and migration of LAC cell lines similar to overexpression of MIRN45.
PDGF-A/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.
regulation of vesicle endocytosis was mediated at the molecular level by N-cadherin in a release activity-dependent manner. Because of its endocytosis enhancing function, N-cadherin might play an important role in the coupling of vesicle exo- and endocytosis.
Results indicate that embryos that express N-cad show altered BMP activity, resulting in an atrophied epiblast, inappropriate loss of cells into the amniotic cavity and inefficient patterning of the extraembryonic mesoderm.
The authors propose that AmotL1 is an essential effector of the N-cadherin mediated endothelial/pericyte junctional complex.
Reelin directly promotes N-cadherin-dependent neuronal adhesion, causing neuronal aggregation.
N-cadherin has different effects on osteolineage cells depending upon their differentiation stage.
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 expression is tightly regulated by the clock and wavefront system in the posterior PSM 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 cooperate to regulate radial migration in mouse brain via the protein tyrosine phosphatase 1B (PTP1B) and alpha- and beta-catenins.
N-cadherin-null enteric neural crest cells do not respond to C3a co-attraction. C3a regulates cell migration in a N-cadherin-dependent process.
Study demonstrates a critical role of presynaptic cadherin/catenin/p140Cap cell adhesion complexes in stabilizing functional synapses and spines in the developing neocortex.
Knock-down of ZBED6 in insulin-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.
N-cadherin modulates Lrp6/PTHR1 interaction, restraining the intensity of parathyroid hormone-induced beta-catenin signaling
Specific deletion of Cdh2 in Sertoli cells leads to altered meiotic progression and subfertility of mice.
CRP suppresses expression of N-cadherin (p < 0.01), a mesenchymal marker of EMT, and ZEB-1, an EMT-related transcription factor (p < 0.01). These findings suggest that CRP inhibits EMT in a MCA-38 tumor-bearing mouse model.
these studies suggest that N-cadherin may represent a viable therapeutic target to prevent the dissemination of MM PCs and delay MM disease progression.
N-cadherin is involved in neuronal activity-dependent regulation of myelinating capacity of zebrafish individual oligodendrocytes in vivo.
N-cadherin-defective endodermal cells resembled ectodermal cells; expression of N-cadherin sufficient to induce internalization of ectodermal cells
In zebrafish, E-cadherin 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 signaling.
Throughout somitogenesis, Cadherin2 promotes extracellular matrix (ECM) assembly along tissue boundaries and inhibits ECM assembly in the tissue mesenchyme.
Cdon 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 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/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) and N-cadherin (Ncad)
zebrafish N-cadherin restricts cell proliferation in the dorsal region of the neural tube by regulating cell-cycle length.
Protocadherin-19 and N-cadherin interact to control cell movements during anterior neurulation
the ratio of the number of cells undergoing neurogenic cell division to the total number of cells undergoing mitosis was decreased in retinas of n-cadherin knockout zebrafish.
Cadherin-2 plays a key role during zebrafish granule cell migration by continuously coordinating cell-cell contacts and cell polarity through the remodeling of adherens junctions.
Both Cdh2 and Cdh4 immunoreactivities were specifically up-regulated in regenerating retina and/or the optic pathway and both may be important for regeneration of injured retinal ganglion cell axons
cell adhesion mediated by N-cadherin is of major importance for retinal lamination and involved in maintenance of the lens epithelial sheet, but is not essential for the formation of photoreceptor ultrastructure or for synaptogenesis.
has several distinct and crucial functions during the establishment of retinal organization
Zebrafish N-cadherin, encoded by the glass onion locus, plays an essential role in retinal patterning.
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, N-cadherin (neuronal)
, calcium-dependent adhesion protein, neuronal
, neural cadherin
, cadherin 2, type 1, N-cadherin (neuronal)
, Neural cadherin
, cadherin 2, type 1 preproprotein
, cadherin 2 type 1 N-cadherin (neuronal)
, glass onion