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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
PDGF-A (show PDGFA Proteins)/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 Proteins) was mediated through N-cadherin and noncanonical TGF-beta (show TGFB1 Proteins) 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 Proteins) expression is tightly regulated by the clock and wavefront system in the posterior PSM (show SH2B1 Proteins) 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 Proteins) cooperate to regulate radial migration in mouse brain via the protein tyrosine phosphatase 1B (PTP1B (show PTPN1 Proteins)) and alpha- and beta-catenins.
N-cadherin-null enteric neural crest cells do not respond to C3a (show C3 Proteins) co-attraction. C3a (show C3 Proteins) regulates cell migration in a N-cadherin-dependent process.
Study demonstrates a critical role of presynaptic cadherin/catenin/p140Cap (show SRCIN1 Proteins) cell adhesion complexes in stabilizing functional synapses and spines in the developing neocortex.
Knock-down of ZBED6 in insulin (show INS Proteins)-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 Proteins) 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 Proteins) signaling.
Throughout somitogenesis, Cadherin2 promotes extracellular matrix (ECM (show MMRN1 Proteins)) assembly along tissue boundaries and inhibits ECM (show MMRN1 Proteins) assembly in the tissue mesenchyme.
Cdon (show CDON Proteins) 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 Proteins) 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 Proteins)/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 Proteins)) and N-cadherin (Ncad)
Tumor-promoting role of N-cadherin in thyroid cancer was closely related to the activities of the MAPK/Erk (show MAPK1 Proteins), the phosphatidylinositol-3-kinase (PI3K (show PIK3CA Proteins))/Akt (show AKT1 Proteins) 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 (show EXOC4 Proteins) regulates N-cadherin expression by controlling Smad3 (show SMAD3 Proteins) and Smad4 (show SMAD4 Proteins) expression through CBP (show CREBBP Proteins), 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 Proteins) 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 Proteins).
Results show that mesenchymal N-cadherin-expressing (Ncad+) cells and MCAs invade much more efficiently than E-cadherin (show CDH1 Proteins)-expressing (Ecad (show CDH1 Proteins)+) 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 Proteins)) and its targeting of N-cadherin. Knockdown of N-cadherin inhibited invasion and migration of LAC (show LCT Proteins) cell lines similar to overexpression of MIRN45.
Genetic mutations in CDH2-encoded N-cadherin may represent a novel pathogenetic basis for arrhythmogenic cardiomyopathy.
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