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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
A study with nonsyndromic cleft lip with or without cleft palate (NSCL (zeige NHLH1 Proteine)+/-P) cases (N=292) and controls (N=287) established association of a SNP in intron 2 of CDH2 with NSCL (zeige NHLH1 Proteine)+/-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 (zeige ITK Proteine) marker, have limited prognostic value in glioma. Nonetheless, the EMT (zeige ITK Proteine) 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 (zeige MAPK1 Proteine), the phosphatidylinositol-3-kinase (PI3K (zeige PIK3CA Proteine))/Akt (zeige AKT1 Proteine) 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 (zeige EXOC4 Proteine) regulates N-cadherin expression by controlling Smad3 (zeige SMAD3 Proteine) and Smad4 (zeige SMAD4 Proteine) expression through CBP (zeige CREBBP Proteine), 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 (zeige TERT Proteine) 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 (zeige BCL11A Proteine).
Results show that mesenchymal N-cadherin-expressing (Ncad+) cells and MCAs invade much more efficiently than E-cadherin (zeige CDH1 Proteine)-expressing (Ecad (zeige CDH1 Proteine)+) 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.
PDGF-A (zeige PDGFA Proteine)/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.
The authors propose that AmotL1 is an essential effector of the N-cadherin mediated endothelial/pericyte junctional complex.
Reelin (zeige RELN Proteine) directly promotes N-cadherin-dependent neuronal adhesion, causing neuronal aggregation.
N-cadherin has different effects on osteolineage cells depending upon their differentiation stage.
Migration of bone marrow-mesenchymal stem cells in response to TGF-beta (zeige TGFB1 Proteine) was mediated through N-cadherin and noncanonical TGF-beta (zeige TGFB1 Proteine) 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 (zeige PCDH8 Proteine) expression is tightly regulated by the clock and wavefront system in the posterior PSM (zeige SH2B1 Proteine) 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 (zeige CDH4 Proteine) cooperate to regulate radial migration in mouse brain via the protein tyrosine phosphatase 1B (PTP1B (zeige PTPN1 Proteine)) and alpha- and beta-catenins.
N-cadherin-null enteric neural crest cells do not respond to C3a (zeige C3 Proteine) co-attraction. C3a (zeige C3 Proteine) regulates cell migration in a N-cadherin-dependent process.
In zebrafish, E-cadherin (zeige CDH1 Proteine) 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 (zeige ERBB2 Proteine) signaling.
Throughout somitogenesis, Cadherin2 promotes extracellular matrix (ECM (zeige MMRN1 Proteine)) assembly along tissue boundaries and inhibits ECM (zeige MMRN1 Proteine) assembly in the tissue mesenchyme.
Cdon (zeige CDON Proteine) 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 (zeige SOX3 Proteine) 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 (zeige ELAVL3 Proteine)/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 (zeige PCDH19 Proteine)) and N-cadherin (Ncad)
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