Browse our N-Cadherin Proteins (CDH2)

Human Cadherin 2 (CDH2) interaction partners

1. This study showed that the significant N-cadherin expression especially in high-grade meningioma group.

2. 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 (show FGFR1 Proteins) interaction.

3. Twist, E-cadherin (show CDH1 Proteins), and N-cadherin protein were differently expressed in endometrioid adenocarcinoma tissues and in normal endometrium which indicates their potential function for endometrioid adenocarcinoma development.

4. 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

5. Regulatory networks specifying cortical interneurons from human embryonic stem cells reveal roles for CHD2 in interneuron development

6. mechanistic experiments revealed that ADAM10 (show ADAM10 Proteins)-RNAi resulted in an increase in E-cadherin (show CDH1 Proteins) and a decrease in N-cadherin and vimentin (show VIM Proteins) expression. Our study implies that high expression of ADAM10 (show ADAM10 Proteins) promotes the proliferation and migration of hypopharyngeal squamous cell carcinoma (HSCC). These findings may help to provide a method for treatment of HSCC

7. A study with nonsyndromic cleft lip with or without cleft palate (NSCL (show NHLH1 Proteins)+/-P) cases (N=292) and controls (N=287) established association of a SNP in intron 2 of CDH2 with NSCL (show NHLH1 Proteins)+/-P as a risk factor.

8. Results show that N-cadherin is highly expressed in 70% of patients with glioma. However, N-cadherin, as a representative EMT (show ITK Proteins) marker, have limited prognostic value in glioma. Nonetheless, the EMT (show ITK Proteins) process in gliomas may be compounded by enhanced N-cadherin expression supported by unfavorable prognostic outcomes.

9. Findings reveal the importance of CDH2-mediated cell contacts in preserving features of the juvenile nucleus pulposus cell phenotype.

10. 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.

Xenopus laevis Cadherin 2 (CDH2) interaction partners

1. 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.

2. the switch from E- to N-cadherin during epithelial-mesenchymal transition is essential for acquisition of Contact inhibition of locomotion behavior.

Mouse (Murine) Cadherin 2 (CDH2) interaction partners

1. 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.

2. 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.

3. The authors propose that AmotL1 is an essential effector of the N-cadherin mediated endothelial/pericyte junctional complex.

4. Reelin (show RELN Proteins) directly promotes N-cadherin-dependent neuronal adhesion, causing neuronal aggregation.

5. N-cadherin has different effects on osteolineage cells depending upon their differentiation stage.

6. 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.

7. 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.

8. 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

9. Loss of N-cadherin in the context of oncogenic K-ras leads to increased pancreatic intraepithelial neoplasia (PanIN) incidence and progression.

10. 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.

Zebrafish Cadherin 2 (CDH2) interaction partners

1. N-cadherin-defective endodermal cells resembled ectodermal cells; expression of N-cadherin sufficient to induce internalization of ectodermal cells

2. In zebrafish, E-cadherin (show CDH1 Proteins) is expressed in lens epithelium, whereas N-cadherin is required for lens fiber growth

3. 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.

4. 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.

5. Cdon (show CDON Proteins) is required to localize N-cadherin to the cell membrane in migratory neural crest cells for directed migration.

6. 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.

7. 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.

8. 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.

9. N-cadherin regulates motor axon growth and branching without severely affecting the mechanisms that control axonal target selection.

10. Slit-Robo signaling downregulates N-cadherin activity to allow apical retraction in newly generated retinal ganglion cells.