Browse our Cadherin 4 Proteins (CDH4)

Mouse (Murine) Cadherin 4 (CDH4) interaction partners

1. 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.

2. Pioneer axon outgrowth was rescued in vivo by selective replacement of R-cadherin by electroporation into cultured Pax6 mutant embryos

3. analysis of subpopulations of HSCs for expression of cell surface adhesion molecules found that R-cadherin was preferentially expressed by HSCs functionally targeting neovascularization in the developing retina

4. Killer cell lectin-like receptor G1 (KLRG1) ligation by R-cadherin may regulate the cytotoxicity of killer cells to prevent damage to tissues expressing cadherins.

5. suggest that R-cad is an adhesion molecule of the mammary epithelium, which acts as a critical regulator of the normal phenotype

Zebrafish Cadherin 4 (CDH4) interaction partners

1. 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

2. analyzed expression patterns of three zebrafish classical (type I) cadherins (cadherin-1, -2, and -4) in the embryonic zebrafish cranial ganglia and lateral line system

3. Cadherin-4 was not detected in the embryonic Zebrafish cerebellum, but it was expressed in the Purkinje cells of the larval and adult cerebellum.

4. Cdh4 is necessary for neural retina survival and differentiation

5. Results indicate that Cdh4 plays a role in the normal formation of the zebrafish lateral line system and a subset of the cranial ganglia.

Human Cadherin 4 (CDH4) interaction partners

1. CDH4 overexpression activates c-Jun via the JNK pathway, while CDH4 knockdown suppresses both tumor xenograft growth and lung colonization.

2. CDH4 may play a negative role in the growth and metastasis of salivary adenoid cystic carcinoma via co-expression with E-cadherin.

3. Low expression of CDH4 is associated with lung cancer.

4. Further knockdown R-cadherin in linc-cdh4-2 stably overexpressed cells, could significantly upregulate the protein levels of RAC1 and improve the cell migration and invasion abilities. Taken together, the novel linc-cdh4-2 may negatively regulate the motility of the HCC cells through targeting R-cadherin-RAC1 signaling pathway.

5. Data show that low expression of R-cadherin is associated with the poor prognosis in gastric cancer.

6. P-cadherin expression correlated with tumor progression and could be an independent predictor for bladder cancer survival.

7. R-cadherin adherens junction formation facilitates a mesenchymal to epithelial-like transition in MDA-MB-231 cells.

8. Findings identify an important role of CHD4 in controlling homologous recombination repair to maintain genome stability and establish the potential therapeutic implications of targeting CHD4 deficiency in tumors.

9. a novel putative tumor suppressor gene that can be frequently and tumor-specifically inactivated by its promoter methylation in nasopharyngeal carcinoma

10. R-cadherin induces cell motility when expressed in epithelial cells, and this increased motility is dependent upon Rho GTPase activity.

11. CDH4 may act as a tumor suppressor gene in human gastrointestinal tumors and can potentially be used as an early diagnostic marker for gastrointestinal tumorigenesis

12. the degradation of E-cadherin in response to expression of R-cadherin is due to competition for p120(ctn)

Caenorhabditis elegans (C. elegans) Cadherin 4 (CDH4) interaction partners

1. loss of the cell adhesion molecule (CAM) CDH-4/Fat-like cadherin causes dendrites to be ordered randomly, despite remaining bundled. Loss of the CAMs PTP-3/LAR or SAX-7/L1CAM causes dendrites to adopt an altered order, which becomes increasingly random as animals grow.

2. The fat-like cadherin CDH-4 acts cell-non-autonomously in anterior-posterior neuroblast migration.

3. CDH-4 functions to ensure that proper cell contacts are made and maintained during development.