ADAM Metallopeptidase Domain 23 (Adam23) ELISA Kits

Mouse (Murine) ADAM Metallopeptidase Domain 23 (Adam23) interaction partners

1. ADAM23 expression on DCs partially governs antigen-presentation capacities to responder CD4(+) T cells. Knockdown did not alter the maturation profile of DCs but impaired cognate T cell responses, decreased antigen-specific clonal expansion, and decreased Th cytokine production. Targeting the alpha(v)beta(3) integrin receptors resulted in similar phenotypes indicating their role in the ADAM23 response.

2. Interaction proteomics revealed the interactors of Caspr2, including CNTN2, KCNAs, members of the ADAM family (ADAM22, ADAM23 and ADAM11), members of LGI family and MAGUKs (DLGs and MPPs).

3. Adam23 knockdown up-regulates P27KIP1 in P19/ADAM23 knockdown cells, one reason that P19/ADAM23 knockdown cells can differentiate into neurons without retinoic acid induction.

4. Data suggest that leucine-rich glioma inactivated 3 (LGI3) may be a candidate adipokine that is perturbed in obesity and suppresses adipogenesis through its receptor, ADAM23.

5. Data suggest that LGI1 binding to ADAM23 is necessary to correctly pattern neuronal morphology, and altered anatomical patterning contributes to autosomal dominant partial epilepsy with auditory features.

6. These results suggest ADAM23 may play roles in both early and later stage of neuronal differentiation.

7. PrP(C) is a novel molecular partner for ADAM23 in the nervous systems.

8. Functional role of ADAM23 during lung cancer metastatic progression by negatively modulating alpha(v)beta(3) integrin activation.

Human ADAM Metallopeptidase Domain 23 (Adam23) interaction partners

1. The relationships between the decreased methylation levels of the SNAI2 and ADAM23 genes and cancer de-differentiation and haematogenous dissemination, respectively, indicate novel functions of those genes in the invasive processes.

2. Our results demonstrate that ADAM23 expression is likely involved in the progression of epithelial ovarian cancer

3. ADAM23 regulates neuronal differentiation by triggering specific signaling pathways during human neural progenitor cells differentiation.

4. these results support the existence of a second mechanism, alternative to inhibition of protein secretion, by which ADLTE-causing LGI1 mutations exert their loss-of-function effect extracellularly, and suggest that interactions of LGI1 with both ADAM22 and ADAM23 play an important role in the molecular mechanisms leading to utosomal dominant lateral temporal epilepsy

5. Our data provide evidence that ADAM23 plays a role in suppression of cancer cell progression through interaction with aVb3 integrin, and suggest that downregulation of ADAM23 in SP cells may contribute toward providing a cancer stem cell phenotype

6. High ADAM23 gene methylation is associated with gastric tumor aggressiveness.

7. quantification of CXCL12 and ADAM23 methylation could be useful for the prediction of advanced stage of BC

8. Intratumoral heterogeneity of ADAM23 promotes tumor growth and metastasis through LGI4 and nitric oxide signals.

9. The expression level of ADAM23 is likely to be involved in the progression of non-small-cell lung carcinoma, and its downregulation is probably correlated with promoter methylation.

10. a SP1 binding site (-202/-190) that binds SP1 at the proximal promoter of human ADAM23 gene was indentified.

11. Together, these results indicate that ADAM23 down-regulation by methylation in brain tumors is a rare event and it may help explain why brain tumor metastases are rarely found elsewhere in the body.

12. ADAM23 is frequently silenced in gastric cancers by homozygous deletion or aberrant promoter methylation.

13. ADAM23 may be down-regulated by aberrant promoter hypermethylation during the progression of colorectal cancer.

14. PrP(C) is a novel molecular partner for ADAM23 in the nervous systems.

15. Functional role of ADAM23 during lung caner metastatic progression by negatively modulating alpha(v)beta(3) integrin activation.