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 (show CD4 ELISA Kits)(+) 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 (show CNTNAP2 ELISA Kits), including CNTN2 (show CNTN2 ELISA Kits), KCNAs, members of the ADAM family (ADAM22 (show ADAM22 ELISA Kits), ADAM23 and ADAM11 (show ADAM11 ELISA Kits)), members of LGI family and MAGUKs (DLGs and MPPs (show MPHOSPH6 ELISA Kits)).

3. Adam23 knockdown up-regulates P27KIP1 (show CDKN1B ELISA Kits) 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 (show LGI3 ELISA Kits)) may be a candidate adipokine that is perturbed in obesity and suppresses adipogenesis through its receptor, ADAM23.

5. Data suggest that LGI1 (show LGI1 ELISA Kits) 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 (show PRNP ELISA Kits)) 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. ADAM23 regulates neuronal differentiation by triggering specific signaling pathways during human neural progenitor cells differentiation.

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

3. 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

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

5. quantification of CXCL12 (show CXCL12 ELISA Kits) and ADAM23 methylation could be useful for the prediction of advanced stage of BC

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

7. 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.

8. a SP1 (show PSG1 ELISA Kits) binding site (-202/-190) that binds SP1 (show PSG1 ELISA Kits) at the proximal promoter of human ADAM23 gene was indentified.

9. 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.

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