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Adam23 encodes a member of the ADAM (a disintegrin and metalloprotease domain) family. Additionally we are shipping Adam23 Antibodies (70) and Adam23 Kits (3) and many more products for this protein.
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Interaction proteomics revealed the interactors of Caspr2 (show CNTNAP2 Proteins), including CNTN2 (show CNTN2 Proteins), KCNAs, members of the ADAM family (ADAM22 (show ADAM22 Proteins), ADAM23 and ADAM11 (show ADAM11 Proteins)), members of LGI family and MAGUKs (DLGs and MPPs (show MPHOSPH6 Proteins)).
Adam23 knockdown up-regulates P27KIP1 (show CDKN1B Proteins) in P19 (show CDKN2D Proteins)/ADAM23 knockdown cells, one reason that P19 (show CDKN2D Proteins)/ADAM23 knockdown cells can differentiate into neurons without retinoic acid induction.
Data suggest that leucine-rich glioma inactivated 3 (LGI3 (show LGI3 Proteins)) may be a candidate adipokine that is perturbed in obesity and suppresses adipogenesis through its receptor, ADAM23.
Data suggest that LGI1 (show LGI1 Proteins) binding to ADAM23 is necessary to correctly pattern neuronal morphology, and altered anatomical patterning contributes to autosomal dominant partial epilepsy with auditory features.
These results suggest ADAM23 may play roles in both early and later stage of neuronal differentiation.
PrP(C (show PRNP Proteins)) is a novel molecular partner for ADAM23 in the nervous systems.
Functional role of ADAM23 during lung cancer metastatic progression by negatively modulating alpha(v)beta(3) integrin activation.
these results support the existence of a second mechanism, alternative to inhibition of protein secretion, by which ADLTE (show LGI1 Proteins)-causing LGI1 (show LGI1 Proteins) mutations exert their loss-of-function effect extracellularly, and suggest that interactions of LGI1 (show LGI1 Proteins) with both ADAM22 (show ADAM22 Proteins) and ADAM23 play an important role in the molecular mechanisms leading to utosomal dominant lateral temporal epilepsy
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
High ADAM23 gene methylation is associated with gastric tumor aggressiveness.
quantification of CXCL12 (show CXCL12 Proteins) and ADAM23 methylation could be useful for the prediction of advanced stage of BC
Intratumoral heterogeneity of ADAM23 promotes tumor growth and metastasis through LGI4 and nitric oxide signals.
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.
a SP1 (show PSG1 Proteins) binding site (-202/-190) that binds SP1 (show PSG1 Proteins) at the proximal promoter of human ADAM23 gene was indentified.
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.
ADAM23 is frequently silenced in gastric cancers by homozygous deletion or aberrant promoter methylation.
ADAM23 may be down-regulated by aberrant promoter hypermethylation during the progression of colorectal cancer.
This gene encodes a member of the ADAM (a disintegrin and metalloprotease domain) family. Members of this family are membrane-anchored proteins structurally related to snake venom disintegrins, and have been implicated in a variety of biological processes involving cell-cell and cell-matrix interactions, including fertilization, muscle development, and neurogenesis. This gene is highly expressed in the brain and may function as an integrin ligand in the brain.
, a disintegrin and metalloprotease domain 23
, disintegrin and metalloproteinase domain-containing protein 23
, metalloproteinase-like, disintegrin-like, and cysteine-rich protein 3
, a disintegrin and metallopeptidase domain 23