Disintegrin and metalloproteinase domain-containing protein 23 is a non-catalytic protein that in humans is encoded by the ADAM23 gene. [5][6] It is a member of the ADAM family of extracellular matrix metalloproteinases.

Mar 30, 2025 · ADAM23 (ADAM Metallopeptidase Domain 23) is a Protein Coding gene. Diseases associated with ADAM23 include Epilepsy, Familial Temporal Lobe, 1 and Anterograde Amnesia. Among its related pathways are Nervous system development and …

Mar 24, 2014 · Here, we show that invasive breast tumors exhibit significant ADAM23-ITH and that this heterogeneity is critical for tumor growth and metastasis.

In this study, the functional role of ADAM23 in DCs is characterized using RNAi approaches. Read‐out indices reveal that antigen‐specific responder CD4 + T cells had impaired activation, proliferation, and production of cytokines upon priming by ADAM23 knockdown DC.

Aug 18, 2017 · ADAM23 is widely expressed in the embryonic central nervous system and plays an important role in tissue formation. In this study, we showed that ADAM23 contributes to cell survival and is involved in neuronal differentiation during the differentiation of human neural progenitor cells (hNPCs).

Dec 1, 2004 · Our analysis of ADAM23 expression in cultured cerebellar granule cells (CGCs) furthermore suggested that this protein is synthesized as a glycosylated precursor of about 100 kD whose maturation depends on cleavage by furin or a related enzyme.

Results indicate that ADAM23 is likely involved in breast cancer (BC) progression and dissemination of mesenchymal circulating tumor cells. ADAM23 methylation has the potential to function as a novel prognostic marker.

Mar 5, 2024 · Clinical resource with information about ADAM23, Genome-wide association study in a Swedish population yields support for greater CNV and MHC involvement in schizophrenia compared with bipolar disorder., and available tests.

Jan 15, 2021 · Our findings suggest that regulation of ADAM23 endocytosis/stability could be exploited therapeutically in diseases in which ADAM23 is directly involved, such as epilepsy, cancer progression and cardiac hypertrophy.

Our results demonstrate that the expression level of ADAM23 is likely to be involved in the progression of NSCLC and its downregulation is probably correlated with promoter methylation. These findings may provide potential diagnostic and prognostic information about NSCLC.