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Adam23 encodes a member of the ADAM (a disintegrin and metalloprotease domain) family.
Showing 10 out of 74 products:
Human Polyclonal Adam23 Primary Antibody für ELISA - ABIN4252567
Takada, Imoto, Tsuda, Nakanishi, Ichikura, Mochizuki, Mitsufuji, Hosoda, Hirohashi, Ohki, Inazawa: ADAM23, a possible tumor suppressor gene, is frequently silenced in gastric cancers by homozygous deletion or aberrant promoter hypermethylation. in Oncogene 2005
Human Polyclonal Adam23 Primary Antibody für IHC, IHC (p) - ABIN4278231
Costa, Barnabé, Li, Dias, Machado, Asprino, Cavalher, Ferreira, Del Mar Inda, Nagai, Malnic, Duarte, Leite, de Barros, Carraro, Chammas, Armelin, Cavenee, Furnari, Camargo: Intratumoral heterogeneity of ADAM23 promotes tumor growth and metastasis through LGI4 and nitric oxide signals. in Oncogene 2015
ADAM23 expression on DCs partially governs antigen-presentation capacities to responder CD4 (zeige CD4 Antikörper)(+) 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.
Interaction proteomics revealed the interactors of Caspr2 (zeige CNTNAP2 Antikörper), including CNTN2 (zeige CNTN2 Antikörper), KCNAs, members of the ADAM family (ADAM22 (zeige ADAM22 Antikörper), ADAM23 and ADAM11 (zeige ADAM11 Antikörper)), members of LGI family and MAGUKs (DLGs and MPPs (zeige MPHOSPH6 Antikörper)).
Adam23 knockdown up-regulates P27KIP1 (zeige CDKN1B Antikörper) in P19 (zeige CDKN2D Antikörper)/ADAM23 knockdown cells, one reason that P19 (zeige CDKN2D Antikörper)/ADAM23 knockdown cells can differentiate into neurons without retinoic acid induction.
Data suggest that leucine-rich glioma inactivated 3 (LGI3 (zeige LGI3 Antikörper)) may be a candidate adipokine that is perturbed in obesity and suppresses adipogenesis through its receptor, ADAM23.
Data suggest that LGI1 (zeige LGI1 Antikörper) 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 (zeige PRNP Antikörper)) 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.
ADAM23 regulates neuronal differentiation by triggering specific signaling pathways during human neural progenitor cells differentiation.
these results support the existence of a second mechanism, alternative to inhibition of protein secretion, by which ADLTE (zeige LGI1 Antikörper)-causing LGI1 (zeige LGI1 Antikörper) mutations exert their loss-of-function effect extracellularly, and suggest that interactions of LGI1 (zeige LGI1 Antikörper) with both ADAM22 (zeige ADAM22 Antikörper) 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 (zeige CXCL12 Antikörper) 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 (zeige LGI4 Antikörper) 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 (zeige PSG1 Antikörper) binding site (-202/-190) that binds SP1 (zeige PSG1 Antikörper) 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.
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