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ADAM10(DC)(-/-) mice are resistant to IgE-mediated anaphylaxis.
In the present study, we report that Nrxn3beta is processed by the metalloproteases ADAM10, ADAM17 (show ADAM17 Proteins), and by the intramembrane-cleaving protease gamma-secretase, producing secreted neurexin3beta (sNrxn3beta) and a single intracellular domain (Nrxn3beta-ICD). Thea (show ACOT11 Proteins) authors show that sNrxn3beta produced by the cells of the dentate gyrus increases the spine density of newborn neurons.
the synaptic localization of APP (show APP Proteins), ADAM10, and BACE1 (show BACE Proteins) in the mouse cerebral cortex, was examined.
Pharmacological inhibition of ADAM10 reduces sEphrin-B2 levels in bronchoalveolar lavage and prevents lung fibrosis in mice. Consistent with the mouse data, ADAM10-sEphrin-B2 signaling is upregulated in fibroblasts from human subjects with idiopathic pulmonary fibrosis.
Xenoestrogens biphenol-A and nonylphenol stimulate the release of EGFR (show EGFR Proteins)-ligands by differentially activating ADAM17 (show ADAM17 Proteins) or ADAM10.
study confirms the importance of ICOSL (show ICOSLG Proteins) shedding in ICOS (show ICOS Proteins)/ICOSL (show ICOSLG Proteins) function and expression and it identifies ADAM10 as the most important sheddase for controlling ICOSL (show ICOSLG Proteins) levels
Tspan3 (show TSPAN3 Proteins) is a central endocytic membrane component regulating the expression of ADAM10, presenilin and the amyloid precursor protein (show APP Proteins).
these results show that ADAM10-Notch (show NOTCH1 Proteins) signaling in ovarian somatic cells governs the primordial follicle formation by controlling the development of ovarian pregranulosa cells.
Findings provide evidence that ADAM10, and not ADAM17 (show ADAM17 Proteins), is indispensable for proper retinal development as a regulator of NOTCH (show NOTCH1 Proteins) signaling.
this study shows that during positive selection in the spleen, B-cell receptor signaling causes immature type 1 transitional B cells to become receptive to Notch (show NOTCH1 Proteins) ligands via Taok3 (show TAOK3 Proteins)-mediated surface expression of ADAM10
elevated expression of ADAM10 was associated with the pathogenesis and development of immune thrombocytopenia
Report overexpression of ADAM10 in oral squamous cell carcinomas, especially in OSCC with metastasis.
High ADAM10 expression is associated with meningococcal purpura fulminans.
The findings of the present study suggested that miR320a may function as a tumor suppressor in GC progression and potential therapeutic strategies for GC may be based on the miR320a/ADAM10 axis.
Insulin-like growth factor-1 (show IGF1 Proteins) activates different catalytic subunits p110 (show CUX1 Proteins) of PI3K (show PIK3CA Proteins) in a cell-type-dependent manner to induce lipogenesis-dependent epithelial-mesenchymal transition through the regulation of ADAM10 and ADAM17 (show ADAM17 Proteins).
mechanistic experiments revealed that ADAM10-RNAi resulted in an increase in E-cadherin (show CDH1 Proteins) and a decrease in N-cadherin (show CDH2 Proteins) and vimentin (show VIM Proteins) expression. Our study implies that high expression of ADAM10 promotes the proliferation and migration of hypopharyngeal squamous cell carcinoma (HSCC). These findings may help to provide a method for treatment of HSCC
Notch (show NOTCH1 Proteins) is ligand activated and undergoes DTX4 (show DTX4 Proteins)-mediated ubiquitylation and bilateral endocytosis before ADAM10 processing
therapies against ADAM10 and ADAM17 (show ADAM17 Proteins) may promote cancer stem cell migration away from the tumourigenic niche resulting in a differentiated phenotype that is more susceptible to treatment.
Presence of anti-ADAM10 auto-Antibodies seems to reflect the increased tumor expression of the immunogenic immature-ADAM10 in a group of Colorectal cancer patients, and is associated with a favourable prognosis in patients at stage III of the disease.
ADAM10 and ADAM17 (show ADAM17 Proteins) are the best characterized members of the ADAM (A Disintegrin and Metalloproteinase) - family of transmembrane proteases. Both are involved diverse physiological and pathophysiological processes.For ADAM17 (show ADAM17 Proteins) phosphatidylserine exposure is required to then induce its shedding function.
A dramatic decline in ephrinB2 (show EFNB2 Proteins) protein levels on the absence of flotillin-1 (show FLOT1 Proteins) expression is specific, and is partly the result of an increased susceptibility to cleavage by the metalloprotease ADAM10.
significantly increased expression of ADAM10 in the ISR versus non-ISR segment in diabetic minipigs
Data show that ADAM10 and APLP2 (show APLP2 Proteins) are expressed in proximal tubule cells, and that ADAM10 activity has a pronounced effect on expression of specific brush-border proteins.
Intracellular trafficking of ADAM10 critically requires a novel sorting signal within its cytoplasmic domain.
N-glycosylation is crucial for ADAM10 processing and resistance to proteolysis, and results suggest that it is required for full-enzyme activity.
Members of the ADAM family are cell surface proteins with a unique structure possessing both potential adhesion and protease domains. This gene encodes and ADAM family member that cleaves many proteins including TNF-alpha and E-cadherin.
a disintegrin and metalloprotease domain 10a
, ADAM metallopeptidase domain 10
, disintegrin and metalloproteinase domain-containing protein 10
, ADAM10 metallopeptidase
, disintegrin and metalloproteinase domain-containing protein 10-like
, ADAM 10
, a disintegrin and metalloprotease domain (ADAM) 10
, a disintegrin and metalloprotease domain 10
, kuzbanian protein homolog
, mammalian disintegrin-metalloprotease
, a disintegrin and metalloproteinase domain 10
, a disintegrin and metallopeptidase domain 10
, myelin-associated metalloproteinase