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Data show that tetraspanin15 (Tspan15) is abundantly expressed in brain, where it specifically interacts with endogenous a disintegrin and metalloproteinase 10 (ADAM10).
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ADAM10(DC)(-/-) mice are resistant to IgE-mediated anaphylaxis.
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In the present study, we report that Nrxn3beta is processed by the metalloproteases ADAM10, ADAM17, and by the intramembrane-cleaving protease gamma-secretase, producing secreted neurexin3beta (sNrxn3beta) and a single intracellular domain (Nrxn3beta-ICD). Thea authors show that sNrxn3beta produced by the cells of the dentate gyrus increases the spine density of newborn neurons.
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the synaptic localization of APP, ADAM10, and BACE1 in the mouse cerebral cortex, was examined.
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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.
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Xenoestrogens biphenol-A and nonylphenol stimulate the release of EGFR-ligands by differentially activating ADAM17 or ADAM10.
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study confirms the importance of ICOSL shedding in ICOS/ICOSL function and expression and it identifies ADAM10 as the most important sheddase for controlling ICOSL levels
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Tspan3 is a central endocytic membrane component regulating the expression of ADAM10, presenilin and the amyloid precursor protein.
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these results show that ADAM10-Notch signaling in ovarian somatic cells governs the primordial follicle formation by controlling the development of ovarian pregranulosa cells.
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Findings provide evidence that ADAM10, and not ADAM17, is indispensable for proper retinal development as a regulator of NOTCH signaling.
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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 ligands via Taok3-mediated surface expression of ADAM10
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Thus, Leda-1/Pianp is constitutively processed by proprotein convertases, sheddases including MMPs and ADAM10/17 and intramembrane protease gamma-secretase.
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ADAM10 was dispensable for alpha-toxin-dependent xenophagic targeting of S. aureus, whereas a role for alpha-toxin attack on the plasma membrane was confirmed.
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ADAM10 was essentially involved in maxillofacial bone development. ADAM10 conditional knock-out KO mice present craniofacial dysmorphia and bone defects. Impaired osteoblast differentiation,proliferation and apoptosis underlie the bone deformity.
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Newborn mice deficient in ADAM10 exhibited organ-specific vascular defects.
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Findings demonstrate the direct requirement of ADAM10 in cortical radial migration and reveal the underlying mechanism by linking ADAM10-initiated regulated intramembrane proteolysis of Notch to the regulation of microtubule cytoskeleton through transcriptional control of Dcx expression
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our data afford the new insight that miR-103a inhibited abdominal aortic aneurysm (AAA) growth via targeting ADAM10, which might be a promising therapeutic strategy to alleviate AAA.
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ADAM10 gene was predominantly expressed in the neurons of the cerebral cortex, hippocampus, thalamus and cerebellar granular cells in adult mouse CNS.
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Matrix metalloproteases ADAM10 and TACE (ADAM17) cleave AXL receptor tyrosine kinase (Axl) in lupus-prone leukocytes.
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Loss of ADAM10 in murine liver results in hepatocyte necrosis and concomitant liver fibrosis. ADAM10 directly regulates expression of bile acid transporters but is dispensable for Notch2-dependent formation of the biliary system. Differentiation of liver progenitor cells to hepatocytes is augmented in the absence of ADAM10.
