Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
A dramatic decline in ephrinB2 protein levels on the absence of flotillin-1 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 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.
Study provides evidence that ADAM10 is important for the growth of embryonic dorsal root ganglion neurons.
The authors report three distinct ADAM10 mutations in RAK, thereby expanding the mutation spectrum in this gene. The findings suggest that these mutations cause either diminished ADAM10 activity or reduced stability and availability of functional protein, leading to haploinsufficiency.
in BP pathogenesis, membrane-bound ADAM10 expressed on activated CD15+ granulocytes in circulation, along with soluble ADAM10 in local lesions, causes Sema4D cleavage from the membrane of CD15+ granulocytes and results in a high level of circulating sSema4D.
transcription factor TBX2 is able to restrain ADAM10 gene expression and that this mechanism might play a role in regulating cellular processes in health, development and disease.
SNPs of ADAM10 are involved in hepatocellular carcinoma progression
SNHG20 could function as an oncogenic long non-coding RNA by regulating miR-140-5p-ADAM10 axis and MEK/ERK signaling pathway in cervical cancer.
restoration of ADAM10 expression partially reversed the effects of miR152 on cell proliferation and apoptosis in rheumatoid arthritisfibroblastlike synoviocytes.
Mechanisms underlying ADAM10 downregulation by miR-140-5p and suggests that dysfunctional regulation of ADAM10 expression is exacerbated by AD-related neurotoxic effects.
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 activates different catalytic subunits p110 of PI3K in a cell-type-dependent manner to induce lipogenesis-dependent epithelial-mesenchymal transition through the regulation of ADAM10 and ADAM17.
mechanistic experiments revealed that ADAM10-RNAi resulted in an increase in E-cadherin and a decrease in N-cadherin and vimentin 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 is ligand activated and undergoes DTX4-mediated ubiquitylation and bilateral endocytosis before ADAM10 processing
therapies against ADAM10 and ADAM17 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 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 phosphatidylserine exposure is required to then induce its shedding function.
A better understanding of the regulatory mechanisms controlling the expression, subcellular localization and activity of ADAM10 will likely uncover suitable drug targets which will allow a more specific and fine-tuned modulation of its proteolytic activity
In the present study, the authors show that deletion of a triple serine (3S) motif (Ser-359 to Ser-361) adjacent to the cleavage site is sufficient to prevent IL-6R cleavage by ADAM17, but not ADAM10. We find that the impaired shedding is caused by the reduced distance between the cleavage site and the plasma membrane.
Data show that tetraspanin15 (Tspan15) is abundantly expressed in brain, where it specifically interacts with endogenous a disintegrin and metalloproteinase 10 (ADAM10).
ADAM10(DC)(-/-) mice are resistant to IgE-mediated anaphylaxis.
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.
the synaptic localization of APP, ADAM10, and BACE1 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-ligands by differentially activating ADAM17 or ADAM10.
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
Tspan3 is a central endocytic membrane component regulating the expression of ADAM10, presenilin and the amyloid precursor protein.
these results show that ADAM10-Notch 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, is indispensable for proper retinal development as a regulator of NOTCH 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 ligands via Taok3-mediated surface expression of ADAM10
Thus, Leda-1/Pianp is constitutively processed by proprotein convertases, sheddases including MMPs and ADAM10/17 and intramembrane protease gamma-secretase.
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.
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.
Newborn mice deficient in ADAM10 exhibited organ-specific vascular defects.
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
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.
ADAM10 gene was predominantly expressed in the neurons of the cerebral cortex, hippocampus, thalamus and cerebellar granular cells in adult mouse CNS.
Matrix metalloproteases ADAM10 and TACE (ADAM17) cleave AXL receptor tyrosine kinase (Axl) in lupus-prone leukocytes.
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.
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 metalloproteinase domain 10
, disintegrin and metalloproteinase domain-containing protein 10
, ADAM metallopeptidase domain 10
, ADAM10 metallopeptidase
, a disintegrin and metalloprotease domain 10a
, ADAM 10
, kuzbanian protein homolog
, a disintegrin and metalloprotease domain 10
, mammalian disintegrin-metalloprotease
, myelin-associated metalloproteinase
, a disintegrin and metalloprotease domain (ADAM) 10
, a disintegrin and metallopeptidase domain 10
, disintegrin and metalloproteinase domain-containing protein 10-like
, ADAM metallopeptidase domain 10b
, a disintegrin and metalloprotease domain 10b