Browse our anti-ADAM10 (ADAM10) Antibodies

Xenopus laevis ADAM Metallopeptidase Domain 10 (ADAM10) interaction partners

1. 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.

Pig (Porcine) ADAM Metallopeptidase Domain 10 (ADAM10) interaction partners

1. significantly increased expression of ADAM10 in the ISR versus non-ISR segment in diabetic minipigs

Cow (Bovine) ADAM Metallopeptidase Domain 10 (ADAM10) interaction partners

1. 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.

2. Intracellular trafficking of ADAM10 critically requires a novel sorting signal within its cytoplasmic domain.

3. N-glycosylation is crucial for ADAM10 processing and resistance to proteolysis, and results suggest that it is required for full-enzyme activity.

Human ADAM Metallopeptidase Domain 10 (ADAM10) interaction partners

1. ADAM10 inhibition is worth considering as a therapeutic perspective in mesothelioma context.

2. These results demonstrated the contributory role of APP cleavage on its oncogenic roles in breast cancer. ADAM10 was the key alpha-secretase. APP and ADAM10 co-expression was associated with worse survival in non-luminal breast cancers.

3. SNHG1 promoted GC cell proliferation and invasion via modulating the miR-140/ADAM10 axis

4. Study provides evidence that ADAM10 is important for the growth of embryonic dorsal root ganglion neurons.

5. 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.

6. 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.

7. 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.

8. SNPs of ADAM10 are involved in hepatocellular carcinoma progression

9. 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.

10. restoration of ADAM10 expression partially reversed the effects of miR152 on cell proliferation and apoptosis in rheumatoid arthritisfibroblastlike synoviocytes.

11. Mechanisms underlying ADAM10 downregulation by miR-140-5p and suggests that dysfunctional regulation of ADAM10 expression is exacerbated by AD-related neurotoxic effects.

12. elevated expression of ADAM10 was associated with the pathogenesis and development of immune thrombocytopenia

13. Report overexpression of ADAM10 in oral squamous cell carcinomas, especially in OSCC with metastasis.

14. High ADAM10 expression is associated with meningococcal purpura fulminans.

15. 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.

16. 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.

17. 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

18. Notch is ligand activated and undergoes DTX4-mediated ubiquitylation and bilateral endocytosis before ADAM10 processing

19. 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.

20. 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.

Mouse (Murine) ADAM Metallopeptidase Domain 10 (ADAM10) interaction partners

1. ADAM10, which cleaves CX3CL1 into a secreted form, is upregulated specifically in layer IV neurons and in microglia following whisker lesioning. Inhibition of ADAM10 phenocopies Cx3cr1(-/-) and Cx3cl1(-/-) synapse elimination defects.

2. Study showed that administering vascular endothelial growth factor concurrently increased the expression of disintegrin and metalloproteinase domain-containing protein 10 and decreased the expression of beta-site APP cleaving enzyme 1, which contributes to the enhanced clearance of amyloid-beta in vivo.

3. The results of this study suggested that increased seizure activity in the Adam10 knockdown TLE mice is dependent on hippocampal neuroinflammation.

4. This study demonstrates the involvement of ADAM10 and PI3K/Akt signaling in mediating RLX-induced Notch-1 activation.

5. Data show that tetraspanin15 (Tspan15) is abundantly expressed in brain, where it specifically interacts with endogenous a disintegrin and metalloproteinase 10 (ADAM10).

6. ADAM10(DC)(-/-) mice are resistant to IgE-mediated anaphylaxis.

7. 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.

8. the synaptic localization of APP, ADAM10, and BACE1 in the mouse cerebral cortex, was examined.

9. 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.

10. Xenoestrogens biphenol-A and nonylphenol stimulate the release of EGFR-ligands by differentially activating ADAM17 or ADAM10.

11. 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

12. Tspan3 is a central endocytic membrane component regulating the expression of ADAM10, presenilin and the amyloid precursor protein.

13. these results show that ADAM10-Notch signaling in ovarian somatic cells governs the primordial follicle formation by controlling the development of ovarian pregranulosa cells.

14. Findings provide evidence that ADAM10, and not ADAM17, is indispensable for proper retinal development as a regulator of NOTCH signaling.

15. 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

16. Thus, Leda-1/Pianp is constitutively processed by proprotein convertases, sheddases including MMPs and ADAM10/17 and intramembrane protease gamma-secretase.

17. 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.

18. 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.

19. Newborn mice deficient in ADAM10 exhibited organ-specific vascular defects.

20. 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