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Human ADAM10 ELISA Kit for Sandwich ELISA - ABIN414771
Van Crombruggen, Holtappels, De Ruyck, Derycke, Tomassen, Bachert: RAGE processing in chronic airway conditions: involvement of Staphylococcus aureus and ECP. in The Journal of allergy and clinical immunology 2012
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study confirms the importance of ICOSL (show ICOSLG ELISA Kits) shedding in ICOS (show ICOS ELISA Kits)/ICOSL (show ICOSLG ELISA Kits) function and expression and it identifies ADAM10 as the most important sheddase for controlling ICOSL (show ICOSLG ELISA Kits) levels
Tspan3 (show TSPAN3 ELISA Kits) is a central endocytic membrane component regulating the expression of ADAM10, presenilin and the amyloid precursor protein (show APP ELISA Kits).
these results show that ADAM10-Notch (show NOTCH1 ELISA Kits) 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 ELISA Kits), is indispensable for proper retinal development as a regulator of NOTCH (show NOTCH1 ELISA Kits) 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 ELISA Kits) ligands via Taok3 (show TAOK3 ELISA Kits)-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 (show PLC ELISA Kits)-dependent xenophagic targeting of S. aureus, whereas a role for alpha-toxin (show PLC ELISA Kits) 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 (show NOTCH1 ELISA Kits) to the regulation of microtubule cytoskeleton through transcriptional control of Dcx (show DCX ELISA Kits) expression
The ADAM17 (show ADAM17 ELISA Kits) messenger RNA (mRNA) and protein levels were significantly higher in the inferior turbinate than in nasal polyps (p < 0.05). The ADAM10 mRNA and protein levels did not differ significantly between NPs (show NPS ELISA Kits) and inferior turbinates (p > 0.05). ADAM10 and ADAM17 (show ADAM17 ELISA Kits) were expressed primarily in inflammatory cells, submucosal glandular cells, and lining epithelial cells.
study confirms the importance of ICOSL (show ICOSLG ELISA Kits) shedding in ICOS (show CTLA4 ELISA Kits)/ICOSL (show ICOSLG ELISA Kits) function and expression and it identifies ADAM10 as the most important sheddase for controlling ICOSL (show ICOSLG ELISA Kits) levels
Inhibition of ADAM10 suppressed the expansion of NK cells and reduced the expression of CD16 (show CD16 ELISA Kits).
Platelet ADAM10 protein expression in patients with AD [Alzheimer's Disease] was positively influenced by serotoninergic medication
Endothelial Tspan5 (show TSPAN5 ELISA Kits)- and Tspan17-ADAM10 complexes may regulate inflammation by maintaining normal VE-cadherin (show CDH5 ELISA Kits) expression and promoting T lymphocyte transmigration.
Regulation of ADAM10 by the TspanC8 subgroup of tetraspanins, namely Tspan5 (show TSPAN5 ELISA Kits), 10, 14, 15, 17 and 33 is reviewed.
active ADAM10 form marks cancer stem-like cells with active Notch (show NOTCH1 ELISA Kits) signaling, known to mediate chemoresistance.
Data show that tetraspanin 33 (tspan33 (show TSPAN33 ELISA Kits)) is an early activation marker, and that disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) protein expression does not correlate with Tspan33 (show TSPAN33 ELISA Kits) expression in B cells.
High ADAM10 expression is associated with metastasis of hepatocellular carcinoma.
A dramatic decline in ephrinB2 (show EFNB2 ELISA Kits) protein levels on the absence of flotillin-1 (show FLOT1 ELISA Kits) 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 ELISA Kits) 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