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The disintegrin-like metalloproteinase ADAM10 is involved in constitutive cleavage of CX3CL1 (fractalkine) and regulates CX3CL1-mediated cell-cell adhesion.
It is demonstrated that ADAM10 is involved in the constitutive cleavage of CX3CL1 and thereby may regulate the recruitment of monocytic cells to CX2CL1-expressing cell layers and prevent de-adhesion of bound THP-1 cells. Expand
ADAM10 mediates E-cadherin shedding and regulates epithelial cell-cell adhesion, migration, and beta-catenin translocation.
It is shown that E-cadherin is cleaved specifically by ADAM (a disintegrin and metalloprotease) 10 in its ectodomain, and the data strongly suggest that this protease constitutes a major regulatory element for the multiple functions of E-bodies under physiological as well as pathological conditions. Expand
ADAM10 cleavage of N‐cadherin and regulation of cell–cell adhesion and β‐catenin nuclear signalling
It is demonstrated here that neuronal cadherin (N‐cadherin) is cleaved specifically by the disintegrin and metalloproteinase ADAM10 in its ectodomain, leading to the conclusion that this protease constitutes a central switch in the signalling pathway from N‐cADherin at the cell surface to β‐catenin/LEF‐1‐regulated gene expression in the nucleus. Expand
A soluble form of the receptor for advanced glycation endproducts (RAGE) is produced by proteolytic cleavage of the membrane‐bound form by the sheddase a disintegrin and metalloprotease 10 (ADAM10)
It is shown here that most soluble RAGE, either produced by cell lines or present in human blood, is not recognized by an anti‐esRAGE antibody, and the data do not disprove the interpretation that high levels of soluble forms of RAGE protect against chronic inflammation, but suggest that they correlate with high Levels of ongoing inflammation. Expand
The "a disintegrin and metalloprotease" (ADAM) family of sheddases: physiological and cellular functions.
  • K. Reiss, P. Saftig
  • Medicine, Biology
  • Seminars in cell & developmental biology
  • 1 April 2009
There is an exciting increase of evidence that members of the disintegrin and metalloprotease (ADAM) family critically regulate cell adhesion, migration, development and signalling. ADAMs areExpand
Phenotypic and Biochemical Analyses of BACE1- and BACE2-deficient Mice*
The data indicate that BACE2 could indeed contribute to Aβ generation in the brains of Alzheimer disease and, in particular, Down syndrome patients and call for some caution when claiming that no major side effects should be expected from blocking BACE1 activity. Expand
ADAM10 Regulates Endothelial Permeability and T-Cell Transmigration by Proteolysis of Vascular Endothelial Cadherin
ADAM10 is identified as a novel regulator of vascular permeability and a hitherto unknown function of ADAM10 in the regulation of VE-cadherin–dependent endothelial cell functions and leukocyte transendothelial migration is demonstrated. Expand
The "A Disintegrin And Metalloproteases" ADAM10 and ADAM17: novel drug targets with therapeutic potential?
This review will cover the emerging roles of both ADAM10 and ADAM17 in the regulation of major physiological and developmental pathways and the suitability of specifically modulating the activities of both proteases as a feasible way to inhibit inflammatory states, cancer and neurodegeneration. Expand
ADAM10, the Rate-limiting Protease of Regulated Intramembrane Proteolysis of Notch and Other Proteins, Is Processed by ADAMS-9, ADAMS-15, and the γ-Secretase*
ADAM10 performs a dual role in cells, as a metalloprotease when it is membrane-bound, and as a potential signaling protein once cleaved by ADAM9/15 and the γ-Secretase. Expand
Correction for Substrate Selectivity of Epidermal Growth Factor-Receptor Ligand Sheddases and their Regulation by Phorbol Esters and Calcium Influx
It is demonstrated that dysregulated EGFR-ligand shedding may be caused by increased expression of constitutively active sheddases or activation of different sheddase by distinct stimuli, including phorbol esters and calcium influx. Expand