EC Number   |
Application |
Reference |
|---|
   3.4.24.56 | analysis |
immunocapture-based assay that uses the fluorogenic peptide substrate (7-methoxycoumarin-4-yl)acetyl-RPPGFSAFK-2,4-dinitrophenyl and allows the specific measurement of insulin-degrading enzyme activity in brain tissue homogenates. The fluorogenic substrate can be cleaved by a number of enzymes including neprilysin endothelin-converting enzyme-1 and angiotensin-converting enzyme, as well as IDE. Discrimination between these individual enzymes is not readily achieved in tissue homogenates, even in the presence of selective inhibitors and pH conditions. Immunocapture with antibody to the inactive domain of IDE prior to the addition of fluorogenic substrate allows sensitive, linear at 156-2500 ng/ml, and specific measurement of IDE activity and negligible cross-reactivity with neprilysin, endothelin-converting enzyme-1 or angiotensin-converting enzyme |
699678 |
| 3.4.24.56 | medicine |
after the development of first amyloid beta plaques in brain of transgenic mice with alzheimer's disease-like neuropathology, cortical mRNAand protein levels of IDE are significantly up-regulated in the transgenic mice compared to their non-transgenic littermates. Up-regulation of IDE mRNA-levels occurrs in parallel with increased amyloid beta40 and amyloid beta42 production. A significant positive correlation is observed between protein levels of IDE and full-length amyloid precursor protein in the cerebral cortex |
700455 |
| 3.4.24.56 | medicine |
beta-site amyloid precursor protein-cleaving enzyme BACE2 overexpression in cultured cells lowers net amyloid beta levels to a greater extent than multiple, well-established amyloid beta-degrading proteases, including neprilysin and endothelinconverting enzyme-1, while showing comparable effectiveness to insulin degrading enzyme |
734728 |
| 3.4.24.56 | medicine |
enzyme is a cellular receptor for both cell-free and cell-associated Varicella-zoster virus. Enzyme interacts with Varicella-zoster virus glycoprotein E through its extracellular domain. Downregulation of enzyme by siRNA, or blocking with antibody inhibited Varicella-zoster infection. Transfection of cell lines impaired for infection with a plasmid expressing human enzyme results in increased entry and increased infection by Varicella-zoster virus |
668184 |
| 3.4.24.56 | medicine |
enzyme is capable of cleavage of the 34 amino acid peptides resulting from internal proteolysis of genetically defect type 2 transmembrane protein BRI2 in patients with familial British dementia or familial Danish dementia. Enzymic degradation of peptide is more efficient with monomeric peptide than with aggregated peptide. Proteolysis of monomeric soluble peptide precursors by enzyme may delay peptide ABri and ADan aggregation in vivo |
667412 |
| 3.4.24.56 | medicine |
IDE represents a target for the development of a new class of drugs for the treatment of Alzheimer's disease that lowers amyloid beta-peptide levels by increasing ist rate of catabolism |
652488 |
| 3.4.24.56 | medicine |
in isolated brain microvessels from patients with Alzheimers disease with cerebral amyloid angiopathy enzyme protein level is up to 44% increased, but enzyme activity is significantly reduced |
667412 |
| 3.4.24.56 | medicine |
in patients with diabetes, the degradation of insulin by wound fluid correlates with glucose control, patients with worse outcomes have higher wound fluid insulin degradation. Reduction of enzyme activity in the wound fluid as potential therapeutic target |
669620 |
| 3.4.24.56 | medicine |
in patients with V97L mutation of presenilin 1, insulysin activity on the plasma membranes is reduction concomitantly with increased levels of extracellular and intracellular amyloid beta42. In the presenilin 1 V97L mutant-transfected SH-SY5Y cell line, increase of intracellular amyloid beta42 is associated with decreased expression and activity of insulysin in the cytosol and endoplasmic reticulum |
697748 |
| 3.4.24.56 | medicine |
inverse correlation between insulysin activity levels and brain Abeta peptide levels suggest that modulation of insulysin activity may alter the risk for Alzheimer's disease |
653595 |
