3.4.24.56: insulysin
This is an abbreviated version!
For detailed information about insulysin, go to the full flat file.
Word Map on EC 3.4.24.56
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3.4.24.56
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alzheimer
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neprilysin
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abeta
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hippocampus
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dementia
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mellitus
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cerebral
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morris
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amyloid-beta
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metalloprotease
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maze
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neuroprotective
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amyloidogenic
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tau
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beta-amyloid
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neurodegenerative
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presenilin
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endothelin-converting
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senile
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gamma-secretase
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beta-protein
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125i-insulin
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abeta-degrading
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hyperinsulinemia
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metalloendopeptidase
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bacitracin
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beta-secretase
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late-onset
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amylin
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microglia
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medicine
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adam10
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non-amyloidogenic
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glutathione-insulin
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enzyme-1
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b-chains
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analysis
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ad-like
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anti-ide
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exosite
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beta-peptide
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abeta1-40
- 3.4.24.56
- alzheimer
- neprilysin
- abeta
- hippocampus
- dementia
- mellitus
- cerebral
-
morris
- amyloid-beta
- metalloprotease
-
maze
-
neuroprotective
-
amyloidogenic
- tau
- beta-amyloid
- neurodegenerative
-
presenilin
-
endothelin-converting
-
senile
- gamma-secretase
- beta-protein
- 125i-insulin
-
abeta-degrading
- hyperinsulinemia
- metalloendopeptidase
- bacitracin
- beta-secretase
-
late-onset
- amylin
- microglia
- medicine
- adam10
-
non-amyloidogenic
-
glutathione-insulin
- enzyme-1
- b-chains
- analysis
-
ad-like
-
anti-ide
-
exosite
- beta-peptide
- abeta1-40
Reaction
Degradation of insulin, glucagon and other polypeptides. No action on proteins =
Synonyms
ADE, amyloid degrading enzyme, cgd6_5510, EC 3.4.22.11, EC 3.4.99.10, EC 3.4.99.45, gamma-endorphin-generating enzyme, IDE, INS20-19, insulin degrading enzyme, Insulin protease, Insulin proteinase, Insulin-degrading enzyme, Insulin-degrading neutral proteinase, Insulin-glucagon protease, Insulin-specific protease, Insulinase, Insulysin, Metalloinsulinase, More, pitrilysin metallopeptidase 1, Pitrm1
ECTree
3.4.24.56 insulysinAdvanced search results
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results (Application
Application on EC 3.4.24.56 - insulysin
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APPLICATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
analysis
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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
medicine
medicine
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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
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
medicine
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stimulation of enzyme activity can provide a useful therapeutic approach in treatment of diseases caused by amyloidosis, like Alzheimer's disease, type2 non-insulin-dependent diabetes and the spongiform encephalopathies such as Creutzfeldt-Jakob disease
medicine
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substrate amyloid beta-protein is an essential factor in the pathogenesis of Alzheimer's disease
medicine
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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
medicine
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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
medicine
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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
medicine
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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
medicine
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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
medicine
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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
medicine
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study on cortical expression of insulysin and neprilysin in sporadic and familial Alzheimer's disease samples carrying the E280A presenilin-1 missense mutation. Insulysin is linked with aggregated amyloid beta40 isoform while neprilysin negatively correlates with amyloid angiopathy. Neprilysin, but not insulysin, is over-expressed in dystrophic neurites, both proteases are immunoreactive in activated astrocytes but not in microglia and insulysin is the only one detected in astrocytes of white matter from familial alzheimer's disease cases
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
medicine
peptide inhibitors cand function as potentially meaningful candidates for the development of type-2 diabetes therapeutics
medicine
the enzyme modulates blood glucose levels by cleaving insulin, a hormone that promotes glucose clearance. It also degrades glucagon, a hormone that elevates glucose levels and opposes the effect of insulin. Insulin-degrading enzyme inhibitors to treat diabetes, therefore, should prevent insulin-degrading enzyme-mediated insulin degradation, but not glucagon degradation. Using a high-throughput screen for non-active-site ligands, potent and highly specific small-molecule inhibitors are discovered that alter substrate selectivity of insulin-degrading enzyme. X-ray co-crystal structures, including an insulin-degrading enzyme-ligand-glucagon ternary complex, reveal substrate-dependent interactions that enable these inhibitors to potently block insulin binding while allowing glucagon cleavage, even at saturating inhibitor concentrations
medicine
therapeutic and/or preventative approaches combining resveratrol and insulin-degrading enzyme may hold promise for sporadic Alzheimer's disease
