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PMID |
Sentence |
1 |
721253
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The liver insulinase activity of diabetic dogs after acetazolamide administration was also studied to evaluate the role of this enzyme for the destruction of exogenous insulin.
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2 |
3536368
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These results suggest that the decreased clearance of insulin is due to the decreased receptor binding and the decreased receptor-mediated degradation, but is not due to the decreased degradation by IDE.
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3 |
3327177
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Relations between lowered blood capability to degenerate insulin in diabetes mellitus and a rise of antiinsulinase activity of the plasma with preserved normal insulinase activity of erythrocytic hemolysate were established.
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4 |
3067001
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The increased insulin responsiveness of R rats was not due to an increase in insulin binding or to a decrease in insulin degradation (measured with intact cells or as cytosolic insulinase activity).
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5 |
8055784
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The observed increase in the amount of degraded insulin may reflect an increase in the activity of insulinase, an enzyme bound to the cell membrane and partly present in the cytoplasm.
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6 |
12634421
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To establish whether IDE hypofunction decreases Abeta and insulin degradation in vivo and chronically increases their levels, we characterized mice with homozygous deletions of the IDE gene (IDE --).
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7 |
12634421
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IDE deficiency resulted in a >50% decrease in Abeta degradation in both brain membrane fractions and primary neuronal cultures and a similar deficit in insulin degradation in liver.
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8 |
12941771
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We investigated the role of insulin-degrading enzyme (IDE) in amylin degradation, amyloid deposition, and cytotoxicity in RIN-m5F insulinoma cells.
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9 |
12941771
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The IDE inhibitor bacitracin inhibited amylin degradation by 78% and insulin degradation by 100%.
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10 |
12941771
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IDE inhibition by bacitracin impaired amylin degradation, increased amyloid formation, and increased amylin-induced cytotoxicity, suggesting a role for IDE in amylin clearance and the prevention of amylin aggregation.
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11 |
15850385
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Deletion of insulin-degrading enzyme (IDE) in mice causes accumulation of cerebral amyloid beta-protein (Abeta), hyperinsulinemia, and glucose intolerance.
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12 |
15850385
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Here, we systematically characterize human IDE mRNAs, identify a novel splice form, and compare its subcellular distribution, kinetic properties, and ability to degrade Abeta to the known isoform.
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13 |
16186174
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Finally, using in vitro cellular models of amyloid precursor protein (APP)-processing and Abeta generation/clearance, we confirmed that human recombinant (hr)CTGF may increase Abeta1-40 and Abeta1-42 peptide steady-state levels, possibly through a mechanism that involves gamma-secretase activation and decreased insulin-degrading enzyme (IDE) steady-state levels in a MAP kinase (MAPK)/ phosphatidylinositol 3-kinase (PI-3K)/protein kinase-B (AKT)1-dependent manner.
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14 |
16574064
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Insulin degrading enzyme (IDE), a zinc metalloprotease, can specifically recognize and degrade insulin, as well as several amyloidogenic peptides such as amyloid beta (Abeta) and amylin.
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15 |
16574064
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Fluorescence polarization assays using labeled insulin reveal that IDE-N has reduced affinity to insulin relative to wild type IDE.
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16 |
16894402
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Functions and expression of insulysin, an enzyme involved in the degradation of neurotoxic amyloid peptides and insulin, are usually impaired or reduced in Alzheimer's disease and diabetes.
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17 |
17066144
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Functions and expression of insulysin, an enzyme involved in the degradation of neurotoxic amyloid peptides and insulin, are usually impaired or reduced in Alzheimer's disease and diabetes.
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18 |
18221786
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We describe the development and optimisation of an immunocapture-based assay that uses the fluorogenic peptide substrate (Mca-RPPGFSAFK(Dnp)) and allows the specific measurement of insulin-degrading enzyme (IDE) activity in brain tissue homogenates.
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19 |
18221786
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We tested a panel of IDE antibodies to isolate and capture IDE from brain tissue homogenates and found that immunocapture with antibody to the inactive domain of IDE prior to the addition of fluorogenic substrate allows sensitive (linear at 156-2500ng/ml) and specific measurement of IDE activity and negligible cross-reactivity with NEP, ACE or ECE-1.
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20 |
19154729
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S-nitrosylation of IDE enzyme did not affect the insulin degradation products produced by the enzyme, nor did NO affect insulin binding to IDE as determined by cross-linking studies.
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21 |
19383491
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Finally, we demonstrate that PPARgamma participates in the insulin-induced IDE expression in neurons.
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22 |
19383491
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These results suggest that PPARgamma transcriptionally induces IDE expression which provides a novel mechanism for the use of PPARgamma agonists in both DM2 and AD therapies.
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23 |
19896952
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Furthermore, IDE exhibits a remarkable ability to preferentially degrade structurally similar peptides such as the selective degradation of insulin-like growth factor (IGF)-II and transforming growth factor-alpha (TGF-alpha) over IGF-I and epidermal growth factor, respectively.
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24 |
19896952
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Our amylin-bound IDE structure offers insight into how the structural constraint from a disulfide bond in amylin can alter IDE cleavage sites.
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25 |
21212741
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As mis-regulated insulin signaling in peripheral tissues is known to cause similar phenotypes, our data suggest a role for Drosophila IDE in determining the level of insulin-like peptides made by IPCs that systemically activate insulin signaling.
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26 |
20414044
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ECE-1 activity was significantly decreased both in the hippocampus and cortex of diabetic rats, while for IDE significantly lower activity occurred only in the cortex.
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27 |
20414044
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The hippocampus of diabetic rats showed significant decrease in mRNA levels of NEP and ECE-1 and moderate increase in IDE mRNA level.
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28 |
21448434
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Insulin-degrading enzyme (IDE) is a thiol sensitive peptidase that degrades insulin and amyloid ?, and has been linked to type 2 diabetes mellitus and Alzheimer's disease.
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29 |
21185309
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From these criteria, we predict that IDE can cleave and inactivate ubiquitin (Ub).
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30 |
21185309
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IDE is known to bind the cytoplasmic intermediate filament protein nestin with high affinity.
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31 |
19809796
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This study validates and confirms the association of IDE polymorphisms with T2DM risk in the prospective German cohort and provides novel evidence of influences of IDE genetic variants on insulin metabolism.
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32 |
20498699
|
Significantly, our results reveal that insulin signaling is normally regulated by IDE activity not only extracellularly but also within cells, supporting the longstanding view that IDE inhibitors could hold therapeutic value for the treatment of diabetes.
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