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1 egradation by enzymes such as neprilysin and insulin degrading enzyme.
2 mechanisms, including elevated expression of insulin-degrading enzyme.
3 ulin clearance due to down-regulation of the insulin-degrading enzyme.
4 of two endopeptidases, neprilysin (NEP) and insulin-degrading enzyme.
5 ecursor protein, presenilin 1, neprylisin or insulin-degrading enzyme.
6 retion and by inhibiting its degradation via insulin-degrading enzyme.
7 onstrated this activity can be attributed to insulin degrading enzyme, a previously described member
8 olytic degradation of monomeric Abeta by the insulin-degrading enzyme, a major Abeta-degrading enzyme
10 TNF-alpha directly reduced the expression of insulin degrading enzyme and chaperone molecules (heat s
11 activities of other Abeta-degrading enzymes, insulin degrading enzyme and neprilysin, were unchanged.
12 e zinc-dependent insulin-degrading proteases insulin-degrading enzyme and cathepsin D were impaired;
13 minal fragment, and Abeta-degrading enzymes (insulin-degrading enzyme and neprilysin) in APP/CCL2 and
14 transition metal is an essential cofactor in insulin-degrading enzyme and several key Zn2+ finger tra
15 AD) markers, synaptophysin, APP, neprilysin, insulin-degrading enzyme and transthyretin in MCAT, Abet
16 nt of mRNA/protein changes in neprilysin and insulin-degrading enzyme and, instead, may involve neuro
20 e-2 diabetes, and the identification of IDE (insulin-degrading enzyme) as a diabetes susceptibility g
22 metabolism and alternate processing, such as insulin degrading enzyme, endothelin-converting enzyme-1
25 0 and Abeta42) with the fully active form of insulin degrading enzyme (IDE) through unrestrained, all
26 nverting the twelve cysteine residues in rat insulin degrading enzyme (IDE) to serines resulted in a
31 increase in NO results in S-nitrosylation of insulin-degrading enzyme (IDE) and dynamin-related prote
32 Previously, we showed that gE interacts with insulin-degrading enzyme (IDE) and facilitates VZV infec
33 hat they result in altered expression of the insulin-degrading enzyme (Ide) and fibroblast growth fac
38 cently found that homozygous deletion of the insulin-degrading enzyme (IDE) gene in mice results in a
57 re we show that transgenic overexpression of insulin-degrading enzyme (IDE) or neprilysin (NEP) in ne
58 a hormone vital for glucose homeostasis, and insulin-degrading enzyme (IDE) plays a key role in its c
60 ves gamma-secretase activation and decreased insulin-degrading enzyme (IDE) steady-state levels in a
64 e and find that it is indistinguishable from insulin-degrading enzyme (IDE), a thiol metalloendopepti
67 main that interacts with a putative receptor insulin-degrading enzyme (IDE), replicated as extensivel
68 cated in the non-coding region (intron 1) of insulin-degrading enzyme (IDE), was the most strongly as
69 genetic system for functional studies of the insulin-degrading enzyme (IDE), which cleaves and inacti
70 terminal region also mediates binding to the insulin-degrading enzyme (IDE), which is proposed to be
71 One candidate gene in this region is the insulin-degrading enzyme (IDE), which, in the GK rat mod
76 adation in MDM is sensitive to lysosomal and insulin degrading enzyme inhibitors but insensitive to p
77 panning the 5' untranslated region region of insulin-degrading enzyme is associated with serum cotini
80 l new biomarkers, a P. falciparum homolog of insulin-degrading enzyme (PfIDEh) met our search criteri
81 r sites as wild-type Abeta by neprilysin and insulin-degrading enzyme, the two most widely studied Ab
82 o a 1-h incubation with either neprilysin or insulin degrading enzyme, whereas the monomer is rapidly
84 rotease Ste23 in yeast, a homologue of human insulin-degrading enzyme, which is required for efficien
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