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IDE encodes a zinc metallopeptidase that degrades intracellular insulin, and thereby terminates insulins activity, as well as participating in intercellular peptide signalling by degrading diverse peptides such as glucagon, amylin, bradykinin, and kallidin. Additionally we are shipping Insulin-Degrading Enzyme Antibodies (134) and Insulin-Degrading Enzyme Kits (50) and many more products for this protein.
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Human IDE Protein expressed in HEK-293 Cells - ABIN2723516
Kim, Lone, Saghatelian: Analysis of the proteolysis of bioactive peptides using a peptidomics approach. in Nature protocols 2013
elevated IDE expression, in the skeletal muscle, seems to be mediated by activation of AMPK-ACC pathway, in response to exercise
IDE inhibition did notincrease amyloid formation or beta-cell loss.
This study demonstrated that the Decreased IDE and IGF2 expression in the cerebral cortex of pups by early life lead exposure.
Findings show a key role of Pla2g3 (show PLA2G3 Proteins) on the reduction of IDE, and suggest that cerebrum specific increase of Pla2g3 (show PLA2G3 Proteins) is involved in the initiation and/or progression of Alzheimer disease.
Abeta (show APP Proteins) level reduction by CALHM1 (show CALHM1 Proteins) could be explained by an increase in extracellular Abeta (show APP Proteins) degradation by insulin-degrading enzyme.
Data suggest that protein restriction down-regulates expression of insulysin (insulin degrading enzyme) in liver and subsequently reduced insulin (show INS Proteins) clearance.
IDE deficiency in bone marrow-derived cells results in larger atherosclerotic lesions, increased lesion-associated Abeta (show APP Proteins) and RAGE (show AGER Proteins), and higher serum cholesterol in male, Ldlr (show LDLR Proteins)(-/-) mice.
The type 2 diabetes-associated gene ide is required for insulin secretion and suppression of alpha-synuclein levels in beta-cells.
this study identified an upstream promoter element which blocks the reverse transcription of mouse IDE.
Data show that in the absence of insulin-degrading enzyme (IDE), full-length calcitonin gene-related peptide (CGRP (show CALCA Proteins)) levels are elevated in vivo.
People with allelic variation in four genes related to cardiovascular diseases and metabolism were more likely to die: apolipoprotein (APO (show C9orf3 Proteins))C1 GG and AG carriers, APOE (show APOE Proteins) varepsilon4 carriers, insulin-degrading enzyme (IDE) TC carriers, and phosphatidylinositol 3-kinase (PI3KCB) GG carriers.
Data suggest the possibility of development of insulin-degrading enzyme (IDE)-based drugs for the treatment of the late-onset form of Alzheimer's disease (AD).
the mechanistic and molecular features of IDE-26S proteasome (show Psmd4 Proteins) interaction in a cell experimental model, is reported.
No significant associations have been found between other IDE gene single nucleotide polymorphisms of rs4646953, rs2251101 and rs1544210 with Alzheimer disease.
results demonstrate that the polymorphisms rs1887922 and rs1999764 of the IDE gene are associated with late-onset Alzheimer disease susceptibility in the Xinjiang Han population
Cognitive impairment is more frequent among those exposed to the C allele of the rs2209972 SNP of the insulin degrading enzyme gene.
IDE does not play a major role in MHC class I antigen processing, confirming the dominant and almost exclusive role of the proteasome in cytosolic production of MHC class I ligands.
using combinational in silico investigations, study identified that pathogenic nonsynonymous mutations corresponding to p.I54F, p.P122T, p.T533R, p.P581A and p.Y609A have more potential role in structural and functional deviations of IDE activity
Our study provided evidence to IDE, PON1 (show PON1 Proteins), WFS1 (show WFS1 Proteins), POU2F1 (show POU2F1 Proteins), IL1alpha (show IL1A Proteins) and IL1beta (show IL1B Proteins) associated with T2D in Pakistanis.
An upstream promoter element which blocks the antisense transcription of the human IDE promoter, was identified.
This gene encodes a zinc metallopeptidase that degrades intracellular insulin, and thereby terminates insulins activity, as well as participating in intercellular peptide signalling by degrading diverse peptides such as glucagon, amylin, bradykinin, and kallidin. The preferential affinity of this enzyme for insulin results in insulin-mediated inhibition of the degradation of other peptides such as beta-amyloid. Deficiencies in this protein's function are associated with Alzheimer's disease and type 2 diabetes mellitus but mutations in this gene have not been shown to be causitive for these diseases. This protein localizes primarily to the cytoplasm but in some cell types localizes to the extracellular space, cell membrane, peroxisome, and mitochondrion. Alternative splicing results in multiple transcript variants encoding distinct isoforms. Additional transcript variants have been described but have not been experimentally verified.
, insulin-degrading enzyme
, insulin-degrading enzyme-like
, insulin protease
, Abeta-degrading protease