|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for IDE(NM_004969.3) Search again
Product ID:
HQP009349
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
INSULYSIN
Gene Description:
insulin degrading enzyme
Target Gene Accession:
NM_004969.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
|
|
| A | B |
|
Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
|
Summary
This gene may belong to a protease family responsible for intercellular peptide signalling. Though its role in the cellular processing of insulin has not yet been defined, insulin-degrading enzyme is thought to be involved in the termination of the insulin response. [provided by RefSeq].
Gene References into function
- Insulin-degrading enzyme rapidly removes the beta-amyloid precursor protein intracellular domain (AICD).
- IDE knockout mice show significantly elevated levels of blood insulin, brain beta-amyloid, and brain amyloid-precursor protein intracellular domain, providing key in vivo evidence that IDE degrades both extracellular and intracellular peptides.
- analysis of over 2,400 samples provides no compelling evidence that variation in IDE contributes to diabetes susceptibility in humans
- when intracellular long-chain fatty acid concentrations are elevated, they may act directly on insulin-degrading enzyme to decrease insulin metabolism and alter insulin action in intact cells and this mechanism may contribute to insulin resistance
- Polymorphism in this enzyme are associated with NIDDM in men.
- IDE gene polymorphisms do not confer susceptibility to early- or late-onset AD at least in a Japanese population.
- Biochemical characteristics of insulin degradation in wound fluid were consistent with characteristics of insulin-degrading enzyme. Reduction in insulin-degrading activity in wound fluid is potential therapeutic target.
- This study provides strong evidence for pathogenic variant(s) in the 276-kb region harboring IDE that influence intermediate Alzheimer's disease phenotypes and risk for AD.
- genomic region in the proximity of IDE that may contribute to Alzheimer and Parkinson disease in a similar manner.
- IDE gene promoter region variants are associated with AD in subjects without an epsilon4 allele
- Polymorphism in/near IDE contributes to a large proportion of variance in plasma insulin levels and correlated traits.
- The C allele of single-nucleotide polymorphism IDE2 associated with Alzheimer disease. There may be a possible synergic interaction between IDE & APOE epsilon4.
- IDE is targeted to mitochondria via alternative initiation of translation.
- a defect in Abeta proteolysis by IDE contributes to the accumulation of this peptide in the cortical microvasculature
- To test the hypothesis that insulin might upregulate IDE via a negative feedback control mechanism, we used both in vitro and in vivo strategies to determine the impact of insulin signaling on IDE levels.
- Results indicate that alleles of IDE contribute to variability in A beta deposition in the AD brain and suggest that this relationship may have relevance for the degree of cognitive dysfunction in AD patients.
- This study systematically characterizes IDE mRNAs, identifies a novel, catalytically inefficient splice form and compares its subcellular distribution, kinetic properties and ability to degrade amyloid beta protein to the known isoform.
- Common genetic variation at IDE is unlikely to confer clinically significant risk of type 2 diabetes in Caucasians.
- Beta-amyloid degradation is largely the result of the action of IDE, as it is blocked by insulin in the medium, a competitive substrate of IDE. IDE could be an important therapeutic target to decrease the amount of Abeta in the cerebrovasculature.
- IDE-N is the catalytic domain and IDE-C facilitates substrate recognition as well as plays a key role in the oligomerization of IDE.
- Different reconstructed insulin-degrading enzyme haplotypes were associated with Alzheimers disease and lower cognitive ability.
- The combined genotype data from 1269 late-onset AD cases and 980 controls yielded a significant association to IDE_9 located in the 3'-end of the IDE gene after conservative multiple testing Bonferroni correction (p = 0.005).
- protein structures of human IDE in complex with four substrates (insulin B chain, amyloid-beta peptide (1-40), amylin and glucagon)
- cellular receptor for infection by varicella-zoster virus. Interacts with VZV glycoprotein E.
- First demonstration of IDE in normal and neoplastic human mammary tissues, providing an experimental starting point towards exploring a potential role of IDE in the control of tumor progression.
- This study suggests IDE may be indirectly related to dementia via its regulation of insulin levels, but it is not a major gene for Alzheimer's.
- the genetic linkage of AD in this set of chromosome 10-linked AD families may be the result of systemic defects in IDE activity in the absence of altered IDE expression
- SNPs rs4646953 & rs4646955 are associated with Alzheimer disease in Finnish patients, conferring an approximately two-fold increased risk.
- Variations in IDE may contribute to diabetes susceptibility in the Korean population.
- The single nucleotide polymorphism rs2209972 in the human IDE gene is associated with metabolic features of polycystic ovary syndrome women in a Chinese population.
- This shows that IDE is involved in cellular insulin metabolism and provides further evidence that insulin inhibits protein degradation via an interaction with IDE.
- Polymorphisms in the IDE-KIF11-HHEX gene locus are associated with susceptibility to type 2 diabetes across the boundary of race.
- Importance of the distribution of the enzyme in brain and pituitary is discussed in relation to its main known substrataes.
- the catalytic domain of insulin-degrading enzyme forms a denaturant-resistant complex with amyloid beta peptide
- Results suggest a relationship between a gene that is intimately involved in insulin metabolism and the determination of lifespan in humans.
- predict that alkylation of C812 and C819 disrupts substrate binding, whereas alkylation of C178 interferes with the apposition of active-site domains and subtly repositions zinc-binding residues
- IDE protein was expressed in all the tissues assessed and all the tumor cell lines except for Raji and HL-60.
- Insulin-degrading enzyme protein expression was found in normal tissues of the kidney, liver, lung, brain, breast and skeletal muscle, as well as in breast and ovarian cancer tissues.
- kinetics and regulation of human IDE with short peptides
- present study provides evidence that IDE promoter polymorphisms that significantly decrease IDE expression levels are associated with development of sporadic lzheimer disease
- Allele and genotype frequency distribution for three markers of insulinase differed only in the sample of females between T2D patients and control , while only in case of rs7078413 SNP genotype frequencies varied significantly in the total population