INT43085

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Context Info
Confidence 0.39
First Reported 1983
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 28
Total Number 30
Disease Relevance 19.96
Pain Relevance 3.45

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

cytosol (Ide) mitochondrion (Ide) extracellular space (Ide)
ATPase activity (Ide) nucleus (Ide)
Anatomy Link Frequency
brain 3
plasma 2
liver 1
hepatocytes 1
muscle 1
Ide (Mus musculus)
Pain Link Frequency Relevance Heat
Enkephalin 16 100.00 Very High Very High Very High
narcan 3 99.80 Very High Very High Very High
antagonist 2 99.62 Very High Very High Very High
Opioid 6 99.40 Very High Very High Very High
Eae 70 99.14 Very High Very High Very High
tolerance 104 98.64 Very High Very High Very High
Neuropeptide 7 96.56 Very High Very High Very High
amygdala 90 92.72 High High
Hippocampus 2 91.52 High High
fibrosis 1 88.48 High High
Disease Link Frequency Relevance Heat
Alzheimer's Dementia 248 100.00 Very High Very High Very High
Insulin Resistance 45 100.00 Very High Very High Very High
Impaired Glucose Tolerance 79 99.96 Very High Very High Very High
Targeted Disruption 484 99.86 Very High Very High Very High
Amyloid Plaque 34 99.32 Very High Very High Very High
Disease 483 99.24 Very High Very High Very High
Diabetes Mellitus 493 97.64 Very High Very High Very High
Hyperinsulinism 13 93.56 High High
Sprains And Strains 140 91.52 High High
Diabetic Nephropathy 1 90.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The specific activity of IDE on T40 was demonstrated by a dose dependent inhibition with insulin (a natural IDE substrate) or 1,10-phenanthroline (a zinc metalloprotease inhibitor)(Figure 2B).
Negative_regulation (inhibition) of insulin
1) Confidence 0.39 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1920558 Disease Relevance 0.13 Pain Relevance 0
Bulatao and Carlson [14] observed the hypoglycaemic effect of insulin in dogs was associated with an increase in the height and frequency of gastric contractions and gastric tonus.
Negative_regulation (effect) of insulin
2) Confidence 0.36 Published 2006 Journal BMC Pharmacol Section Body Doc Link PMC1444921 Disease Relevance 0 Pain Relevance 0.04
Each group of overnight fasted mice was administered insulin subcutaneously (s.c) 2 ?
Negative_regulation (administered) of insulin
3) Confidence 0.36 Published 2006 Journal BMC Pharmacol Section Body Doc Link PMC1444921 Disease Relevance 0 Pain Relevance 0
Later studies indicated the acceleration of gastric emptying [11] and other parts of intestine [16] were due to the hypoglycaemic effect of insulin.
Negative_regulation (effect) of insulin in other parts
4) Confidence 0.36 Published 2006 Journal BMC Pharmacol Section Body Doc Link PMC1444921 Disease Relevance 0 Pain Relevance 0.06
It is possible that the loss of IDE and neprilysin in AD brain is due to the loss of neurons that produce these two enzymes or the hypofunction of live neurons as it has been reported for choline acetyltransferase (ChAT) in AD.
Negative_regulation (loss) of IDE in neurons associated with disease
5) Confidence 0.34 Published 2009 Journal Mol Neurodegener Section Body Doc Link PMC2726140 Disease Relevance 0.92 Pain Relevance 0.05
Reduction in hippocampal IDE protein levels were reported and were associated with the APOE-4 allele presence in the AD patients [38].
Negative_regulation (Reduction) of IDE associated with disease
6) Confidence 0.34 Published 2009 Journal Mol Neurodegener Section Body Doc Link PMC2726140 Disease Relevance 0.74 Pain Relevance 0.04
IDE activity was decreased in soluble fractions from the brain of AD patients compared to normal control brains [48], which suggests that a decrease in enzyme activity could be responsible for the increased accumulation of pathologic amyloid peptides during AD.
Negative_regulation (decreased) of IDE in brains associated with alzheimer's dementia and disease
7) Confidence 0.34 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1920558 Disease Relevance 0.55 Pain Relevance 0
These mice were recently reported to exhibit glucose intolerance, insulin resistance and a decrease in 2-deoxyglucose uptake in cultured hepatocytes, which adds evidence for an important role of extracellular nucleotides in glucose homeostasis, probably at least in part through the P2Y1 receptor [33].
Negative_regulation (decrease) of insulin in hepatocytes associated with insulin resistance and impaired glucose tolerance
8) Confidence 0.25 Published 2005 Journal Purinergic Signal Section Body Doc Link PMC2096536 Disease Relevance 0.41 Pain Relevance 0
IDE has been proposed to be an amyloid scavenger recognizing structural ?
Negative_regulation (scavenger) of IDE associated with alzheimer's dementia
9) Confidence 0.25 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1920558 Disease Relevance 0.28 Pain Relevance 0
Therefore, if modification of hAChE by IDE occurs in vivo, both IDE and NEP deficiencies could alter the brain levels of CSR species and increase the risk of oligomerisation and fibril deposition.
Negative_regulation (deficiencies) of IDE in brain
10) Confidence 0.25 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1920558 Disease Relevance 0.05 Pain Relevance 0
IDE cleaves a broad range of peptides and has been proposed to be an amyloid scavenger recognizing structural ?
Negative_regulation (scavenger) of IDE associated with alzheimer's dementia
11) Confidence 0.25 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1920558 Disease Relevance 1.06 Pain Relevance 0.08
Furthermore, insulin can modulate tau phosphorylation in vitro [17] and in non-transgenic mice, depletion of insulin results in increased tau phosphorylation, with no concomitant formation of pathological tau deposits [18], [19].
Negative_regulation (depletion) of insulin associated with targeted disruption and eae
12) Confidence 0.18 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2775636 Disease Relevance 1.87 Pain Relevance 0.14
Specifically, we showed that depletion of insulin upon STZ injection and consequently, chronically increased blood glucose levels causes hyperphosphorylation of tau, a protein associated with AD.
Negative_regulation (depletion) of insulin in blood associated with disease
13) Confidence 0.18 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2775636 Disease Relevance 0.79 Pain Relevance 0.04
While co-morbidity is difficult to address in humans, transgenic mice offer the selective advantage to determine whether reduction in insulin levels can exacerbate a pre-existing tau pathology.
Negative_regulation (reduction) of insulin associated with targeted disruption
14) Confidence 0.18 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2775636 Disease Relevance 1.40 Pain Relevance 0.12
, to examine the relative contribution of two insulin-sensitive tissues, muscle and liver, towards the insulin sensitization phenotype originally observed in the global GSK-3?
Negative_regulation (sensitization) of insulin in liver
15) Confidence 0.16 Published 2011 Journal PLoS ONE Section Abstract Doc Link PMC3017066 Disease Relevance 0.68 Pain Relevance 0.04
Since there was a lack of insulin-sensitization in the tissue-specific deletions of GSK-3?
Negative_regulation (lack) of insulin
16) Confidence 0.16 Published 2011 Journal PLoS ONE Section Body Doc Link PMC3017066 Disease Relevance 0.28 Pain Relevance 0
Insulin deficiency and consequently, increased glucose levels exacerbated the histopathology of pR5, with accelerated tau deposition and NFT formation.


Negative_regulation (deficiency) of Insulin
17) Confidence 0.13 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2775636 Disease Relevance 1.02 Pain Relevance 0.10
Here, we hypothesized that depletion of insulin may accelerate the tau pathology in a mouse model that is prone to develop NFTs.
Negative_regulation (depletion) of insulin
18) Confidence 0.13 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2775636 Disease Relevance 0.62 Pain Relevance 0.06
Defective insulin signalling and altered glucose metabolism have also been found in AD [14]–[16].
Negative_regulation (Defective) of insulin associated with disease
19) Confidence 0.13 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2775636 Disease Relevance 2.06 Pain Relevance 0.13
Interestingly, this was not associated with the formation of insoluble tau aggregates or NFTs, suggesting that hyperphosphorylation of tau upon insulin depletion in itself is not sufficient to induce its deposition.
Negative_regulation (depletion) of insulin
20) Confidence 0.13 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2775636 Disease Relevance 0.62 Pain Relevance 0.22

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