INT213792

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Context Info
Confidence 0.45
First Reported 2007
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 3
Total Number 5
Disease Relevance 1.00
Pain Relevance 0.20

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

plasma membrane (Igf1r) kinase activity (Igf1r)
Igf1r (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 45 99.12 Very High Very High Very High
cerebral cortex 1 96.24 Very High Very High Very High
Inflammatory response 7 61.12 Quite High
Somatostatin 17 41.40 Quite Low
Central nervous system 7 5.00 Very Low Very Low Very Low
Pain 5 5.00 Very Low Very Low Very Low
isoflurane 5 5.00 Very Low Very Low Very Low
interstitial cystitis 4 5.00 Very Low Very Low Very Low
substance P 3 5.00 Very Low Very Low Very Low
Inflammatory stimuli 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 56 99.12 Very High Very High Very High
Hypertrophy 45 93.52 High High
Microcephaly 1 88.56 High High
Obesity 9 75.48 Quite High
Targeted Disruption 48 70.72 Quite High
Dislocations 7 64.32 Quite High
Lifespan 33 62.16 Quite High
Body Weight 5 60.68 Quite High
Microphthalmia 23 36.00 Quite Low
Increased Venous Pressure Under Development 1 10.60 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This cortical IGF-1R activation may be due to a compensatory local increase of ligand.
Positive_regulation (activation) of IGF-1R
1) Confidence 0.45 Published 2008 Journal PLoS Biology Section Body Doc Link PMC2573928 Disease Relevance 0.34 Pain Relevance 0.05
In addition, inflammation associated with PAR2 stimulation led to an up-regulation of serpine 1, WT1, cyclin D1, IGF1R, and cathepsin K.


Positive_regulation (up-regulation) of IGF1R associated with inflammation
2) Confidence 0.32 Published 2007 Journal BMC Immunol Section Body Doc Link PMC2000913 Disease Relevance 0.30 Pain Relevance 0.15
At no time point following acute resistance exercise was there an increase in IGF-1R tyrosine phosphorylation (Figure 1), suggesting that the IGF-1R is not activated by acute resistance exercise.


Neg (not) Positive_regulation (activated) of IGF-1R
3) Confidence 0.27 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2905373 Disease Relevance 0.12 Pain Relevance 0
Insulin and insulin-like growth factor activation of mTORC1 is dependent on the activation of the IGF-1 receptor [44], the generation of PI(3,4,5)P3 at the membrane, and the subsequent activation of PKB [45], [46].
Positive_regulation (activation) of IGF-1 receptor
4) Confidence 0.18 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2905373 Disease Relevance 0.16 Pain Relevance 0
We found no increase in IGF-1 receptor tyrosine phosphorylation or IRS1/2 associated p85 following resistance exercise and, from 30 minutes, p85 associated with IRS1/2 was reduced.
Neg (no) Positive_regulation (increase) of IGF-1 receptor
5) Confidence 0.18 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2905373 Disease Relevance 0.07 Pain Relevance 0

General Comments

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