INT190664

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Context Info
Confidence 0.52
First Reported 2006
Last Reported 2010
Negated 2
Speculated 3
Reported most in Body
Documents 3
Total Number 5
Disease Relevance 4.29
Pain Relevance 0.10

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

Golgi apparatus (Prnp) endoplasmic reticulum (Prnp) nucleolus (Prnp)
plasma membrane (Prnp) nucleus (Prnp) cytoplasm (Prnp)
Anatomy Link Frequency
brain 4
Prnp (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 16 82.00 Quite High
iatrogenic 6 69.00 Quite High
long-term potentiation 2 51.36 Quite High
Thalamus 14 5.00 Very Low Very Low Very Low
Hippocampus 10 5.00 Very Low Very Low Very Low
Eae 8 5.00 Very Low Very Low Very Low
medulla 6 5.00 Very Low Very Low Very Low
anesthesia 5 5.00 Very Low Very Low Very Low
Central nervous system 4 5.00 Very Low Very Low Very Low
cerebral cortex 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Sprains And Strains 163 99.12 Very High Very High Very High
Targeted Disruption 75 95.92 Very High Very High Very High
Creutzfeldt Jakob Disease 151 92.92 High High
Brain Disease 2 87.36 High High
Prion Diseases 92 86.00 High High
Disease 160 83.08 Quite High
Congenital Anomalies 8 82.64 Quite High
Stress 16 82.16 Quite High
Encephalitis 8 82.00 Quite High
Genetic Predisposition To Disease 2 81.72 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These changes were not dependent on PrPSc formation, since the protein accumulated in the brain to the same levels as in the untreated mice.
Neg (not) Regulation (dependent) of PrPSc Neg (not) Binding (formation) of in brain
1) Confidence 0.52 Published 2010 Journal PLoS Pathogens Section Abstract Doc Link PMC2951383 Disease Relevance 0.72 Pain Relevance 0
It is, however, possible that mechanisms other than the PrP primary sequence contribute to the species barrier, for instance binding of PrPC [45] or PrPSc [46,47] to other proteins or to cellular factors.
Spec (possible) Regulation (contribute) of PrPC Binding (binding) of
2) Confidence 0.24 Published 2006 Journal PLoS Pathogens Section Body Doc Link PMC1383487 Disease Relevance 0.87 Pain Relevance 0
It is, however, possible that mechanisms other than the PrP primary sequence contribute to the species barrier, for instance binding of PrPC [45] or PrPSc [46,47] to other proteins or to cellular factors.
Spec (possible) Regulation (contribute) of PrPSc Binding (binding) of
3) Confidence 0.24 Published 2006 Journal PLoS Pathogens Section Body Doc Link PMC1383487 Disease Relevance 0.92 Pain Relevance 0
These changes were not dependent on PrPSc formation, since the protein accumulated in the brain to the same levels as in the untreated mice.
Neg (not) Regulation (dependent) of PrPSc Neg (not) Binding (formation) of in brain
4) Confidence 0.23 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2951383 Disease Relevance 0.77 Pain Relevance 0.07
Biophysical measurements suggest that this powerful effect of residue 129 on prion strain selection is likely to be mediated via its effect on the conformation of PrPSc or its precursors or on the kinetics of their formation, as it has no measurable effect on the folding, dynamics or stability of PrPC[5,174].
Regulation (effect) of PrPSc Spec (likely) Binding (conformation) of associated with sprains and strains
5) Confidence 0.19 Published 2010 Journal Neuropathology and Applied Neurobiology Section Body Doc Link PMC3017745 Disease Relevance 1.02 Pain Relevance 0.03

General Comments

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