INT241451

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Context Info
Confidence 0.09
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.10
Pain Relevance 0.21

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

signal transduction (Ngfr) nuclear envelope (Ngfr) Golgi apparatus (Ngfr)
cell adhesion (Mag) plasma membrane (Ngfr) nucleus (Ngfr)
Anatomy Link Frequency
neurite 1
Mag (Mus musculus)
Ngfr (Mus musculus)
Pain Link Frequency Relevance Heat
dorsal root ganglion 1 99.20 Very High Very High Very High
Central nervous system 29 86.40 High High
Peripheral nervous system 3 67.72 Quite High
Spinal cord 19 25.72 Quite Low
cINOD 6 5.00 Very Low Very Low Very Low
Kinase C 5 5.00 Very Low Very Low Very Low
cva 5 5.00 Very Low Very Low Very Low
ischemia 3 5.00 Very Low Very Low Very Low
adenocard 1 5.00 Very Low Very Low Very Low
Intracerebroventricular 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Ganglion Cysts 1 98.72 Very High Very High Very High
Shock 2 37.84 Quite Low
Spinal Cord Injury 16 26.08 Quite Low
Injury 6 24.68 Low Low
Paralysis 1 21.28 Low Low
Disease 18 5.00 Very Low Very Low Very Low
Stroke 15 5.00 Very Low Very Low Very Low
Targeted Disruption 7 5.00 Very Low Very Low Very Low
Cv General 3 Under Development 3 5.00 Very Low Very Low Very Low
Optic Nerve Injuries 3 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Initially, we reported that p75NTR is required for neurite outgrowth inhibition by MAG by using postnatal dorsal root ganglion (DRG) neurons from mutant mice with a mutation in the p75NTR gene (Yamashita et al 2002).
MAG Positive_regulation (required) of p75NTR in neurite associated with ganglion cysts and dorsal root ganglion
1) Confidence 0.09 Published 2008 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2500253 Disease Relevance 0.10 Pain Relevance 0.21

General Comments

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