INT201741

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Context Info
Confidence 0.01
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 1.00
Pain Relevance 0

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

cytoplasm (Rhoa, Ngfr) plasma membrane (Rhoa, Ngfr) nucleus (Rhoa, Ngfr)
cell differentiation (Rhoa) nuclear envelope (Ngfr) mitochondrion (Rhoa)
Anatomy Link Frequency
neurite 1
Rhoa (Mus musculus)
Ngfr (Mus musculus)
Pain Link Frequency Relevance Heat
withdrawal 1 43.08 Quite Low
Glutamate 2 30.96 Quite Low
Inflammation 9 5.00 Very Low Very Low Very Low
cytokine 8 5.00 Very Low Very Low Very Low
Hippocampus 7 5.00 Very Low Very Low Very Low
Eae 6 5.00 Very Low Very Low Very Low
long-term potentiation 5 5.00 Very Low Very Low Very Low
Kinase C 5 5.00 Very Low Very Low Very Low
Neurotransmitter 5 5.00 Very Low Very Low Very Low
Central nervous system 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Death 56 99.16 Very High Very High Very High
Brain Injury 1 91.04 High High
Apoptosis 133 86.12 High High
Toxicity 15 77.20 Quite High
Stress 32 75.36 Quite High
Parkinson's Disease 8 73.12 Quite High
Disease 127 65.12 Quite High
Amyloid Plaque 5 5.92 Low Low
Neurodegenerative Disease 36 5.00 Very Low Very Low Very Low
Cognitive Disorder 16 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Finally, p75NTR receptor has been found to directly interact with RhoA, a member of the Ras-GTP binding proteins and a regulator of actin assembly in many cell types, suggesting a role for this receptor in the neurite outgrowth and reorganization of the actin cytoscheleton, a function that is negatively modulated by neurotrophin binding [168].


RhoA Binding (interact) of p75NTR receptor in neurite
1) Confidence 0.01 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1775042 Disease Relevance 1.00 Pain Relevance 0

General Comments

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