INT230972

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Context Info
Confidence 0.18
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.07
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.

Golgi apparatus (SHH) endoplasmic reticulum (SHH) embryo development (SHH)
cell-cell signaling (SHH) signal transducer activity (SHH) peptidase activity (SHH)
Anatomy Link Frequency
neural 2
SHH (Homo sapiens)
Pain Link Frequency Relevance Heat
Neurotransmitter 6 48.32 Quite Low
Dopamine 2 13.44 Low Low
antagonist 8 5.00 Very Low Very Low Very Low
Glutamate 6 5.00 Very Low Very Low Very Low
Glutamate receptor 5 5.00 Very Low Very Low Very Low
agonist 3 5.00 Very Low Very Low Very Low
cytokine 2 5.00 Very Low Very Low Very Low
Spinal cord 2 5.00 Very Low Very Low Very Low
Neuritis 2 5.00 Very Low Very Low Very Low
Action potential 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Neurodegenerative Disease 9 68.20 Quite High
Obesity 3 5.00 Very Low Very Low Very Low
Neuritis 2 5.00 Very Low Very Low Very Low
Neurological Disease 2 5.00 Very Low Very Low Very Low
Apoptosis 2 5.00 Very Low Very Low Very Low
Death 2 5.00 Very Low Very Low Very Low
Adhesions 2 5.00 Very Low Very Low Very Low
Osteoporosis 2 5.00 Very Low Very Low Very Low
Disease 2 5.00 Very Low Very Low Very Low
Injury 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
More interestingly, in comparison of genes associated during neural differentiation process of human embryonic stem cells or human brain with our results, we also found increased expression of PENK, STK4, IGFBP4, Slc17a6, Slc6A1, Nurr1, Nrp2, Moxd1, Shh and Neurod2 [36,37].
Positive_regulation (increased) of Gene_expression (expression) of Shh in neural
1) Confidence 0.18 Published 2008 Journal BMC Genomics Section Body Doc Link PMC2358905 Disease Relevance 0.07 Pain Relevance 0

General Comments

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