INT135582

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Context Info
Confidence 0.06
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Abstract
Documents 1
Total Number 2
Disease Relevance 1.02
Pain Relevance 1.87

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

mitochondrion (Prkce) endoplasmic reticulum (Prkce) enzyme binding (Prkce)
cytoplasm (Prkce) cell proliferation (Prok2) cytosol (Prkce)
Anatomy Link Frequency
neuronal 4
Prok2 (Rattus norvegicus)
Prkce (Mus musculus)
Pain Link Frequency Relevance Heat
qutenza 4 100.00 Very High Very High Very High
bradykinin 2 98.84 Very High Very High Very High
antagonist 2 98.32 Very High Very High Very High
Pain 2 96.64 Very High Very High Very High
nociceptor 4 95.68 Very High Very High Very High
Hyperalgesia 10 94.96 High High
dorsal root ganglion 6 93.88 High High
agonist 4 83.08 Quite High
Inflammation 2 35.20 Quite Low
Neuropeptide 2 25.00 Low Low
Disease Link Frequency Relevance Heat
Hyperalgesia 10 94.96 High High
Ganglion Cysts 6 93.88 High High
INFLAMMATION 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Bv8 enhanced the inward current carried by the heat and capsaicin receptor, transient receptor potential vanilloid 1 (TRPV1) via a pathway involving activation of protein kinase Cepsilon (PKCepsilon), because Bv8 caused translocation of PKCepsilon to the neuronal membrane and because PKC antagonists reduced both the enhancement of current carried by TRPV1 and behavioral hyperalgesia in rodents.
Bv8 Positive_regulation (caused) of Localization (translocation) of PKCepsilon in neuronal associated with hyperalgesia, qutenza and antagonist
1) Confidence 0.06 Published 2006 Journal J. Neurosci. Section Abstract Doc Link 16687502 Disease Relevance 0.49 Pain Relevance 0.91
Bv8 enhanced the inward current carried by the heat and capsaicin receptor, transient receptor potential vanilloid 1 (TRPV1) via a pathway involving activation of protein kinase Cepsilon (PKCepsilon), because Bv8 caused translocation of PKCepsilon to the neuronal membrane and because PKC antagonists reduced both the enhancement of current carried by TRPV1 and behavioral hyperalgesia in rodents.
Bv8 Positive_regulation (caused) of Localization (translocation) of PKCepsilon in neuronal associated with hyperalgesia, qutenza and antagonist
2) Confidence 0.05 Published 2006 Journal J. Neurosci. Section Abstract Doc Link 16687502 Disease Relevance 0.53 Pain Relevance 0.97

General Comments

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