INT190778

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Context Info
Confidence 0.50
First Reported 2006
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 2
Total Number 3
Disease Relevance 1.49
Pain Relevance 0.55

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

lyase activity (Adcy1) plasma membrane (Adcy1) nucleus (Adcy1)
Anatomy Link Frequency
AC2 2
acute muscle 2
Adcy1 (Mus musculus)
Pain Link Frequency Relevance Heat
Pain 35 100.00 Very High Very High Very High
Inflammation 18 99.32 Very High Very High Very High
IPN 9 82.56 Quite High
antagonist 22 78.36 Quite High
Lasting pain 4 60.40 Quite High
Kinase C 22 50.52 Quite High
Neuropathic pain 1 37.84 Quite Low
Hyperalgesia 2 30.92 Quite Low
qutenza 1 21.72 Low Low
Fibrositis 1 7.88 Low Low
Disease Link Frequency Relevance Heat
Myalgia 29 100.00 Very High Very High Very High
INFLAMMATION 18 99.32 Very High Very High Very High
Targeted Disruption 51 92.16 High High
Injury 3 83.84 Quite High
Inflammatory Pain 9 82.56 Quite High
Pain 10 60.40 Quite High
Nociception 11 57.08 Quite High
Neuropathic Pain 29 37.84 Quite Low
Hyperalgesia 2 30.92 Quite Low
Myositis 1 9.16 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The contribution of AC1 and AC8 to the behavioral responses to acute muscle pain induced by intramuscular injection of 10 ?
Positive_regulation (induced) of Gene_expression (contribution) of AC1 in acute muscle associated with pain and myalgia
1) Confidence 0.50 Published 2006 Journal Mol Pain Section Body Doc Link PMC1395303 Disease Relevance 1.49 Pain Relevance 0.45
We found that Ishikawa cells express mRNA for AC1, AC3, AC4, AC5, AC6, AC7, AC9 and the soluble AC (SAC), but not AC2 or AC8 isoforms (data not shown).
Neg (not) Positive_regulation (not) of Neg (not) Gene_expression (express) of AC1 in AC2
2) Confidence 0.18 Published 2010 Journal Cell Signal Section Body Doc Link PMC2791881 Disease Relevance 0 Pain Relevance 0.10
As shown in Fig. 3C, transfection with AC3 siRNA completely abolished the potentiation of Butaprost-stimulated cAMP by PGF significantly (P < 0.001) while AC1 siRNA transfection had no effect on cAMP accumulation.
Positive_regulation (transfection) of Gene_expression (transfection) of AC1
3) Confidence 0.18 Published 2010 Journal Cell Signal Section Body Doc Link PMC2791881 Disease Relevance 0 Pain Relevance 0

General Comments

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