INT302940

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Context Info
Confidence 0.37
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 1.53
Pain Relevance 0.10

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 (Smpd3) Golgi apparatus (Smpd3) cell cycle (Smpd3)
response to stress (Smpd3)
Anatomy Link Frequency
fibroblasts 1
Smpd3 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 8 84.76 Quite High
agonist 12 65.84 Quite High
cytokine 6 5.00 Very Low Very Low Very Low
metalloproteinase 2 5.00 Very Low Very Low Very Low
anesthesia 2 5.00 Very Low Very Low Very Low
Inflammatory response 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Stress 38 99.60 Very High Very High Very High
Apoptosis 126 99.24 Very High Very High Very High
INFLAMMATION 10 84.76 Quite High
Necrosis 6 75.36 Quite High
Osteogenic Sarcomas 4 66.36 Quite High
Toxicity 16 34.12 Quite Low
Leukemia 2 24.96 Low Low
Death 10 5.00 Very Low Very Low Very Low
Osteogenesis Imperfecta 8 5.00 Very Low Very Low Very Low
Alzheimer's Dementia 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
was apparently independent of nSMase2 and SM hydrolysis in murine fibroblasts, since similar apoptosis was observed in nSMase2-deficient cells, and since rescuing the activity of the nSMase2 did not alter the apoptosis induced by TNF?
nSMase2 Binding (activity) of in fibroblasts associated with apoptosis
1) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2843740 Disease Relevance 1.02 Pain Relevance 0.04
In order to define the specific contributions of nSMase2 to these stress responses, the activation of the SM/Cer pathway by TNF?
nSMase2 Binding (contributions) of associated with stress
2) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2843740 Disease Relevance 0.51 Pain Relevance 0.06

General Comments

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