INT266658

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Context Info
Confidence 0.05
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 0.21
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 (SH3BP5, AKT1) signal transduction (SH3BP5, AKT1) cell differentiation (AKT1)
nucleoplasm (AKT1) transport (AKT1) mitochondrion (SH3BP5)
SH3BP5 (Homo sapiens)
AKT1 (Homo sapiens)
Pain Link Frequency Relevance Heat
metalloproteinase 6 50.00 Quite Low
Inflammation 30 27.52 Quite Low
cytokine 4 22.12 Low Low
COX2 2 20.32 Low Low
Angina 4 5.00 Very Low Very Low Very Low
Inflammatory mediators 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
Fibrosarcoma 2 93.80 High High
Leukemia 2 64.80 Quite High
Death 2 52.32 Quite High
INFLAMMATION 34 27.52 Quite Low
Rupture 8 5.00 Very Low Very Low Very Low
Atherosclerotic Plaque 6 5.00 Very Low Very Low Very Low
Cv General 3 Under Development 4 5.00 Very Low Very Low Very Low
Atherosclerosis 4 5.00 Very Low Very Low Very Low
Metabolic Disorder 2 5.00 Very Low Very Low Very Low
Cardiovascular Disease 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Inhibition of Akt by SH-5 was associated with attenuation of MMP-9 secretion in AA stimulated MonoMac 6 cells.
SH-5 Negative_regulation (Inhibition) of Akt
1) Confidence 0.05 Published 2009 Journal Lipids Health Dis Section Body Doc Link PMC2667508 Disease Relevance 0.15 Pain Relevance 0
To test the phophatidylinositol signalling system downstream of PI3K we treated the MonoMac 6 cells for 30 min with various concentrations of phosphatidyl inositol analog, SH-5, an inhibitor of Akt.
SH-5 Negative_regulation (inhibitor) of Akt
2) Confidence 0.03 Published 2009 Journal Lipids Health Dis Section Body Doc Link PMC2667508 Disease Relevance 0.06 Pain Relevance 0

General Comments

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