INT275156

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Context Info
Confidence 0.03
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 4
Disease Relevance 2.89
Pain Relevance 0.40

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

aging (Agt) intracellular (Rac1) enzyme binding (Rac1)
GTPase activity (Rac1) extracellular matrix organization (Agt) cytoplasm (Rac1)
Anatomy Link Frequency
myocytes 2
fibroblasts 2
Agt (Rattus norvegicus)
Rac1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Inflammation 188 79.36 Quite High
fibrosis 24 59.92 Quite High
Inflammatory response 28 5.00 Very Low Very Low Very Low
Inflammatory marker 20 5.00 Very Low Very Low Very Low
metalloproteinase 20 5.00 Very Low Very Low Very Low
cva 16 5.00 Very Low Very Low Very Low
Bioavailability 8 5.00 Very Low Very Low Very Low
cytokine 8 5.00 Very Low Very Low Very Low
Catecholamine 4 5.00 Very Low Very Low Very Low
antagonist 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Heart Arrhythmia 1148 90.04 High High
INFLAMMATION 236 79.36 Quite High
Coronary Heart Disease 12 77.36 Quite High
Fibrosis 32 59.92 Quite High
Adhesions 12 21.36 Low Low
Thrombosis 4 8.48 Low Low
Left Ventricular Dysfunction 8 7.36 Low Low
Coronary Artery Disease 56 5.28 Low Low
Recurrence 112 5.00 Very Low Very Low Very Low
Myocardial Infarction 108 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In cultured atrial myocytes and fibroblasts, Ang II induced tyrosine phosphorylation of STAT3 through a Rac1-dependent mechanism, which was inhibited by dominant-negative Rac1, losartan, and simvastatin.
Ang II Positive_regulation (induced) of Rac1 in myocytes
1) Confidence 0.03 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2704895 Disease Relevance 0.72 Pain Relevance 0.10
In cultured atrial myocytes and fibroblasts, Ang II induced tyrosine phosphorylation of STAT3 through a Rac1-dependent mechanism, which was inhibited by dominant-negative Rac1, losartan, and simvastatin.
Ang II Positive_regulation (induced) of Rac1 in myocytes
2) Confidence 0.03 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2704895 Disease Relevance 0.73 Pain Relevance 0.10
In cultured atrial myocytes and fibroblasts, Ang II induced tyrosine phosphorylation of STAT3 through a Rac1-dependent mechanism, which was inhibited by dominant-negative Rac1, losartan, and simvastatin.
Ang II Positive_regulation (induced) of Rac1 in fibroblasts
3) Confidence 0.01 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2704895 Disease Relevance 0.72 Pain Relevance 0.10
In cultured atrial myocytes and fibroblasts, Ang II induced tyrosine phosphorylation of STAT3 through a Rac1-dependent mechanism, which was inhibited by dominant-negative Rac1, losartan, and simvastatin.
Ang II Positive_regulation (induced) of Rac1 in fibroblasts
4) Confidence 0.01 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2704895 Disease Relevance 0.73 Pain Relevance 0.10

General Comments

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