INT290401

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Context Info
Confidence 0.64
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 3
Disease Relevance 1.81
Pain Relevance 0.07

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

cell differentiation (Mef2a) nucleus (Mef2a) DNA binding (Mef2a)
Anatomy Link Frequency
cardiomyocytes 1
heart 1
Mef2a (Mus musculus)
Pain Link Frequency Relevance Heat
fibrosis 30 73.32 Quite High
anesthesia 9 5.00 Very Low Very Low Very Low
ketamine 6 5.00 Very Low Very Low Very Low
imagery 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Hypertrophy 27 98.96 Very High Very High Very High
Coronary Heart Disease 39 91.48 High High
Stress 24 81.32 Quite High
Myocardial Infarction 9 78.96 Quite High
Targeted Disruption 6 76.08 Quite High
Fibrosis 30 73.32 Quite High
Injury 3 58.48 Quite High
Heart Disease 6 55.64 Quite High
Left Ventricular Hypertrophy 30 54.92 Quite High
Congenital Anomalies 6 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Western blot analysis indicated that MEF2C was reduced in the order of 75%, while no change could be observed in the expression of MEF2A in cells treated with siMEF2C, in comparison with cells treated with siGFP (Figure 1E, F).
Gene_expression (expression) of MEF2A
1) Confidence 0.64 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.05 Pain Relevance 0
Accordingly, forced expressions of MEF2A, C and D in mice heart were demonstrated to be sufficient to drive intolerance to pressure overload, ventricular chamber dilation and contractile dysfunction[8], [9], [10].
Gene_expression (expressions) of MEF2A in heart
2) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.76 Pain Relevance 0.03
Overexpression of MEF2A or MEF2C in cultured cardiomyocytes induces sarcomere degeneration and cardiomyocytes elongation, suggesting that activation of these members may compose signaling pathways responsible for pathologic hypertrophy [8].
Gene_expression (Overexpression) of MEF2A in cardiomyocytes associated with hypertrophy
3) Confidence 0.57 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 1.00 Pain Relevance 0.04

General Comments

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