INT290401

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

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 anesthesia 9 5.00 ketamine 6 5.00 imagery 3 5.00

Disease Link Frequency Relevance Heat Hypertrophy 27 98.96 Coronary Heart Disease 39 91.48 Stress 24 81.32 Myocardial Infarction 9 78.96 Targeted Disruption 6 76.08 Fibrosis 30 73.32 Injury 3 58.48 Heart Disease 6 55.64 Left Ventricular Hypertrophy 30 54.92 Congenital Anomalies 6 5.00

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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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