INT277586

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Context Info
Confidence 0.59
First Reported 2009
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 36
Total Number 37
Disease Relevance 11.03
Pain Relevance 0.86

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 (Mef2c) nucleus (Mef2c) DNA binding (Mef2c)
protein complex (Mef2c) cytoplasm (Mef2c)
Anatomy Link Frequency
ventricle 7
myocardium 2
cardiomyocytes 2
lungs 2
heart 2
Mef2c (Mus musculus)
Pain Link Frequency Relevance Heat
fibrosis 330 98.84 Very High Very High Very High
depression 3 40.08 Quite Low
anesthesia 99 31.68 Quite Low
ketamine 66 29.36 Quite Low
imagery 35 5.00 Very Low Very Low Very Low
antagonist 16 5.00 Very Low Very Low Very Low
cocaine 12 5.00 Very Low Very Low Very Low
Spinal cord 9 5.00 Very Low Very Low Very Low
Eae 6 5.00 Very Low Very Low Very Low
Analgesic 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Repression 25 100.00 Very High Very High Very High
Stress 264 99.00 Very High Very High Very High
Fibrosis 330 98.84 Very High Very High Very High
Hypertrophy 306 97.80 Very High Very High Very High
Left Ventricular Hypertrophy 330 97.28 Very High Very High Very High
Coronary Heart Disease 429 94.68 High High
Tuberous Sclerosis 33 93.48 High High
Congenital Anomalies 78 92.60 High High
Adhesions 34 91.08 High High
Targeted Disruption 87 85.80 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Remarkably, our results also show that depletion of MEF2C attenuated the interstitial fibrosis and the rise of ANP expression, without affecting the left ventricular function, indicating that depletion of MEF2C may reduce the adverse effects of pressure overload.
Negative_regulation (depletion) of MEF2C associated with fibrosis
1) Confidence 0.59 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.39 Pain Relevance 0.05
We detected that the depletion of MEF2C also results in lowered levels of both PGC-1?
Negative_regulation (depletion) of MEF2C
2) Confidence 0.59 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2794538 Disease Relevance 0.72 Pain Relevance 0.08
The treatment with siMEF2C was accompanied by marked reduction of MEF2C transcripts, but not of those from MEF2A, MEF2B or MEF2D (Figure 2C-F), after normalization to GAPDH.
Negative_regulation (reduction) of MEF2C
3) Confidence 0.59 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0 Pain Relevance 0
Therefore, we next examined if depletion of MEF2C could change the expression of PGC-1?
Negative_regulation (depletion) of MEF2C
4) Confidence 0.59 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0 Pain Relevance 0
Therefore, we next examined if depletion of MEF2C influences the rises of mtDNA copy number induced by pressure overload in mice left ventricle.
Spec (examined) Negative_regulation (depletion) of MEF2C in ventricle
5) Confidence 0.59 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.19 Pain Relevance 0.03
The data indicate that depletion of MEF2C is sufficient to markedly attenuate the hypertrophic growth and myocardial fibrosis of overloaded left ventricle by a mechanism dependent on defective activation of mTOR/S6K pathway.
Negative_regulation (depletion) of MEF2C in ventricle associated with fibrosis
6) Confidence 0.59 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.46 Pain Relevance 0.05
Conceivably, depletion of MEF2C results in changes in the abundance of mtDNA and energy metabolism in overloaded left ventricle.
Negative_regulation (depletion) of MEF2C in ventricle
7) Confidence 0.59 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.21 Pain Relevance 0.04
Depletion of MEF2C did not change the left ventricular diameter or fractional shortening (Figure 4B, C).
Negative_regulation (Depletion) of MEF2C
8) Confidence 0.51 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.44 Pain Relevance 0.07
Additionally, MEF2C depletion was accompanied by defective activation of S6K in response to pressure overload.
Negative_regulation (depletion) of MEF2C
9) Confidence 0.51 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2794538 Disease Relevance 0.73 Pain Relevance 0.09
Depletion of MEF2C markedly attenuated the rises of the mtDNA:nDNA ratio induced by aortic banding.
Negative_regulation (Depletion) of MEF2C
10) Confidence 0.51 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.05 Pain Relevance 0
Thus HDAC4 repression of RUNX2 and MEF2C is critical for normal bone development.
Negative_regulation (repression) of MEF2C associated with repression
11) Confidence 0.48 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2720538 Disease Relevance 0.40 Pain Relevance 0
Therefore it is highly likely that the expressed HDAC4 1-747 retains its binding to and repression of MEF2C and Runx2 in vivo, explaining the lack of chondrocyte hypertrophy in our mutant mice.
Negative_regulation (repression) of MEF2C in chondrocyte associated with hypertrophy and repression
12) Confidence 0.48 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2720538 Disease Relevance 0.72 Pain Relevance 0
We found that blood pressure, heart rate, left ventricular structure and function of sham-operated mice were unaffected by siMEF2C, indicating that depletion of MEF2C does not influence basal cardiac function or structure.
Negative_regulation (depletion) of MEF2C in heart
13) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.36 Pain Relevance 0.03
Overall, these data support the notion that depletion of MEF2C attenuates the load-induced replication of mtDNA and likely in mitochondrial biogenesis in mice left ventricle, associated to a defect in the regulation of PGC-1?
Negative_regulation (depletion) of MEF2C in ventricle
14) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.15 Pain Relevance 0
Remarkably, the restoration of the activity of this signaling complex after supplementation with leucine was accompanied by suppression of the anti-hypertrophic of MEF2C depletion, indicating that the defective activation of mTOR/S6K pathway is a critical component of the beneficial effects of MEF2C depletion in the cardiac phenotype of TAC mice.
Negative_regulation (depletion) of MEF2C
15) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.28 Pain Relevance 0
These findings represent new evidences that MEF2C depletion attenuates the hypertrophic responses to mechanical stress and highlight the potential of MEF2C to be a target for new therapies to cardiac hypertrophy and failure.



Negative_regulation (depletion) of MEF2C associated with stress and coronary heart disease
16) Confidence 0.43 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2794538 Disease Relevance 0.80 Pain Relevance 0.09
Accordingly, we have shown here that MEF2C depletion markedly attenuated the rise of PGC-1?
Negative_regulation (depletion) of MEF2C
17) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.28 Pain Relevance 0
Thus, we reasoned that supplementation with leucine might rescue the defective activation of mTOR/S6K complex after depletion of MEF2C.
Negative_regulation (depletion) of MEF2C
18) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.23 Pain Relevance 0
Finally, we found that supplementation with leucine attenuated the anti-hypertrophic effect of MEF2C depletion, as indicated by gravimetry and histological data shown in Figure 7D, E.
Negative_regulation (depletion) of MEF2C
19) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.32 Pain Relevance 0.03
In conclusion, we used RNAi strategy to deplete MEF2C in the left ventricle of adult mice and understand the role of this factor in the responses of the left ventricle to mechanical stress.
Negative_regulation (deplete) of MEF2C in ventricle associated with stress
20) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.42 Pain Relevance 0.04

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