INT248543

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Context Info
Confidence 0.69
First Reported 2008
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 7
Total Number 9
Disease Relevance 2.82
Pain Relevance 0.18

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
myocyte 1
P19 1
cardiogenic 1
hearts 1
Mef2c (Mus musculus)
Pain Link Frequency Relevance Heat
fibrosis 60 96.12 Very High Very High Very High
antagonist 32 66.32 Quite High
Potency 2 36.24 Quite Low
imagery 31 5.00 Very Low Very Low Very Low
anesthesia 20 5.00 Very Low Very Low Very Low
ketamine 12 5.00 Very Low Very Low Very Low
Action potential 11 5.00 Very Low Very Low Very Low
isoflurane 4 5.00 Very Low Very Low Very Low
ischemia 3 5.00 Very Low Very Low Very Low
Inflammation 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Coronary Heart Disease 78 99.84 Very High Very High Very High
Embryonal Carcinoma 46 99.44 Very High Very High Very High
Left Ventricular Hypertrophy 60 97.64 Very High Very High Very High
Stress 50 97.48 Very High Very High Very High
Hypertrophy 54 97.16 Very High Very High Very High
Fibrosis 60 96.12 Very High Very High Very High
Targeted Disruption 13 88.56 High High
Adhesions 8 86.96 High High
Teratoma 10 80.48 Quite High
Death 4 76.80 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Consistent with this hypothesis, data from previous studies indicate that activation of MEF2C may mediate myocardial adverse events invoked by pathological stress[8].
Positive_regulation (activation) of MEF2C associated with stress
1) Confidence 0.69 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.42 Pain Relevance 0.05
Signaling molecules potentially involved in MEF2C activation[12], [13], [18] were also examined to exclude off-target effects of siMEF2C.
Positive_regulation (activation) of MEF2C
2) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.09 Pain Relevance 0
Conversely, the activation of this pathway might be involved, together with changes in mitochondrial biogenesis and function, to the detrimental effects of MEF2C activation in cardiac hypertrophy.
Positive_regulation (activation) of MEF2C associated with coronary heart disease
3) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.29 Pain Relevance 0
However, it is still uncertain whether these genes are involved in the hypertrophic growth induced by MEF2C activation.
Positive_regulation (activation) of MEF2C
4) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.41 Pain Relevance 0.03
Moreover, mTOR overactivation has been shown to cause increased mitochondrial biogenesis and accumulation of reactive oxygen species in distinct model systems[36], suggesting that the activation of mTOR pathway might be responsible for the detrimental effects of MEF2C activation and vice-versa to the beneficial effects of MEF2C depletion in the mechanically overloaded hearts.
Positive_regulation (activation) of MEF2C in hearts
5) Confidence 0.47 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.17 Pain Relevance 0
The knockdown of myocardial MEF2C induced by specific small interfering RNA (siRNA) has been shown to attenuate hypertrophy, interstitial fibrosis and the rise of ANP levels in aortic banded mice.
Positive_regulation (induced) of MEF2C associated with fibrosis and hypertrophy
6) Confidence 0.47 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2794538 Disease Relevance 0.66 Pain Relevance 0.08
Differentiation into beating EBs was accompanied by mesodermal differentiation and dramatic activation of TWIST1, TBX5, and MEOX transcription, as well as the very clear induction of nearly all of the early cardiogenic genes, including FOXC1, ISL2, HAND1, GATA4, 5, and 6, FOXH1, and MEF2C.
Spec (clear) Positive_regulation (induction) of MEF2C in cardiogenic
7) Confidence 0.25 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2565131 Disease Relevance 0.16 Pain Relevance 0
Exposure of EC P19 cells to OT and OT-GKR increased GATA-4 mRNA (Fig. 6A), the transcription factor involved in cardiac development, and Mef2c mRNA (Fig. 6B), the gene involved in cardiac morphogenesis and myogenesis.
Positive_regulation (increased) of Mef2c in P19 associated with embryonal carcinoma
8) Confidence 0.20 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2964328 Disease Relevance 0.28 Pain Relevance 0.03
We established that the OTR-nitric oxide-cGMP pathway is essential for the OT-elicited differentiation of P19 stem cells into CM in association with elevation of transcription factors GATA-4 and myocyte-specific enhancer factor 2c (Mef2c) [12].
Positive_regulation (elevation) of Mef2c in myocyte
9) Confidence 0.18 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2964328 Disease Relevance 0.35 Pain Relevance 0

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