INT277602

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Context Info
Confidence 0.39
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 10
Total Number 10
Disease Relevance 4.35
Pain Relevance 0.16

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
cardiomyocytes 2
heart 2
myocyte 1
ventricle 1
chondrocyte 1
Mef2c (Mus musculus)
Pain Link Frequency Relevance Heat
fibrosis 50 78.44 Quite High
depression 4 40.68 Quite Low
antagonist 16 25.84 Quite Low
cocaine 16 5.00 Very Low Very Low Very Low
anesthesia 15 5.00 Very Low Very Low Very Low
Spinal cord 12 5.00 Very Low Very Low Very Low
ketamine 10 5.00 Very Low Very Low Very Low
Eae 8 5.00 Very Low Very Low Very Low
Analgesic 8 5.00 Very Low Very Low Very Low
Acute pain 8 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Repression 33 100.00 Very High Very High Very High
Myocardial Infarction 16 98.00 Very High Very High Very High
Hypertrophy 57 97.80 Very High Very High Very High
Coronary Heart Disease 65 96.60 Very High Very High Very High
Targeted Disruption 38 93.12 High High
Left Ventricular Hypertrophy 50 88.56 High High
Stress 40 86.44 High High
Embryonal Carcinoma 23 80.60 Quite High
Fibrosis 50 78.44 Quite High
Hyperplasia 1 73.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In vitro assays have established that aa 119-208 is sufficient to interact with MEF2 and HDAC1 [4], [8].
MEF2 Binding (interact) of
1) Confidence 0.39 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2720538 Disease Relevance 0.43 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.
MEF2C Binding (depletion) of in heart
2) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.36 Pain Relevance 0.03
Besides the left ventricle, depletion of MEF2C was confirmed to occur in cardiomyocytes harvested from mice treated with siMEF2C, thereby demonstrating the susceptibility of this cell type to the effects of systemically delivered siRNA.
MEF2C Binding (depletion) of in cardiomyocytes
3) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.18 Pain Relevance 0.03
There is also evidence associating MEF2 transcription factors with common forms of human heart failure[14].
MEF2 Binding (associating) of in heart associated with myocardial infarction
4) Confidence 0.36 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.85 Pain Relevance 0.06
The expression of MEF2C was reduced in cardiomyocytes harvested from the left ventricle 24 hours after the treatment with siMEF2C to similar levels of myocardial extracts (?
siMEF2C Binding (treatment) of in ventricle
5) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0 Pain Relevance 0
In this context, many studies have shown that overall MEF2 DNA-binding activity is enhanced in cardiomyocytes in response to biomechanical and neurohormonal stimuli[11], [12], [13].
MEF2 Binding (binding) of in cardiomyocytes
6) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794538 Disease Relevance 0.93 Pain Relevance 0.04
The effect of MEF2C deficit on bone formation is mediated through interactions with HDAC4 such that the precocious ossification in HDAC4 null animals is mostly rescued by a single allele deletion of MEF2C.
MEF2C Binding (interactions) of
7) Confidence 0.30 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2720538 Disease Relevance 0.39 Pain Relevance 0
Extensive deletion analysis [4], [6], [8] coupled with in vitro assays have established that amino acids (aa) 1–660 is sufficient to interact with MEF2, Runx2, HDAC1, 14-3-3, and also for phosphorylation and nuclear export [3], [12], [13], [16]–[19].
MEF2 Binding (interact) of
8) Confidence 0.30 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2720538 Disease Relevance 0.14 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.
MEF2C Binding (binding) of in chondrocyte associated with hypertrophy and repression
9) Confidence 0.29 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2720538 Disease Relevance 0.72 Pain Relevance 0
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].
Mef2c Binding (association) of in myocyte
10) Confidence 0.14 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2964328 Disease Relevance 0.35 Pain Relevance 0

General Comments

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