INT280467

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.59
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 8
Disease Relevance 3.33
Pain Relevance 1.21

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

enzyme binding (Mecp2) embryo development (Mecp2) DNA binding (Mecp2)
protein complex (Mecp2) response to stress (Mecp2) cytoplasm (Mecp2)
Anatomy Link Frequency
synapses 2
hypothalamus 1
neurons 1
forebrain 1
Mecp2 (Mus musculus)
Pain Link Frequency Relevance Heat
amygdala 288 99.32 Very High Very High Very High
long-term potentiation 6 98.60 Very High Very High Very High
midbrain 15 86.40 High High
depression 73 80.56 Quite High
antidepressant 62 71.56 Quite High
anesthesia 4 54.92 Quite High
Thalamus 3 42.48 Quite Low
Eae 12 18.20 Low Low
Hippocampus 46 16.28 Low Low
fluoxetine 18 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Repression 2 100.00 Very High Very High Very High
Retts Disease 172 98.52 Very High Very High Very High
Stress 37 97.32 Very High Very High Very High
Anxiety Disorder 57 94.76 High High
Disease 23 92.16 High High
Targeted Disruption 17 88.76 High High
Depression 95 80.56 Quite High
Suicidal Behaviour 123 68.04 Quite High
Death 12 66.96 Quite High
Weight Loss 4 66.24 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Long-term potentiation is reduced in cortical slices of mice mutant for Mecp2 [9], [10] and loss of MeCP2 in mice results in a decrease in the total excitatory synaptic drive, an increase in the total inhibitory drive and an altered number of glutamatergic synapses [11]–[13].
Negative_regulation (loss) of MeCP2 in synapses associated with long-term potentiation
1) Confidence 0.59 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2902516 Disease Relevance 1.03 Pain Relevance 0.10
Although the relevance of these molecular findings to the partial behavioral amelioration induced by EE is yet unknown, they indicate that neurons lacking MeCP2 are unable to respond to EE through canonical pathways.
Negative_regulation (lacking) of MeCP2 in neurons
2) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2902516 Disease Relevance 0.09 Pain Relevance 0.06
Importantly, the availability of mouse models of RTT has allowed researchers to determine that the dysfunctionality caused by lack of MeCP2 is not irrevocable.
Negative_regulation (lack) of MeCP2 associated with retts disease
3) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2902516 Disease Relevance 0.45 Pain Relevance 0.04
Importantly, the other major excitatory projections to the LA, the so-called Thalamo-LA synapses, were unaffected by the absence of Mecp2.
Negative_regulation (absence) of Mecp2 in synapses associated with amygdala
4) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2896423 Disease Relevance 0.20 Pain Relevance 0.39
To conclude, we here show that at excitatory projections to the LA all synaptic effects associated with the absence of Mecp2 were following a developmental time course similar as in WT mice.
Negative_regulation (absence) of Mecp2 associated with amygdala
5) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2896423 Disease Relevance 0 Pain Relevance 0.27
In mice, removal of Mecp2 in the forebrain recapitulates most of behavioral deficits found in global Mecp2 deficient mice, including amygdala-related hyper-anxiety and lack of social interaction, pointing a role of Mecp2 in emotional learning.
Negative_regulation (removal) of Mecp2 in forebrain associated with anxiety disorder and amygdala
6) Confidence 0.43 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2896423 Disease Relevance 0.37 Pain Relevance 0.18
We found that the expression of Crh in hypothalamus was similar in Mecp2?
Negative_regulation (similar) of Mecp2 in hypothalamus
7) Confidence 0.37 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2902516 Disease Relevance 0.41 Pain Relevance 0
Membrane depolarization triggers the calcium-dependent phosphorylation and release of MeCP2 from BDNF promoter III, thereby facilitating transcription.177 On the other hand, membrane depolarization causes increased BDNF transcription, which involves dissociation of the MeCP2-histone deacetylase-mSin3A repression complex from its promoter,177,178 which suggests that DNA methylation-related chromatin remodeling is important for activity-dependent Bdnf gene regulation.
Negative_regulation (repression) of MeCP2-histone associated with repression
8) Confidence 0.12 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2732010 Disease Relevance 0.77 Pain Relevance 0.18

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox