INT272256

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Context Info
Confidence 0.49
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 7
Disease Relevance 2.66
Pain Relevance 0.19

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

plasma membrane (Psd) intracellular (Psd) cytoplasm (Psd)
Anatomy Link Frequency
Shank 1
neurons 1
Psd (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Glutamate receptor 12 85.52 High High
imagery 32 66.44 Quite High
Hippocampus 2 58.28 Quite High
Thalamus 3 57.08 Quite High
addiction 5 54.88 Quite High
tetrodotoxin 36 5.00 Very Low Very Low Very Low
depression 8 5.00 Very Low Very Low Very Low
Central nervous system 5 5.00 Very Low Very Low Very Low
cva 5 5.00 Very Low Very Low Very Low
Action potential 5 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Dementia 108 100.00 Very High Very High Very High
Syndrome 12 93.24 High High
Congenital Anomalies 2 87.20 High High
Agraphia 1 85.24 High High
Dyslexia 1 84.84 Quite High
Aphasia 3 84.16 Quite High
Amnesia 1 83.80 Quite High
Cognitive Disorder 90 82.68 Quite High
Angelman Syndrome 5 82.04 Quite High
Stroke 122 81.44 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In general, the degree of PSD commonly parallel that of motor and functional disability,30–32 however, some studies demonstrated that the degree of dementia did not always parallel that of neurological deficits.45
Protein_catabolism (degree) of PSD associated with dementia
1) Confidence 0.49 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2695209 Disease Relevance 2.21 Pain Relevance 0.09
If a specific E3 mediates the ubiquitination and degradation of a PSD protein, then that PSD protein should accumulate to higher levels when expression of the endogenous E3 is suppressed by RNAi.
Protein_catabolism (degradation) of PSD protein
2) Confidence 0.38 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0.24 Pain Relevance 0
Chronic alterations in synaptic activity result in a coordinated, reversible change in postsynaptic protein composition, with increased activity stimulating degradation of a subset of PSD proteins [3].
Protein_catabolism (degradation) of PSD
3) Confidence 0.34 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0.04
However, this analysis was performed at the population level, and thus did not provide information on the long-term stability of individual PSD sizes.
Protein_catabolism (stability) of PSD
4) Confidence 0.33 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2693930 Disease Relevance 0 Pain Relevance 0.03
To identify specific E3 ligases that mediate degradation of PSD proteins, we performed an RNAi screen of a subset of known and putative E3 enzymes in primary hippocampal neurons.
Protein_catabolism (degradation) of PSD in neurons
5) Confidence 0.25 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0.20 Pain Relevance 0.03
Regulated degradation of postsynaptic density (PSD) proteins by the ubiquitin-proteasome system is believed to play an important role in activity-dependent synaptic remodeling.
Protein_catabolism (degradation) of PSD
6) Confidence 0.25 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0
Stimulating neuronal activity in vitro and in vivo induces the ubiquitination and degradation of GKAP/SAPAP and Shank, major scaffold proteins of the PSD.
Protein_catabolism (degradation) of PSD in Shank
7) Confidence 0.22 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0

General Comments

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