INT220612

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Context Info
Confidence 0.51
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 3
Disease Relevance 2.67
Pain Relevance 0.29

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

endosome (Bace1) peptidase activity (Bace1) Golgi apparatus (Bace1)
endoplasmic reticulum (Bace1) enzyme binding (Bace1)
Bace1 (Mus musculus)
Pain Link Frequency Relevance Heat
ischemia 12 83.04 Quite High
Nerve growth factor 1 32.80 Quite Low
Inflammation 20 5.00 Very Low Very Low Very Low
Central nervous system 11 5.00 Very Low Very Low Very Low
Hippocampus 11 5.00 Very Low Very Low Very Low
Peripheral nervous system 10 5.00 Very Low Very Low Very Low
cINOD 9 5.00 Very Low Very Low Very Low
cytokine 7 5.00 Very Low Very Low Very Low
sodium channel 6 5.00 Very Low Very Low Very Low
Inflammatory response 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Disease 202 98.66 Very High Very High Very High
Apoptosis 25 98.12 Very High Very High Very High
Disease Progression 7 94.04 High High
Cv Unclassified Under Development 10 83.04 Quite High
Transient Ischemic Attack 2 65.64 Quite High
Stroke 7 63.12 Quite High
Injury 11 57.72 Quite High
Targeted Disruption 86 57.00 Quite High
Brain Injury 14 56.60 Quite High
Stress 57 46.00 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Several mechanisms are proposed to induce the BACE1 elevation associated with AD; for example, caspase-3-dependent inactivation of GGA3 leading to decreased lysosomal degradation of BACE1 [38], [39], increased phosphorylation of the translation initiation factor eIF2?
Negative_regulation (decreased) of Protein_catabolism (degradation) of BACE1 associated with disease
1) Confidence 0.51 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2944882 Disease Relevance 0.44 Pain Relevance 0
Indeed, caspase activation during programmed cell death induced the BACE1 increase via a post-translational stabilization of BACE1 and a significant impairment in BACE1 degradation and turnover.
Negative_regulation (impairment) of Protein_catabolism (degradation) of BACE1 associated with apoptosis
2) Confidence 0.37 Published 2007 Journal Current Genomics Section Body Doc Link PMC2647160 Disease Relevance 1.10 Pain Relevance 0.14
Indeed, caspase activation during programmed cell death induced the BACE1 increase via a post-translational stabilization of BACE1 and a significant impairment in BACE1 degradation and turnover.
Negative_regulation (impairment) of Protein_catabolism (degradation) of BACE1 associated with apoptosis
3) Confidence 0.37 Published 2007 Journal Mol Neurodegener Section Body Doc Link PMC2211305 Disease Relevance 1.12 Pain Relevance 0.15

General Comments

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