INT356369

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Context Info
Confidence 0.05
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 0.81
Pain Relevance 0

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

endosome (Mib2) signal transduction (Mib2) ligase activity (Mib2)
cytoplasm (Mib2) signal transducer activity (Mib2)
Mib2 (Mus musculus)
Pain Link Frequency Relevance Heat
fibrosis 72 5.00 Very Low Very Low Very Low
imagery 12 5.00 Very Low Very Low Very Low
Inflammation 8 5.00 Very Low Very Low Very Low
Calcium channel 4 5.00 Very Low Very Low Very Low
cytokine 2 5.00 Very Low Very Low Very Low
tolerance 2 5.00 Very Low Very Low Very Low
Angina 2 5.00 Very Low Very Low Very Low
antagonist 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Muscular Dystrophy 280 88.12 High High
Shock 2 80.40 Quite High
Duchenne Muscular Dystrophy 40 12.56 Low Low
Cardiomyopathy 126 5.00 Very Low Very Low Very Low
Fibrosis 86 5.00 Very Low Very Low Very Low
Dilated Cardiomyopathy 36 5.00 Very Low Very Low Very Low
Death 22 5.00 Very Low Very Low Very Low
Stress 16 5.00 Very Low Very Low Very Low
Congenital Anomalies 12 5.00 Very Low Very Low Very Low
Myocardial Infarction 12 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The disorder is caused by mutations in the dystrophin gene, usually deletions or point mutations that lead to a shift in the reading frame and produce a stop codon, thus causing the complete loss or very reduced and deficient synthesis of dystrophin protein, which forms an integral part of the dystrophin-glycoprotein complex (DGC) [3].
Negative_regulation (reduced) of Gene_expression (synthesis) of dystrophin protein
1) Confidence 0.05 Published 2010 Journal The Open Cardiovascular Medicine Journal Section Body Doc Link PMC3024556 Disease Relevance 0.40 Pain Relevance 0
The disorder is caused by mutations in the dystrophin gene, usually deletions or point mutations that lead to a shift in the reading frame and produce a stop codon, thus causing the complete loss or very reduced and deficient synthesis of dystrophin protein, which forms an integral part of the dystrophin-glycoprotein complex (DGC) [3].
Negative_regulation (deficient) of Gene_expression (synthesis) of dystrophin protein
2) Confidence 0.04 Published 2010 Journal The Open Cardiovascular Medicine Journal Section Body Doc Link PMC3024556 Disease Relevance 0.40 Pain Relevance 0

General Comments

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