INT254804

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Context Info
Confidence 0.04
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 0.97
Pain Relevance 0.17

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

signal transduction (Ecm1) extracellular space (Ecm1) extracellular region (Ecm1)
proteinaceous extracellular matrix (Ecm1) enzyme binding (Ecm1) signal transducer activity (Ecm1)
Anatomy Link Frequency
ECM 2
Ecm1 (Mus musculus)
Pain Link Frequency Relevance Heat
metalloproteinase 2 99.16 Very High Very High Very High
fibrosis 3 94.40 High High
Inflammation 11 75.52 Quite High
Crohn's disease 1 71.52 Quite High
chemokine 7 23.88 Low Low
Inflammatory response 1 11.16 Low Low
cytokine 8 5.00 Very Low Very Low Very Low
palliative 2 5.00 Very Low Very Low Very Low
agonist 2 5.00 Very Low Very Low Very Low
anesthesia 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Cirrhosis 1 97.08 Very High Very High Very High
Fibrosis 3 94.40 High High
Rectal Cancer 1 94.32 High High
Injury 3 92.92 High High
Stomach Cancer 58 81.32 Quite High
INFLAMMATION 12 75.52 Quite High
Disease 7 70.88 Quite High
Inflammatory Bowel Disease 1 69.92 Quite High
Malignant Neoplastic Disease 10 40.52 Quite Low
Cancer 64 37.48 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
, via Smad pathway, regulates ECM-related proteins, including the profibrotic mediator CTGF [4], [26], the inhibitor of ECM degradation, PAI-1, [27], and the main ECM component Type I Collagen (Col-1) [4].
Negative_regulation (inhibitor) of Protein_catabolism (degradation) of ECM
1) Confidence 0.04 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2597201 Disease Relevance 0 Pain Relevance 0
Parsons et al., (2004) [53] have shown TIMP1 to be involved in decreased degradation of extracellular matrix (ECM) by blocking matrix metalloproteinase activity and enhanced survival of hepatic stellate cells which are a major source of ECM, leading to fibrosis in liver following chemical injury.
Negative_regulation (decreased) of Protein_catabolism (degradation) of ECM in ECM associated with fibrosis, cirrhosis, injury and metalloproteinase
2) Confidence 0.01 Published 2010 Journal Cancer Cell Int Section Body Doc Link PMC3004887 Disease Relevance 0.97 Pain Relevance 0.17

General Comments

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