INT346899

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Context Info
Confidence 0.18
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.75
Pain Relevance 0.22

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

cytosol (Nod2) signal transduction (Nod2) plasma membrane (Nod2)
intracellular (Nod2) enzyme binding (Nod2) cytoplasm (Nod2)
Anatomy Link Frequency
plasma 2
Nod2 (Mus musculus)
Pain Link Frequency Relevance Heat
Crohn's disease 20 84.40 Quite High
Inflammation 27 68.64 Quite High
potassium channel 1 50.24 Quite High
Bile 6 5.00 Very Low Very Low Very Low
cytokine 3 5.00 Very Low Very Low Very Low
chemokine 3 5.00 Very Low Very Low Very Low
Inflammatory response 2 5.00 Very Low Very Low Very Low
corticosteroid 1 5.00 Very Low Very Low Very Low
spastic colon 1 5.00 Very Low Very Low Very Low
iatrogenic 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 6 96.72 Very High Very High Very High
Disease 28 83.76 Quite High
Inflammatory Bowel Disease 20 77.76 Quite High
INFLAMMATION 23 68.64 Quite High
Colitis 2 61.44 Quite High
Enteritis 1 59.12 Quite High
Celiac Disease 2 24.24 Low Low
Infection 11 5.00 Very Low Very Low Very Low
Bacterial Respiratory Disease 7 5.00 Very Low Very Low Very Low
Gastritis 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Moreover, Cadwell et al. provided evidence that in ATG16L1 knockout mice, granule exocytosis is abnormal [67, 68], and recently it has been shown that recruitment of ATG16L1 to the site of bacterial entry in the plasma membrane is dependent on activation of NOD2 by bacteria ([69]).
Regulation (dependent) of Positive_regulation (activation) of NOD2 in plasma associated with targeted disruption
1) Confidence 0.18 Published 2010 Journal International Journal of Inflammation Section Body Doc Link PMC2992817 Disease Relevance 0.75 Pain Relevance 0.22

General Comments

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