INT145196

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Context Info
Confidence 0.23
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 5
Total Number 5
Disease Relevance 4.23
Pain Relevance 2.13

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 (Irak3) nucleus (Irak3) kinase activity (Irak3)
cytoplasm (Irak3)
Anatomy Link Frequency
monocytes 3
Irak3 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 20 100.00 Very High Very High Very High
cytokine 17 100.00 Very High Very High Very High
Inflammatory response 8 97.50 Very High Very High Very High
tolerance 50 97.12 Very High Very High Very High
Angina 4 92.60 High High
agonist 3 45.96 Quite Low
palliative 1 5.00 Very Low Very Low Very Low
addiction 1 5.00 Very Low Very Low Very Low
Inflammatory mediators 1 5.00 Very Low Very Low Very Low
chemokine 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 29 100.00 Very High Very High Very High
Acute Coronary Syndrome 24 99.78 Very High Very High Very High
Myocardial Infarction 8 96.40 Very High Very High Very High
Cv General 3 Under Development 4 92.60 High High
Heart Disease 4 83.08 Quite High
Infection 5 53.40 Quite High
Sepsis 10 49.84 Quite Low
Disease 2 33.04 Quite Low
Necrosis 1 21.32 Low Low
Cancer 1 20.96 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We show for the first time that inflammatory responses associated with ACS induce an unresponsiveness state to endotoxin challenge in circulating monocytes, which correlates with expression of IRAK-M, TLR4 and IL-10.
Gene_expression (expression) of IRAK-M in monocytes associated with acute coronary syndrome and inflammatory response
1) Confidence 0.23 Published 2007 Journal J. Endotoxin Res. Section Abstract Doc Link 17621545 Disease Relevance 0.71 Pain Relevance 0.32
Control monocytes cultured for 6 h in supplemented medium (10% serum from ACS patients) expressed IRAK-M, and LPS stimulation failed to induce TNF-alpha and IL-6 in these cultures.
Gene_expression (expressed) of IRAK-M in monocytes associated with acute coronary syndrome
2) Confidence 0.23 Published 2007 Journal J. Endotoxin Res. Section Abstract Doc Link 17621545 Disease Relevance 1.10 Pain Relevance 0.46
Circulating monocytes from all patients, but not from healthy individuals, showed high levels of pro-inflammatory cytokines, TNF-alpha and IL-6, as well as of IRAK-M and IL-10.
Gene_expression (levels) of IRAK-M in monocytes associated with inflammation and cytokine
3) Confidence 0.20 Published 2007 Journal J. Endotoxin Res. Section Abstract Doc Link 17621545 Disease Relevance 1.11 Pain Relevance 0.47
Further, we investigated the consequences of cytokines/IRAK-M expression on the innate immune response to endotoxin.
Gene_expression (expression) of IRAK-M associated with cytokine
4) Confidence 0.18 Published 2007 Journal J. Endotoxin Res. Section Abstract Doc Link 17621545 Disease Relevance 1.14 Pain Relevance 0.48
IRAK-M is a catalytically inactive member of the IRAK kinase family that prevents formation of IRAK-1–TRAF6 complexes downstream of TLR4 (15, 16).
Gene_expression (complexes) of IRAK-M
5) Confidence 0.07 Published 2010 Journal mBio Section Body Doc Link PMC2962435 Disease Relevance 0.17 Pain Relevance 0.41

General Comments

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