INT334223

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Context Info
Confidence 0.25
First Reported 2010
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 1
Total Number 6
Disease Relevance 1.11
Pain Relevance 0.52

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 (Irak4) kinase activity (Irak4) cytoplasm (Irak4)
Irak4 (Mus musculus)
Pain Link Frequency Relevance Heat
cytokine 84 98.48 Very High Very High Very High
Inflammation 96 96.56 Very High Very High Very High
rheumatoid arthritis 30 5.00 Very Low Very Low Very Low
antagonist 18 5.00 Very Low Very Low Very Low
corticosteroid 6 5.00 Very Low Very Low Very Low
agonist 6 5.00 Very Low Very Low Very Low
cINOD 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 96 96.56 Very High Very High Very High
Systemic Lupus Erythematosus 366 92.04 High High
Cancer 24 81.92 Quite High
Necrosis 12 81.44 Quite High
Autoimmune Disease 138 52.68 Quite High
Renal Disease 18 35.40 Quite Low
Disease 96 35.36 Quite Low
Sprains And Strains 12 8.08 Low Low
Apoptosis 30 5.00 Very Low Very Low Very Low
Rheumatoid Arthritis 30 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Briefly, IRAK4 is a kinase that interacts with MyD88 and TRAF6 and is associated with the activation of the downstream transcription factors in TLR signaling.
IRAK4 Binding (associated) of
1) Confidence 0.25 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.24 Pain Relevance 0.05
Kobayashi et al. showed that IRAK-M, which lacks the kinase activity of its counterparts IRAK1 and IRAK4, suppresses the production of proinflammatory cytokines and proposed a model whereby IRAK-M prevents the dissociation of the IRAK1/IRAK4/MyD88 complex to inhibit downstream NF?
IRAK4 Binding (complex) of associated with cytokine
2) Confidence 0.25 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.14 Pain Relevance 0.09
This short form of MyD88 fails to recruit IRAK4, impairing the ability to phosphorylate IRAK1, therefore preventing the activation of NF?
IRAK4 Binding (recruit) of
3) Confidence 0.25 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.12 Pain Relevance 0.16
Kobayashi et al. showed that IRAK-M, which lacks the kinase activity of its counterparts IRAK1 and IRAK4, suppresses the production of proinflammatory cytokines and proposed a model whereby IRAK-M prevents the dissociation of the IRAK1/IRAK4/MyD88 complex to inhibit downstream NF?
IRAK4 Binding (counterparts) of associated with cytokine
4) Confidence 0.25 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.12 Pain Relevance 0.09
They also went on to show that not only do these peptides inhibit dimerization of MyD88, but also inhibit the recruitment of IRAK1 and IRAK4 [88].
IRAK4 Neg (inhibit) Binding (recruitment) of
5) Confidence 0.25 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.33 Pain Relevance 0.04
Likewise, the splice variant IRAK1c acts in a similar manner by interacting with MyD88 and IRAK4.
IRAK4 Binding (interacting) of
6) Confidence 0.24 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.16 Pain Relevance 0.09

General Comments

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