INT142754

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Context Info
Confidence 0.36
First Reported 2007
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 20
Total Number 22
Disease Relevance 9.61
Pain Relevance 3.80

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

cytosol (Myd88) signal transduction (Myd88) plasma membrane (Myd88)
intracellular (Myd88) protein complex (Myd88) cytoplasm (Myd88)
Anatomy Link Frequency
microglial cell 2
macrophage 1
endothelial cells 1
external carotid artery 1
tails 1
Myd88 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 417 99.76 Very High Very High Very High
cytokine 220 99.40 Very High Very High Very High
chemokine 61 98.04 Very High Very High Very High
Inflammatory response 95 95.16 Very High Very High Very High
agonist 56 95.04 Very High Very High Very High
anesthesia 11 85.36 High High
Arthritis 4 75.56 Quite High
Inflammatory mediators 16 73.16 Quite High
COX-2 inhibitor 6 71.60 Quite High
Hyperalgesia 1 70.96 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 470 99.76 Very High Very High Very High
Colitis 69 98.70 Very High Very High Very High
Disease 366 98.66 Very High Very High Very High
Neointima 12 96.56 Very High Very High Very High
Pneumonia 2 95.80 Very High Very High Very High
Chlamydia Infection 2 93.52 High High
Paratuberculosis 20 92.72 High High
Systemic Lupus Erythematosus 366 91.12 High High
Vasculitis 36 90.56 High High
Crystal Associated Disease 75 90.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Inward remodeling was associated with MyD88-dependent and superoxide-initiated cytokine and chemokine production, as well as transient adventitial macrophage accumulation and activation.
MyD88 Binding (associated) of in macrophage associated with chemokine and cytokine
1) Confidence 0.36 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2605224 Disease Relevance 0.34 Pain Relevance 0.26
B activation as a link between MyD88 signaling and cytokine synthesis.


MyD88 Binding (link) of associated with cytokine
2) Confidence 0.36 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2605224 Disease Relevance 0.22 Pain Relevance 0.26
Therefore, disease development at 3 months was mostly independent of microglial cell priming through TLR4 and MyD88.


MyD88 Binding (priming) of in microglial cell associated with disease
3) Confidence 0.32 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2396504 Disease Relevance 0.83 Pain Relevance 0.17
Common carotid arteries decreased in size after ipsilateral external carotid artery ligation in wild-type mice, but not in myeloid differentiation protein-88 (MyD88)–deficient mice.
MyD88 Binding (ligation) of in external carotid artery
4) Confidence 0.31 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2605224 Disease Relevance 0.35 Pain Relevance 0.25
Toll-like receptors and the key adaptor molecule myeloid differentiation factor-88 (MyD88) play a critical role in inducing immunity against this microorganism and are crucial for survival.
MyD88 Binding (crucial) of
5) Confidence 0.31 Published 2007 Journal Physiol. Genomics Section Abstract Doc Link 17374847 Disease Relevance 0.42 Pain Relevance 0.14
In cell culture, heparan sulfate oligosaccharides activated microglial cells by signaling through the Toll-like receptor 4 and the adaptor protein MyD88.
MyD88 Binding (signaling) of in microglial cells
6) Confidence 0.28 Published 2008 Journal PLoS ONE Section Abstract Doc Link PMC2396504 Disease Relevance 0.78 Pain Relevance 0.17
The results of this mimic showed an inhibition of MyD88 and IL-1RI interaction by ablating phosphorylation of MAP kinases [86].
MyD88 Binding (interaction) of
7) Confidence 0.27 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.40 Pain Relevance 0.06
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?
MyD88 Binding (complex) of associated with cytokine
8) Confidence 0.27 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.14 Pain Relevance 0.09
This inhibitor showed similar inhibition of MyD88 signaling indicated by impaired NF?
MyD88 Binding (indicated) of
9) Confidence 0.27 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.38 Pain Relevance 0.03
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].
MyD88 Neg (inhibit) Binding (dimerization) of
10) Confidence 0.27 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.38 Pain Relevance 0.03
Likewise, the splice variant IRAK1c acts in a similar manner by interacting with MyD88 and IRAK4.
MyD88 Binding (interacting) of
11) Confidence 0.26 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.16 Pain Relevance 0.09
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.
MyD88 Binding (interacts) of
12) Confidence 0.26 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2945668 Disease Relevance 0.24 Pain Relevance 0.05
TLR signaling may lead to different responses in distinctive cell types through an interaction with MyD88 unique variants.
MyD88 Binding (interaction) of
13) Confidence 0.23 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2913815 Disease Relevance 0.15 Pain Relevance 0.27
Ligand-induced TLR dimerization permits the binding of cytoplasmic adapter proteins, MyD88, to the TLR cytoplasmic tails [38].
MyD88 Binding (binding) of in tails
14) Confidence 0.23 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2901327 Disease Relevance 0.76 Pain Relevance 0.18
The dominant and founding member of this family of adaptors is myeloid differentiation factor 88 (MyD88), which relays the signal for most TLR family members and tends to predominantly induce an NF-?
myeloid differentiation factor 88 Binding (tends) of
15) Confidence 0.20 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2913815 Disease Relevance 0.05 Pain Relevance 0.20
The dominant and founding member of this family of adaptors is myeloid differentiation factor 88 (MyD88), which relays the signal for most TLR family members and tends to predominantly induce an NF-?
MyD88 Binding (tends) of
16) Confidence 0.20 Published 2010 Journal Mediators of Inflammation Section Body Doc Link PMC2913815 Disease Relevance 0.05 Pain Relevance 0.20
Activation of TLR4 triggers the recruitment of myeloid differentiation factor (MyD88) and initiates NF-?
MyD88 Binding (recruitment) of
17) Confidence 0.19 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3002338 Disease Relevance 0.34 Pain Relevance 0.24
As both IL-1RI and MyD88 are essential for signal transduction on IL-1 binding, these results showed that nonhematopoieitic cells, most probably endothelial cells, are necessary to develop fully the inflammatory response to IL-1?.


MyD88 Binding (binding) of in endothelial cells associated with inflammatory response
18) Confidence 0.19 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2888190 Disease Relevance 1.36 Pain Relevance 0.60
It is plausible that Mycobacteria stimulate TLRs to promote colitis in IL-10-/- mice, which presents a scenario where mycobacterial recognition via TLR and MyD88 activate DCs to control Th1 polarization and expansion.
MyD88 Binding (recognition) of associated with colitis
19) Confidence 0.19 Published 2008 Journal BMC Immunol Section Body Doc Link PMC2443107 Disease Relevance 0.77 Pain Relevance 0.04
This inhibitory effect of HO-1 is mediated through an HO-1 byproduct, CO, which attenuates TLR4/MyD88 complex formation and NF-?
MyD88 Binding (formation) of
20) Confidence 0.15 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3002338 Disease Relevance 0.34 Pain Relevance 0.04

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