INT254205

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Context Info
Confidence 0.19
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 12
Total Number 12
Disease Relevance 3.17
Pain Relevance 1.54

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 (Myd88, Tlr4) plasma membrane (Myd88, Tlr4) intracellular (Myd88, Tlr4)
cytoplasm (Myd88, Tlr4) cytosol (Myd88) protein complex (Myd88)
Anatomy Link Frequency
plasma 1
Myd88 (Mus musculus)
Tlr4 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 260 96.80 Very High Very High Very High
agonist 1 94.28 High High
cytokine 113 86.80 High High
Inflammatory response 35 80.80 Quite High
rheumatoid arthritis 65 78.16 Quite High
COX-2 inhibitor 18 71.60 Quite High
Pain 9 64.24 Quite High
Inflammatory mediators 16 62.40 Quite High
Arthritis 17 52.32 Quite High
antagonist 7 46.64 Quite Low
Disease Link Frequency Relevance Heat
INFLAMMATION 267 96.80 Very High Very High Very High
Infection 36 94.08 High High
Rheumatoid Arthritis 65 78.16 Quite High
Targeted Disruption 14 77.44 Quite High
Lyme Disease 13 70.84 Quite High
Arthritis 20 70.72 Quite High
Pressure And Volume Under Development 6 65.92 Quite High
Pain 9 64.24 Quite High
Disease 34 62.40 Quite High
Shock 3 53.52 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
MyD88-dependent signalling via TLR2 and TLR4 requires the presence of TIRAP and will end after several steps in activation of NF?
MyD88-dependent Binding (signalling) of TLR4
1) Confidence 0.19 Published 2010 Journal Heart Fail Rev Section Body Doc Link PMC3003782 Disease Relevance 0.05 Pain Relevance 0.03
To date, Mal is thought to function as a sorting adaptor for TLR2 and TLR4, recruiting MyD88 to the receptor complex in the plasma membrane, through its ability to interact with phosphatidylinositol-4,5-bisphosphate [42] (Figure 1).
MyD88 Binding (recruiting) of TLR4 in plasma
2) Confidence 0.14 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2592774 Disease Relevance 0.55 Pain Relevance 0.16
Pretreatment with CO-RM2 also inhibited TLR4/MyD88 complex formation, NF-?
MyD88 Binding (formation) of TLR4
3) Confidence 0.10 Published 2010 Journal J Neuroinflammation Section Abstract Doc Link PMC3002338 Disease Relevance 0.16 Pain Relevance 0
In the present study, pretreatment with CO-RM2 attenuated the association between TLR4 and MyD88 (Figure 5D).
MyD88 Binding (association) of TLR4
4) Confidence 0.10 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3002338 Disease Relevance 0.32 Pain Relevance 0.24
In the present study, pretreatment with CO-RM2 attenuated the association between TLR4 and MyD88 (Figure 5D).
MyD88 Binding (association) of TLR4
5) Confidence 0.10 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3002338 Disease Relevance 0.32 Pain Relevance 0.24
We tested the effect of CO-RM2 on LPS-induced protein-protein interaction between TLR4 and its adaptor protein myeloid differentiation factor (MyD88) which was shown to initiate an early activation of NF-?
MyD88 Binding (interaction) of TLR4
6) Confidence 0.10 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3002338 Disease Relevance 0.17 Pain Relevance 0.08
Pretreatment with CO-RM2 also inhibited TLR4/MyD88 complex formation, NF-?
MyD88 Binding (formation) of TLR4
7) Confidence 0.10 Published 2010 Journal J Neuroinflammation Section Abstract Doc Link PMC3002338 Disease Relevance 0.16 Pain Relevance 0
As shown in Figure 5D, pretreatment with CO-RM2 inhibited LPS-induced TLR4/MyD88 complex formation in bEnd.3 cells, indicating that CO attenuated the protein-protein interaction between TLR4 and MyD88 and thus retardation of COX-2 expression induced by LPS.
MyD88 Binding (formation) of TLR4
8) Confidence 0.10 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3002338 Disease Relevance 0.28 Pain Relevance 0.17
As shown in Figure 5D, pretreatment with CO-RM2 inhibited LPS-induced TLR4/MyD88 complex formation in bEnd.3 cells, indicating that CO attenuated the protein-protein interaction between TLR4 and MyD88 and thus retardation of COX-2 expression induced by LPS.
MyD88 Binding (formation) of TLR4
9) Confidence 0.10 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3002338 Disease Relevance 0.28 Pain Relevance 0.17
We tested the effect of CO-RM2 on LPS-induced protein-protein interaction between TLR4 and its adaptor protein myeloid differentiation factor (MyD88) which was shown to initiate an early activation of NF-?
MyD88 Binding (interaction) of LPS
10) Confidence 0.09 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3002338 Disease Relevance 0.17 Pain Relevance 0.08
We tested the effect of CO-RM2 on LPS-induced protein-protein interaction between TLR4 and its adaptor protein myeloid differentiation factor (MyD88) which was shown to initiate an early activation of NF-?
MyD88 Binding (interaction) of LPS
11) Confidence 0.09 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3002338 Disease Relevance 0.17 Pain Relevance 0.08
This hyporesponsiveness has been attributed to the lower affinity of non-CD14-complexed LPS for TLR4 [7], the requirement for CD14 in MyD88-independent signaling [8], and/or the inability of p38, a member of the serine/threonine MAPK family, to be induced in the absence of CD14 [9].
MyD88 Binding (complexed) of LPS
12) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2781632 Disease Relevance 0.57 Pain Relevance 0.28

General Comments

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