INT339467

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Context Info
Confidence 0.46
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 3
Disease Relevance 0.08
Pain Relevance 0.14

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

RNA binding (Eif2ak2) nucleus (Eif2ak2) intracellular (Eif2ak2)
translation (Eif2ak2) kinase activity (Eif2ak2)
Anatomy Link Frequency
macrophages 1
Eif2ak2 (Mus musculus)
Pain Link Frequency Relevance Heat
tolerance 126 99.84 Very High Very High Very High
agonist 9 19.52 Low Low
palliative 3 8.80 Low Low
Inflammation 24 5.00 Very Low Very Low Very Low
cytokine 15 5.00 Very Low Very Low Very Low
Inflammatory mediators 3 5.00 Very Low Very Low Very Low
addiction 3 5.00 Very Low Very Low Very Low
chemokine 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 9 81.52 Quite High
Sepsis 30 24.16 Low Low
INFLAMMATION 27 5.00 Very Low Very Low Very Low
Infection 15 5.00 Very Low Very Low Very Low
Disease 6 5.00 Very Low Very Low Very Low
Bacterial Infection 3 5.00 Very Low Very Low Very Low
Necrosis 3 5.00 Very Low Very Low Very Low
Attention Deficit Hyperactivity Disorder 3 5.00 Very Low Very Low Very Low
Cancer 3 5.00 Very Low Very Low Very Low
Stress 3 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The capacity of SOCS-1 to interact physically with and catalyze degradation of PKR in HEK293T cells supports the possibility that SOCS-1 regulates PKR protein levels during the TLR4-mediated response to LPS.
Protein_catabolism (degradation) of PKR
1) Confidence 0.46 Published 2010 Journal mBio Section Body Doc Link PMC2962435 Disease Relevance 0.08 Pain Relevance 0
The similarity in kinetics between the loss of LPS-inducible PKR activation in tolerant cells between 30 and 90 min following LPS restimulation and the reduction of PKR total protein levels over the same period led us to hypothesize that induced degradation of PKR in tolerance may, in part, be responsible for the failure to observe PKR activation.
Protein_catabolism (degradation) of PKR associated with tolerance
2) Confidence 0.30 Published 2010 Journal mBio Section Body Doc Link PMC2962435 Disease Relevance 0 Pain Relevance 0.09
This result was surprising because our previous observation that proteosome inhibition could restore activation in tolerance (Fig. 3A) had led us to expect that PKR would be inducibly ubiquitinated to a greater degree in tolerant cells, leading to subsequent degradation and, thus, explaining the failure in observing PKR activation in tolerized macrophages.
Protein_catabolism (degradation) of PKR in macrophages associated with tolerance
3) Confidence 0.30 Published 2010 Journal mBio Section Body Doc Link PMC2962435 Disease Relevance 0 Pain Relevance 0.05

General Comments

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