INT253116

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Context Info
Confidence 0.47
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 11
Disease Relevance 2.08
Pain Relevance 0.77

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

intracellular (Tbc1d4) cytoplasm (Tbc1d4)
Anatomy Link Frequency
skeletal muscle 1
Tbc1d4 (Mus musculus)
Pain Link Frequency Relevance Heat
tolerance 66 98.16 Very High Very High Very High
cytokine 187 93.60 High High
anesthesia 11 10.16 Low Low
Inflammation 44 5.60 Low Low
agonist 110 5.00 Very Low Very Low Very Low
ischemia 11 5.00 Very Low Very Low Very Low
metalloproteinase 11 5.00 Very Low Very Low Very Low
Kinase C 11 5.00 Very Low Very Low Very Low
Immobilon 11 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Impaired Glucose Tolerance 33 98.48 Very High Very High Very High
Insulin Resistance 440 95.08 Very High Very High Very High
Targeted Disruption 33 86.64 High High
Obesity 220 77.40 Quite High
Hyperglycemia 11 67.80 Quite High
Body Weight 11 21.60 Low Low
INFLAMMATION 44 5.60 Low Low
Diabetes Mellitus 66 5.00 Very Low Very Low Very Low
Hyperinsulinism 22 5.00 Very Low Very Low Very Low
Hypoxia 11 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Although IL-6 per se activated glucose uptake, a dual effect on insulin action was observed: short-term IL-6 treatment was additive to insulin on activating glucose uptake and AS160 phosphorylation, which resulted in an improvement on glucose tolerance and insulin sensitivity in mice, whereas chronic exposure produced insulin resistance both in vitro and in vivo.
Phosphorylation (phosphorylation) of AS160 associated with tolerance, insulin resistance and impaired glucose tolerance
1) Confidence 0.47 Published 2008 Journal Diabetes Section Body Doc Link PMC2584126 Disease Relevance 0.42 Pain Relevance 0.09
In contrast, complete inhibition of AS160 phosphorylation was observed at 24 h.
Phosphorylation (phosphorylation) of AS160
2) Confidence 0.47 Published 2008 Journal Diabetes Section Body Doc Link PMC2584126 Disease Relevance 0.12 Pain Relevance 0.10
AS160 was phosphorylated by IL-6 and insulin individually, and when combined, an additive effect was produced at 3 h of IL-6 treatment.
Phosphorylation (phosphorylated) of AS160
3) Confidence 0.47 Published 2008 Journal Diabetes Section Body Doc Link PMC2584126 Disease Relevance 0.12 Pain Relevance 0.10
We observed that IL-6 induces the sequential phosphorylation of LKB1, AMPK, and AS160.
Phosphorylation (phosphorylation) of AS160
4) Confidence 0.47 Published 2008 Journal Diabetes Section Body Doc Link PMC2584126 Disease Relevance 0.34 Pain Relevance 0.07
Moreover, no phosphorylation of AMPK or AS160 was detectable, a fact that indicates a reciprocal negative cross talk in the signaling pathways elicited by insulin and IL-6 under chronic treatment with the cytokine.
Phosphorylation (phosphorylation) of AS160 associated with cytokine
5) Confidence 0.47 Published 2008 Journal Diabetes Section Body Doc Link PMC2584126 Disease Relevance 0.27 Pain Relevance 0.08
This increase is a consequence of the activation of AMPK and AKT by IL-6 and insulin, respectively, and is additive to AS160 phosphorylation, as observed in C2C12 cells and in skeletal muscle, in agreement with other reports (3,12,40).
Phosphorylation (phosphorylation) of AS160 in skeletal muscle
6) Confidence 0.47 Published 2008 Journal Diabetes Section Body Doc Link PMC2584126 Disease Relevance 0.07 Pain Relevance 0.04
Furthermore, direct inhibition of AMPK activity with either compound C or siRNA in the presence of IL-6 blocked phosphorylation of AS160 and impeded glucose uptake.
Phosphorylation (phosphorylation) of AS160
7) Confidence 0.47 Published 2008 Journal Diabetes Section Body Doc Link PMC2584126 Disease Relevance 0.22 Pain Relevance 0.06
Separately, IL-6 and insulin activate the phosphorylation of AS160, and together, this effect was additive (Fig. 6C).
Phosphorylation (phosphorylation) of AS160
8) Confidence 0.36 Published 2008 Journal Diabetes Section Body Doc Link PMC2584126 Disease Relevance 0.29 Pain Relevance 0.09
IL-6 treatment for 3 h produced the sequential phosphorylation of LKB1, AMPK, ACC, and AS160 in C2C12 cells, and phosphorylation of ACC and AS160 was prevented by compound C.
Phosphorylation (phosphorylation) of AS160
9) Confidence 0.36 Published 2008 Journal Diabetes Section Body Doc Link PMC2584126 Disease Relevance 0.07 Pain Relevance 0.04
was knocked down with siRNA, a robust 80% reduction of AMPK protein was detected, and, therefore, phosphorylation of AMPK, ACC, and AS160 by IL-6 was completely impaired.


Phosphorylation (phosphorylation) of AS160
10) Confidence 0.36 Published 2008 Journal Diabetes Section Body Doc Link PMC2584126 Disease Relevance 0.09 Pain Relevance 0.07
IL-6 treatment for 3 h produced the sequential phosphorylation of LKB1, AMPK, ACC, and AS160 in C2C12 cells, and phosphorylation of ACC and AS160 was prevented by compound C.
Phosphorylation (phosphorylation) of AS160
11) Confidence 0.32 Published 2008 Journal Diabetes Section Body Doc Link PMC2584126 Disease Relevance 0.07 Pain Relevance 0.03

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