INT289592

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Context Info
Confidence 0.41
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 1.44
Pain Relevance 0.04

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

cytosol (Foxo1) nucleus (Foxo1) DNA binding (Foxo1)
cytoplasm (Foxo1)
Foxo1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Inflammatory response 1 89.60 High High
fibrosis 1 17.92 Low Low
ischemia 8 5.00 Very Low Very Low Very Low
antagonist 5 5.00 Very Low Very Low Very Low
anesthesia 3 5.00 Very Low Very Low Very Low
Central nervous system 1 5.00 Very Low Very Low Very Low
Bioavailability 1 5.00 Very Low Very Low Very Low
beta blocker 1 5.00 Very Low Very Low Very Low
addiction 1 5.00 Very Low Very Low Very Low
Hippocampus 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Aging 5 100.00 Very High Very High Very High
Death 3 96.36 Very High Very High Very High
INFLAMMATION 1 89.60 High High
Stress 2 78.32 Quite High
Herpes Simplex Virus 1 73.76 Quite High
Hepatotoxicity 1 72.48 Quite High
Alzheimer's Dementia 1 71.84 Quite High
Pulmonary Disease 1 71.08 Quite High
Disease 4 70.16 Quite High
Aids-related Complex 22 68.32 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The most prominent mechanism appears its ability to induce several longevity genes including Sirt1, Sirt3, Sirt4, FoxO1, Foxo3a and PBEF [4].
Positive_regulation (induce) of FoxO1 associated with aging
1) Confidence 0.41 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3009730 Disease Relevance 1.32 Pain Relevance 0.04
We also treated N43 immortalized hypothalamic cell line [31] with the Sirt1 activator SA3, which was accompanied by increased FoxO1 binding (Figure 4D).
Positive_regulation (increased) of FoxO1
2) Confidence 0.34 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2790615 Disease Relevance 0.12 Pain Relevance 0

General Comments

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