INT276213

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Context Info
Confidence 0.51
First Reported 2009
Last Reported 2009
Negated 0
Speculated 1
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 0.61
Pain Relevance 0.72

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

aging (Pten, Akt1) enzyme binding (Pten, Akt1) cytoplasm (Pten, Akt1)
nucleus (Pten, Akt1) plasma membrane (Pten, Akt1) nucleoplasm (Akt1)
Anatomy Link Frequency
adipocytes 4
Pten (Rattus norvegicus)
Akt1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Paracetamol 120 93.32 High High
cytokine 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Obesity 4 99.84 Very High Very High Very High
Aging 76 78.20 Quite High
Hyperglycemia 8 36.56 Quite Low
Apoptosis 20 5.00 Very Low Very Low Very Low
Frailty 10 5.00 Very Low Very Low Very Low
Body Weight 8 5.00 Very Low Very Low Very Low
Death 4 5.00 Very Low Very Low Very Low
Hypoxia 2 5.00 Very Low Very Low Very Low
Insulin Resistance 2 5.00 Very Low Very Low Very Low
Hypertrophy 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results are consistent with the alterations in PTEN protein levels and suggest that PTEN may regulate the phosphorylation of Akt Thr308 in skeletal muscle using a mechanism similar to that previously observed in adipocytes [13].
PTEN Spec (may) Regulation (regulate) of Phosphorylation (phosphorylation) of Akt in adipocytes associated with obesity
1) Confidence 0.51 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2712760 Disease Relevance 0.37 Pain Relevance 0.36
It has been reported that the phosphorylation of Thr308 of Akt, but not Ser473, is regulated by PTEN in adipocytes [13].
PTEN Regulation (regulated) of Phosphorylation (phosphorylation) of Akt in adipocytes associated with obesity
2) Confidence 0.38 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2712760 Disease Relevance 0.24 Pain Relevance 0.36

General Comments

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