INT292725

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Context Info
Confidence 0.01
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.10
Pain Relevance 0

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

cytoplasm (GOPC, Akt1) plasma membrane (GOPC, Akt1) transport (Akt1)
aging (Akt1) Golgi apparatus (GOPC) enzyme binding (Akt1)
GOPC (Homo sapiens)
Akt1 (Mus musculus)
Pain Link Frequency Relevance Heat
qutenza 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Stress 11 100.00 Very High Very High Very High
Myeloid Leukemia 12 50.00 Quite Low
Chronic Myeloid Leukemia 8 50.00 Quite Low
Apoptosis 8 5.00 Very Low Very Low Very Low
Shock 7 5.00 Very Low Very Low Very Low
Cancer 5 5.00 Very Low Very Low Very Low
Philadelphia Chromosome 2 5.00 Very Low Very Low Very Low
Blast Crisis 1 5.00 Very Low Very Low Very Low
Alkalosis 1 5.00 Very Low Very Low Very Low
Congenital Anomalies 1 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However the question that needs to be addressed is how diminishing Akt activation by17AAG treatment (Fig 4A) could simultaneously result in induction of stress response by sharply augmenting the Hsp70 levels (Fig 4A). 17AAG blocks the chaperoning activity of Hsp90, prompting degradation of its client protein Akt.
Fig Positive_regulation (augmenting) of Protein_catabolism (degradation) of Akt associated with stress
1) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2806839 Disease Relevance 0.10 Pain Relevance 0

General Comments

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