INT313426

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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 1
Disease Relevance 0.36
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 (Ppp2ca, Bax) cytosol (Ppp2ca, Bax) nucleus (Ppp2ca, Bax)
mitochondrion (Bax) endoplasmic reticulum (Bax) intracellular (Bax)
Ppp2ca (Mus musculus)
Bax (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Dopamine 20 18.16 Low Low
Substantia nigra 9 5.00 Very Low Very Low Very Low
Catecholamine 6 5.00 Very Low Very Low Very Low
midbrain 4 5.00 Very Low Very Low Very Low
adenocard 1 5.00 Very Low Very Low Very Low
Neurotransmitter 1 5.00 Very Low Very Low Very Low
Tetrahydrobiopterin 1 5.00 Very Low Very Low Very Low
Pain 1 5.00 Very Low Very Low Very Low
lidocaine 1 5.00 Very Low Very Low Very Low
Potency 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 3 100.00 Very High Very High Very High
Parkinson's Disease 18 96.32 Very High Very High Very High
Stress 2 41.60 Quite Low
Aging 3 23.12 Low Low
Targeted Disruption 10 5.00 Very Low Very Low Very Low
Toxicity 2 5.00 Very Low Very Low Very Low
Pain 1 5.00 Very Low Very Low Very Low
Disease 1 5.00 Very Low Very Low Very Low
Injury 1 5.00 Very Low Very Low Very Low
Neurodegenerative Disease 1 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It is known that prolonged activation of PP2A can induce apoptosis in part by enhancing pro-apoptotic Bax activity (105), which stimulates ceramide production, a factor also known to contribute to PD pathology (106).
Positive_regulation (activation) of PP2A Positive_regulation (enhancing) of Bax associated with parkinson's disease and apoptosis
1) Confidence 0.46 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2878529 Disease Relevance 0.36 Pain Relevance 0

General Comments

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