INT201769

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Context Info
Confidence 0.00
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.82
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.

cytosol (Akt1, CASP9) nucleus (Akt1, CASP9) transport (Akt1)
aging (Akt1) intracellular (CASP9) enzyme binding (Akt1)
Akt1 (Mus musculus)
CASP9 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 9 5.00 Very Low Very Low Very Low
cytokine 8 5.00 Very Low Very Low Very Low
Hippocampus 7 5.00 Very Low Very Low Very Low
Eae 6 5.00 Very Low Very Low Very Low
long-term potentiation 5 5.00 Very Low Very Low Very Low
Kinase C 5 5.00 Very Low Very Low Very Low
Neurotransmitter 5 5.00 Very Low Very Low Very Low
Central nervous system 4 5.00 Very Low Very Low Very Low
Neuropeptide 2 5.00 Very Low Very Low Very Low
Inflammatory mediators 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 133 100.00 Very High Very High Very High
Death 56 84.24 Quite High
Stress 32 83.36 Quite High
Disease 127 71.04 Quite High
Parkinson's Disease 8 30.64 Quite Low
Tetraploidy 1 11.60 Low Low
Neurodegenerative Disease 36 5.00 Very Low Very Low Very Low
Cognitive Disorder 16 5.00 Very Low Very Low Very Low
Toxicity 15 5.00 Very Low Very Low Very Low
INFLAMMATION 13 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
As shown in Figure 4, IAPs can be induced by NF-kB and Akt, which can also inhibit the intrinsic apoptotic pathway through phosphorylation of both caspase-9 and its inactive form [150].
Akt Negative_regulation (inhibit) of Phosphorylation (phosphorylation) of caspase-9 associated with apoptosis
1) Confidence 0.00 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1775042 Disease Relevance 0.82 Pain Relevance 0

General Comments

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