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Context Info
Confidence 0.06
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 4
Disease Relevance 1.16
Pain Relevance 0.96

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

chromosome organization (Rpa1) nucleus (Rpa1) DNA binding (Rpa1)
cytoplasm (Rpa1)
Anatomy Link Frequency
interneurons 1
Rpa1 (Mus musculus)
Pain Link Frequency Relevance Heat
cINOD 9 99.70 Very High Very High Very High
long-term potentiation 4 84.12 Quite High
midbrain 36 79.80 Quite High
GABAergic 1 78.80 Quite High
Dopamine 1 69.52 Quite High
depression 9 66.04 Quite High
Central nervous system 2 30.60 Quite Low
gABA 11 5.00 Very Low Very Low Very Low
imagery 5 5.00 Very Low Very Low Very Low
Substantia nigra 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Parkinson's Disease 22 86.96 High High
Drug Induced Neurotoxicity 16 81.44 Quite High
INFLAMMATION 3 80.32 Quite High
Death 118 78.20 Quite High
Ataxia 3 77.48 Quite High
Stress 24 74.08 Quite High
Depression 9 66.04 Quite High
Disease 18 5.00 Very Low Very Low Very Low
Hypersensitivity 10 5.00 Very Low Very Low Very Low
Cytomegalovirus Infection 10 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We reported earlier that the activation of presynaptic interneurons during postsynaptic depolarization suppresses RP through activation of postsynaptic metabotropic GABAB receptors (GABABRs) (Kawaguchi and Hirano, 2000).
Negative_regulation (suppresses) of RP in interneurons
1) Confidence 0.06 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0.13 Pain Relevance 0.25
Accordingly, treatment of cells with HBED attenuated the decrease in RPA fluorescence.
Negative_regulation (decrease) of RPA
2) Confidence 0.04 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.62 Pain Relevance 0
A concentration-dependent decrease in RPA fluorescence (corresponding with an increase in Fe2+) was detected following 4 hrs of incubation with 500 µM (13.8±2.4%) and 1000 µM (23.8±1.2%) PQ2+ (Fig. 1c).
Negative_regulation (decrease) of RPA
3) Confidence 0.03 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.25 Pain Relevance 0.10
Here, we explored the potential relationship between chemopreventive NSAIDs and DNA damage responses induced by treatment with topoisomerase-targeting drugs. (1) Sodium salicylate, a non-COX-selective NSAID, was shown to reduce DNA damage-induced RPA and p53 phosphorylation. (2) The formation of enzyme cleavable complexes by topoisomerase-targeting drugs was not affected in the presence of sodium salicylate. (3) The attenuating effect of NSAIDs on the DNA damage responses is COX-2-independent, since COX-2-selective inhibitors failed to inhibit DNA damage-induced phosphorylation of replication protein A (RPA) and p53. (4) This COX-2-independent attenuating effect was mediated through interference of neither nuclear factor kappa B nor extracellular signal-regulated kinase pathways. (5) The activation of ataxia telangiectasia mutated (ATM) kinase and DNA-dependent protein kinase (DNA-PK), two key signal transducers upstream of RPA and p53, was found to be significantly reduced with sodium salicylate treatment. (6) Most importantly, sodium salicylate and other NSAIDs directly inhibited kinase activity of ATM and DNA-PK.
Negative_regulation (reduce) of RPA associated with ataxia and cinod
4) Confidence 0.01 Published 2010 Journal Eur. J. Pharmacol. Section Abstract Doc Link 20406630 Disease Relevance 0.16 Pain Relevance 0.61

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