INT167701

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Context Info
Confidence 0.01
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 1
Total Number 1
Disease Relevance 0.16
Pain Relevance 0.61

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)
Rpa1 (Mus musculus)
Pain Link Frequency Relevance Heat
cINOD 9 99.18 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 1 79.28 Quite High
Ataxia 1 78.44 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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.
Phosphorylation (phosphorylation) of RPA associated with ataxia and cinod
1) 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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