INT100078

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Context Info
Confidence 0.70
First Reported 2002
Last Reported 2009
Negated 1
Speculated 0
Reported most in Abstract
Documents 11
Total Number 11
Disease Relevance 3.60
Pain Relevance 5.86

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

nucleoplasm (PPARG) enzyme binding (PPARG) DNA binding (PPARG)
lipid metabolic process (PPARG) cytoplasm (PPARG) cytosol (PPARG)
PPARG (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 6 100.00 Very High Very High Very High
cINOD 40 99.90 Very High Very High Very High
Inflammation 9 99.54 Very High Very High Very High
diclofenac 32 98.92 Very High Very High Very High
withdrawal 1 95.00 High High
Analgesic 3 92.76 High High
antagonist 4 90.24 High High
Pain 4 89.92 High High
agonist 5 89.28 High High
Cannabinoid 6 86.24 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 17 99.62 Very High Very High Very High
Apoptosis 6 99.28 Very High Very High Very High
Familial Adenomatous Polyposis 3 98.24 Very High Very High Very High
Cancer 12 97.92 Very High Very High Very High
Squamous Cell Carcinoma 5 96.20 Very High Very High Very High
Obesity 1 90.92 High High
Pain 3 89.92 High High
Neuropathic Pain 1 84.24 Quite High
Colon Cancer 3 76.92 Quite High
Colorectal Cancer 6 75.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The ability of various nonsteroidal anti-inflammatory drugs (NSAIDs) to induce PPARgamma activation was also evaluated.
Positive_regulation (induce) of Positive_regulation (activation) of PPARgamma associated with inflammation and cinod
1) Confidence 0.70 Published 2003 Journal Prostaglandins Leukot. Essent. Fatty Acids Section Abstract Doc Link 12711249 Disease Relevance 0.50 Pain Relevance 0.45
The non-steroidal anti-inflammatory drug (NSAID) sulindac induces the transcription of SSAT via activation of PPARgamma.
Positive_regulation (induces) of Positive_regulation (activation) of PPARgamma associated with inflammation and cinod
2) Confidence 0.66 Published 2003 Journal Biochem. Soc. Trans. Section Abstract Doc Link 12653645 Disease Relevance 0.74 Pain Relevance 0.22
Unexpectedly, diclofenac bound PPARgamma at therapeutic concentrations (K(i) = 700 nM) but induced only 2-fold activation of PPARgamma at a concentration of 25 microM and antagonized PPARgamma trans-activation by rosiglitazone.
Positive_regulation (trans) of Positive_regulation (activation) of PPARgamma associated with diclofenac
3) Confidence 0.64 Published 2002 Journal Mol. Pharmacol. Section Abstract Doc Link 11752200 Disease Relevance 0.27 Pain Relevance 0.85
Unexpectedly, diclofenac bound PPARgamma at therapeutic concentrations (K(i) = 700 nM) but induced only 2-fold activation of PPARgamma at a concentration of 25 microM and antagonized PPARgamma trans-activation by rosiglitazone.
Positive_regulation (induced) of Positive_regulation (activation) of PPARgamma associated with diclofenac
4) Confidence 0.64 Published 2002 Journal Mol. Pharmacol. Section Abstract Doc Link 11752200 Disease Relevance 0.23 Pain Relevance 0.82
We suggest that upregulation of PPARgamma expression and activation may be, at least partially, responsible for sulindac's antiproliferative effect.
Positive_regulation (upregulation) of Positive_regulation (activation) of PPARgamma
5) Confidence 0.46 Published 2002 Journal Int. J. Cancer Section Abstract Doc Link 11948457 Disease Relevance 0.58 Pain Relevance 0.17
Our results suggest that EGR-1 induction is a unique property of TGZ, but is independent of PPARgamma activation.
Neg (independent) Positive_regulation (independent) of Positive_regulation (activation) of PPARgamma
6) Confidence 0.46 Published 2004 Journal J. Biol. Chem. Section Abstract Doc Link 14662774 Disease Relevance 0.13 Pain Relevance 0.15
Unexpectedly, diclofenac bound PPARgamma at therapeutic concentrations (K(i) = 700 nM) but induced only 2-fold activation of PPARgamma at a concentration of 25 microM and antagonized PPARgamma trans-activation by rosiglitazone.
Positive_regulation (activation) of Positive_regulation (trans) of PPARgamma associated with diclofenac
7) Confidence 0.43 Published 2002 Journal Mol. Pharmacol. Section Abstract Doc Link 11752200 Disease Relevance 0.27 Pain Relevance 0.85
The results suggest that COX-2 expression by NSAIDs is biologically functional, prostanoid-independent, and involves PPARgamma activation, and provide the first direct evidence that the PPRE in the promoter is required for NSAID-induced COX-2 expression.
Positive_regulation (involves) of Positive_regulation (activation) of PPARgamma associated with cinod
8) Confidence 0.43 Published 2003 Journal J. Immunol. Section Abstract Doc Link 12517972 Disease Relevance 0.07 Pain Relevance 0.37
Data on its mechanism of action are not yet complete; however, the activation of PPAR-gamma, and regulation of eicosanoid and cytokine production, appear to be important for its potential therapeutic effects.
Positive_regulation (important) of Positive_regulation (activation) of PPAR-gamma associated with cytokine
9) Confidence 0.41 Published 2004 Journal Life Sci. Section Abstract Doc Link 15240185 Disease Relevance 0.37 Pain Relevance 0.82
A variety of small molecule ligands including AJA have been shown to induce the activation of PPAR-gamma and, in some cases this has led to the introduction of clinically useful agents.
Positive_regulation (induce) of Positive_regulation (activation) of PPAR-gamma
10) Confidence 0.32 Published 2005 Journal Life Sci. Section Abstract Doc Link 16005906 Disease Relevance 0.24 Pain Relevance 0.38
We, therefore, have identified that PPAR-gamma activation is a requirement for COX-2 induction after diclofenac stimulation of J774.2 cells.
Positive_regulation (requirement) of Positive_regulation (activation) of PPAR-gamma associated with diclofenac
11) Confidence 0.03 Published 2009 Journal Mol. Cell. Biochem. Section Abstract Doc Link 19219624 Disease Relevance 0.18 Pain Relevance 0.80

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