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Context Info
Confidence 0.19
First Reported 1998
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 8
Disease Relevance 2.82
Pain Relevance 1.06

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

mitochondrion (CPOX) small molecule metabolic process (CPOX) oxidoreductase activity (CPOX)
cytoplasm (CPOX)
Anatomy Link Frequency
Caco-2 2
CPOX (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 79 99.48 Very High Very High Very High
metalloproteinase 106 99.12 Very High Very High Very High
cINOD 15 92.32 High High
antagonist 26 89.88 High High
COX-2 inhibitor 24 67.68 Quite High
Kinase C 8 62.84 Quite High
aspirin 3 62.48 Quite High
carrageenan induced 1 60.80 Quite High
Pain 1 53.04 Quite High
Spinal cord 24 52.08 Quite High
Disease Link Frequency Relevance Heat
Cancer 25 100.00 Very High Very High Very High
INFLAMMATION 93 99.48 Very High Very High Very High
Reprotox - General 1 5 96.20 Very High Very High Very High
Colon Cancer 6 94.76 High High
Neuroblastoma 44 94.70 High High
Lung Cancer 6 83.76 Quite High
Sarcoma 79 79.44 Quite High
Herpes Simplex Virus 238 76.00 Quite High
Repression 2 75.00 Quite High
Infection 104 73.44 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Prostaglandins are generated through two isoforms of the enzyme cyclooxygenase, the constitutively expressed cyclooxygenase (Cox)-1 and Cox-2, which is induced at sites of inflammation.
Positive_regulation (generated) of Positive_regulation (induced) of Cox associated with inflammation
1) Confidence 0.19 Published 1998 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 9808683 Disease Relevance 0.22 Pain Relevance 0.13
OVCAR-3 cells showed a constitutive expression of COX-1 and an induction of high levels of COX-2 and PGE(2) after stimulation with interleukin-1beta.
Positive_regulation (levels) of Positive_regulation (induction) of COX in OVCAR-3
2) Confidence 0.16 Published 2003 Journal Oncogene Section Abstract Doc Link 14647459 Disease Relevance 0.42 Pain Relevance 0.13
This unknown target of ATRA would, in turn, be responsible for the activation of a signalling pathway leading to the activation of the COX-2 promoter.
Positive_regulation (leading) of Positive_regulation (activation) of COX
3) Confidence 0.14 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC1769480 Disease Relevance 0.16 Pain Relevance 0.07
Recent studies show that up-regulation of cyclooxygenase-2 (COX-2) in human cancer cells induces activation of matrix metalloproteinases (MMPs) and increase of metastatic potential.
Positive_regulation (induces) of Positive_regulation (up-regulation) of COX associated with cancer and metalloproteinase
4) Confidence 0.11 Published 2001 Journal FEBS Lett. Section Abstract Doc Link 11728453 Disease Relevance 0.41 Pain Relevance 0.29
This requirement for a higher dose of inhibitors to block COX-2 function and PGE2 secretion could be due to the continuous loop of COX activation leading to the maintenance of a constant level of PGE2 in latently infected cells.
Positive_regulation (leading) of Positive_regulation (activation) of COX
5) Confidence 0.11 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 0.50 Pain Relevance 0
Here we observed that ATRA also induces ERK1/2 phosphorylation in SH-SY5Y human neuroblastoma cells (Figure 2c, right) and we confirmed the key role of ERK1/2 phosphorylation for COX-2 up-regulation by ATRA since treatment with PD098059, the selective inhibitor of mitogen-activated protein kinase kinase 1 (MEK-1), was sufficient to abrogate COX-2 promoter activation, to increase COX-2 protein expression and to increase PGE2 production (Figure 2d and Figure 3a right and 3b).
Positive_regulation (activation) of Positive_regulation (increase) of COX in SH-SY5Y associated with neuroblastoma
6) Confidence 0.10 Published 2007 Journal J Neuroinflammation Section Body Doc Link PMC1769480 Disease Relevance 0.15 Pain Relevance 0
Collectively, these observations suggest that AR is an obligatory mediator of growth factor-induced up-regulation of COX-2, PGE(2), and growth of Caco-2 cells, indicating that inhibition of AR may be a novel therapeutic approach in preventing the progression of colon cancer.
Positive_regulation (factor-induced) of Positive_regulation (up-regulation) of COX in Caco-2 associated with colon cancer
7) Confidence 0.10 Published 2006 Journal Cancer Res. Section Abstract Doc Link 17018629 Disease Relevance 0.36 Pain Relevance 0.09
stimulation of HUVEC for 20 h induced COX activity, generating high level of PGE2 and the stable metabolite of prostacyclin, 6-keto-PGF1?
Positive_regulation (stimulation) of Positive_regulation (induced) of COX
8) Confidence 0.04 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1435878 Disease Relevance 0.60 Pain Relevance 0.34

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