INT1762

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Context Info
Confidence 0.43
First Reported 1979
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 64
Total Number 66
Disease Relevance 28.21
Pain Relevance 11.27

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

plasma membrane (PTGER2) signal transducer activity (PTGER2)
Anatomy Link Frequency
PGE2 5
plasma 4
blood 2
osteoblasts 2
HGF 2
PTGER2 (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 379 99.98 Very High Very High Very High
Osteoarthritis 693 99.84 Very High Very High Very High
diclofenac 123 99.78 Very High Very High Very High
antagonist 30 99.64 Very High Very High Very High
metalloproteinase 421 99.58 Very High Very High Very High
COX2 13 99.20 Very High Very High Very High
Potency 6 99.14 Very High Very High Very High
MU agonist 2 99.14 Very High Very High Very High
Inflammation 721 99.12 Very High Very High Very High
COX-2 inhibitor 195 98.14 Very High Very High Very High
Disease Link Frequency Relevance Heat
Ulcers 31 100.00 Very High Very High Very High
Cancer 507 99.88 Very High Very High Very High
Osteoarthritis 731 99.84 Very High Very High Very High
Chronic Sinusitis 25 99.84 Very High Very High Very High
Breast Cancer 376 99.60 Very High Very High Very High
INFLAMMATION 885 99.12 Very High Very High Very High
Asthma 91 99.12 Very High Very High Very High
Nasal Polyps 26 98.92 Very High Very High Very High
Fibrosis 10 98.90 Very High Very High Very High
Disease 241 98.28 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This SNP may act by reducing the PGE2 braking mechanism of inflammation.
Negative_regulation (reducing) of PGE2 associated with inflammation
1) Confidence 0.43 Published 2006 Journal Yonsei Medical Journal Section Body Doc Link PMC2687575 Disease Relevance 0.64 Pain Relevance 0.12
There was a significant negative trend between the doses (10(-7)-10(-3) M) of each of indomethacin, piroxicam, and ibuprofen, and the amounts of PGF2 alpha, PGE2, PGD2, and 15-keto-PGE2 produced.
Negative_regulation (amounts) of PGE2
2) Confidence 0.38 Published 1983 Journal J. Dent. Res. Section Abstract Doc Link 6576002 Disease Relevance 0.16 Pain Relevance 0.16
We studied all aspects of the actual measurement of PGE2 including the extraction efficiency of the PGE2 from the mucosa, the precision of the assay and calculation of the PGE2 content in terms of milligrams of protein in the sample, the inhibition of PGE2 by indomethacin over time, the reproducibility of the measurement within one homogenate, the rate of PGE2 production over time, the effect of adding indomethacin versus snap freezing on PGE2 production, the stability of PGE2 in tissues over time stored in liquid nitrogen, and the variability of the measurement of PGE2 in separate biopsies from one individual.
Negative_regulation (inhibition) of PGE2 in PGE2
3) Confidence 0.34 Published 1995 Journal Cancer Epidemiol. Biomarkers Prev. Section Abstract Doc Link 7606198 Disease Relevance 0.60 Pain Relevance 0.23
The PGE2-dependent stimulation of IGF-1 synthesis was due in part to the cAMP/protein kinase A pathway since both the direct inhibition of this pathway with H-89 and the inhibition of EP2 or EP4 receptors, linked to cAMP production, reduced IGF-1 synthesis.
Negative_regulation (inhibition) of EP2 in PGE2
4) Confidence 0.34 Published 2006 Journal Bone Section Abstract Doc Link 16257278 Disease Relevance 1.24 Pain Relevance 0.69
The inhibitory effect of very low concentrations PGE2 in OA cartilage explants may help to explain the similar inhibitory effects produced by TGF-?
Negative_regulation (effect) of PGE2 in cartilage associated with osteoarthritis
5) Confidence 0.32 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2206385 Disease Relevance 0.41 Pain Relevance 0.25
This protection is believed to be mediated, at least in part, through reduction of prostaglandin E2 (PGE2) levels [7,8], as PGE2 promotes cell growth, migration and angiogenesis and reduce apoptosis [4].
Negative_regulation (reduction) of PGE2 in PGE2 associated with apoptosis
6) Confidence 0.25 Published 2010 Journal BMC Gastroenterol Section Body Doc Link PMC2824707 Disease Relevance 1.21 Pain Relevance 0.22
Blood flow was kept constant during elevation by 20 cm above heart level (preserved autoregulation) except after injection of PGE-2 and LTD-4 20 microM where a significant decrease was observed (defective smooth muscle function).
Negative_regulation (decrease) of PGE-2 in heart
7) Confidence 0.24 Published 1985 Journal Prostaglandins Section Abstract Doc Link 3856899 Disease Relevance 0.08 Pain Relevance 0.18
In addition, PGE2 was down-regulated in chronic rhinosinusitis/nasal polyp tissue compared to chronic rhinosinusitis and normal nasal mucosa and the levels of this eicosanoid inversely correlated to eosinophilic inflammation.
Negative_regulation (regulated) of PGE2 in nasal mucosa associated with rhinitis, inflammation, chronic sinusitis and nasal polyps
8) Confidence 0.22 Published 2006 Journal Respir Res Section Body Doc Link PMC1481584 Disease Relevance 1.19 Pain Relevance 0.16
The ability of ASC to respond to exogenous PGE2 stimulation of cAMP synthesis is inhibited or stimulated by factors that increase or decrease PGE2 levels, respectively, in the cultures.
Negative_regulation (decrease) of PGE2 in ASC
9) Confidence 0.21 Published 1979 Journal Ann. N. Y. Acad. Sci. Section Abstract Doc Link 231404 Disease Relevance 0.34 Pain Relevance 0.21
It is suggested that the gastric tolerability of non-steroidal anti-inflammatory drugs (NSAIDs) is related to their inhibitory potency on PGE2 formation, in the sense that weak inhibitors of PGE2 cause less damage to the gastric mucosa than do strong inhibitors.
Negative_regulation (inhibitors) of PGE2 associated with inflammation, cinod and potency
10) Confidence 0.20 Published 1986 Journal Hepatogastroenterology Section Abstract Doc Link 3456972 Disease Relevance 0.10 Pain Relevance 0.25
is associated with a significant decrease in EP2 mRNA and protein
Negative_regulation (decrease) of EP2
11) Confidence 0.19 Published 2008 Journal PPAR Research Section Body Doc Link PMC2515882 Disease Relevance 0.57 Pain Relevance 0.07
To confirm the results obtained with EP receptor selective agonists, we performed complementary experiments with EP receptor selective antagonists (Fig. 5C). 10 nM PGE2 driven proliferation was severely reduced by EP1 and EP3 specific antagonists whereas an EP4 specific blocker did not ostensibly affect proliferation in these cells.
Negative_regulation (reduced) of PGE2 associated with antagonist and agonist
12) Confidence 0.16 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2615781 Disease Relevance 0 Pain Relevance 0.37
associated with a significant decrease in EP2 mRNA and protein expression.
Negative_regulation (decrease) of EP2
13) Confidence 0.16 Published 2007 Journal PPAR Research Section Body Doc Link PMC2220082 Disease Relevance 0.50 Pain Relevance 0.04
Pterostilbene levels in serum were increased, but were 5-fold lower than the observed IC50 for PGE2 inhibition in LPS-stimulated PBMC.
Negative_regulation (inhibition) of PGE2 in PBMC
14) Confidence 0.15 Published 2005 Journal Planta Med. Section Abstract Doc Link 15931573 Disease Relevance 0 Pain Relevance 0
RESULTS: All of the COX inhibitors caused dose-dependent decreases in IL-1beta-stimulated PGE2, to a maximum of > 90% in all cell lines (P < or = 0.0001).
Negative_regulation (decreases) of PGE2
15) Confidence 0.13 Published 2003 Journal J. Periodontol. Section Body Doc Link 14974816 Disease Relevance 0 Pain Relevance 0
CONCLUSION: From the results of this study we conclude that nimesulide and diclofenac at therapeutic concentrations are potent inhibitors of PGE2 and IL-6 production while they do not modify proteoglycan or IL-8 production.


Negative_regulation (inhibitors) of PGE2 in PGE2
16) Confidence 0.13 Published 1999 Journal Clin. Exp. Rheumatol. Section Body Doc Link 10342040 Disease Relevance 0 Pain Relevance 0
Consistent with this mechanism, a reduction in plasma PGE2 levels was observed in the diclofenac treatment group.
Negative_regulation (reduction) of PGE2 in plasma associated with diclofenac
17) Confidence 0.12 Published 2010 Journal BMC Med Genomics Section Body Doc Link PMC2837611 Disease Relevance 1.58 Pain Relevance 0.92
LPS-induced IL-6 and PGE2 release was only slightly inhibited at high doses, whereas LPS-induced release of IL-8 and matrix metalloprotease (MMP)-9 was not affected.
Negative_regulation (inhibited) of PGE2
18) Confidence 0.09 Published 2004 Journal Scand. J. Rheumatol. Suppl. Section Abstract Doc Link 15515409 Disease Relevance 0.50 Pain Relevance 0.19
As expected, diclofenac treatment decreased PGE2 levels (48.9 ± 10.6 pg/mL (mean ± stdev) at day 9 compared to 55.3 ± 11.9 pg/mL at day0, p = 0.047), as displayed in figure 1.
Negative_regulation (decreased) of PGE2 associated with diclofenac
19) Confidence 0.09 Published 2010 Journal BMC Med Genomics Section Body Doc Link PMC2837611 Disease Relevance 0.48 Pain Relevance 0.46
IND significantly reduced both basal and IL-1 beta-induced PGE2 release and HGF production.
Negative_regulation (reduced) of PGE2 in HGF
20) Confidence 0.08 Published 1998 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 9571196 Disease Relevance 0.23 Pain Relevance 0.36

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