INT76341

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Context Info
Confidence 0.25
First Reported 1998
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 12
Total Number 12
Disease Relevance 6.63
Pain Relevance 2.42

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

signal transduction (Ptger2) plasma membrane (Ptger2) signal transducer activity (Ptger2)
Anatomy Link Frequency
plasma 4
macrophage 2
PGE2 2
Ptger2 (Mus musculus)
Pain Link Frequency Relevance Heat
cINOD 20 100.00 Very High Very High Very High
antagonist 103 99.32 Very High Very High Very High
COX-2 inhibitor 28 99.24 Very High Very High Very High
chemokine 4 96.32 Very High Very High Very High
Inflammatory marker 2 94.64 High High
Inflammatory mediators 3 93.52 High High
Inflammation 130 91.20 High High
cytokine 49 89.24 High High
rheumatoid arthritis 65 87.44 High High
cva 1 84.00 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 120 100.00 Very High Very High Very High
Adenoma 1 99.20 Very High Very High Very High
Hemorrhage 4 99.08 Very High Very High Very High
Cancer 79 97.48 Very High Very High Very High
Stomach Cancer 22 97.12 Very High Very High Very High
Apoptosis 143 94.88 High High
Body Weight 2 94.68 High High
Death 24 91.84 High High
Injury 9 91.28 High High
Dermatitis 1 89.92 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Although we definitively confirm the role of PGE2 and more precisely define its mechanistic activity by identifying EP2 as the crucial PGE2 receptor, these findings beg for further dissection of this important signaling pathway leading to increased M?
Negative_regulation (define) of Positive_regulation (identifying) of EP2
1) Confidence 0.25 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2585850 Disease Relevance 1.26 Pain Relevance 0.18
Orally administered OGT prevented or reduced lethality, intestinal lesions, bleeding, increased serum nitrate/nitrite levels, and reduction of mucosal PGE2 induced by indomethacin.
Negative_regulation (reduction) of Positive_regulation (induced) of PGE2 in PGE2 associated with hemorrhage
2) Confidence 0.19 Published 2007 Journal Biol. Pharm. Bull. Section Abstract Doc Link 17329845 Disease Relevance 0.52 Pain Relevance 0.34
This effect of PGE2 on intracellular cAMP accumulation could be inhibited with the selective EP2 or EP4 receptor antagonists AH6809 and ONOAE2227 and abolished with the combination of EP2 and EP4 receptor antagonists.
Negative_regulation (inhibited) of Positive_regulation (selective) of EP2 associated with antagonist
3) Confidence 0.10 Published 2008 Journal Molecular and Cellular Endocrinology Section Body Doc Link PMC2694994 Disease Relevance 0.21 Pain Relevance 0.22
NNK suppressed humoral and cellular immune responses and increased plasma PGE2 and LTB4 levels.
Negative_regulation (suppressed) of Positive_regulation (increased) of PGE2 in plasma
4) Confidence 0.09 Published 1998 Journal Exp. Lung Res. Section Abstract Doc Link 9659586 Disease Relevance 0.19 Pain Relevance 0.16
In addition, we found that the PGE2 activation of COX-2 promoter and mRNA expression was significantly reduced by the EP2 and EP4 receptor antagonists.
Negative_regulation (reduced) of Positive_regulation (activation) of PGE2 associated with antagonist
5) Confidence 0.08 Published 2008 Journal Molecular and Cellular Endocrinology Section Body Doc Link PMC2694994 Disease Relevance 0 Pain Relevance 0.11
Cardioprotection and the increases in PGE2 and 6-keto-PGF(1-alpha) 48 h after morphine administration were abrogated only by indomethacin, and not by SC-560 or NS-398.
Neg (not) Negative_regulation (abrogated) of Positive_regulation (increases) of PGE2
6) Confidence 0.07 Published 2005 Journal J. Am. Coll. Cardiol. Section Body Doc Link 15893191 Disease Relevance 0 Pain Relevance 0
Accordingly, the present results suggest that the suppression of macrophage infiltration and its activation by anti-inflammatory drugs or inhibitors for PGE2 pathway is, therefore, a possible strategy for chemoprevention against gastric cancer.


Negative_regulation (suppression) of Positive_regulation (activation) of PGE2 in macrophage associated with inflammation, cinod and stomach cancer
7) Confidence 0.04 Published 2008 Journal EMBO J Section Body Doc Link PMC2413189 Disease Relevance 0.99 Pain Relevance 0.15
Mechanistically, the increase may be related to the observed decrease in PGE2, since high levels of PGE2 can inhibit TNF?
Negative_regulation (inhibit) of Positive_regulation (levels) of PGE2
8) Confidence 0.03 Published 2002 Journal Lipids Health Dis Section Body Doc Link PMC139966 Disease Relevance 0.51 Pain Relevance 0.24
Interestingly, siRNA directed against S1P or S1P phosphatase (SPP) also enhanced COX-2 and PGE2 production, whereas siRNA directed against SphK1 inhibited the effects of exogenous Sph and ceramide on the induction of PGE2 indicating that it was the intracellular metabolism of S1P that regulated COX-2 and PGE2 induction.
Negative_regulation (metabolism) of Positive_regulation (induction) of PGE2
9) Confidence 0.03 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2842969 Disease Relevance 0.31 Pain Relevance 0.21
In the present study, we found that pre-induction of HO-1 attenuate LPS-induced expression of COX-2 protein and therefore decreased PGE2 accumulation.
Negative_regulation (decreased) of Positive_regulation (accumulation) of PGE2
10) Confidence 0.02 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC3002338 Disease Relevance 0.69 Pain Relevance 0.17
In addition, although treatment with NS-398 blocked LPS-induced increases in the circulating levels of immunoreactive PGE2, injection of the COX-2 inhibitor did not modulate plasma concentrations of TNF or the CXC chemokine KC.
Negative_regulation (blocked) of Positive_regulation (increases) of PGE2 in plasma associated with chemokine and cox-2 inhibitor
11) Confidence 0.02 Published 2004 Journal Crit Care Section Body Doc Link PMC1065065 Disease Relevance 0.96 Pain Relevance 0.47
Cao and Prescott [33] proposed that Bcl-2 overexpression is probably caused by reductions in arachidonic acid and increases in PGE2 levels.
Negative_regulation (reductions) of Positive_regulation (increases) of PGE2
12) Confidence 0.01 Published 2007 Journal Breast Cancer Res Section Body Doc Link PMC2206712 Disease Relevance 0.99 Pain Relevance 0.17

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