INT35485

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Context Info
Confidence 0.19
First Reported 1985
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 12
Disease Relevance 4.50
Pain Relevance 2.00

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 (PTGIR) cell-cell signaling (PTGIR) signal transducer activity (PTGIR)
Anatomy Link Frequency
blood 1
tail 1
PTGIR (Homo sapiens)
Pain Link Frequency Relevance Heat
aspirin 16 99.04 Very High Very High Very High
Inflammatory response 4 90.28 High High
COX-2 inhibitor 15 88.72 High High
Pain 97 88.16 High High
cINOD 33 88.16 High High
Inflammatory mediators 15 86.48 High High
Pain management 2 86.04 High High
visual analogue scale 18 80.72 Quite High
cytokine 2 78.44 Quite High
agonist 78 76.44 Quite High
Disease Link Frequency Relevance Heat
Disease 214 99.62 Very High Very High Very High
Pressure And Volume Under Development 126 99.12 Very High Very High Very High
Hypertension 31 99.06 Very High Very High Very High
Aseptic Necrosis Of Bone 130 98.80 Very High Very High Very High
Hypercalcemia 2 97.72 Very High Very High Very High
Myocardial Infarction 11 92.64 High High
Stroke 3 90.56 High High
INFLAMMATION 115 89.88 High High
Increased Venous Pressure Under Development 20 89.20 High High
Pain 85 88.16 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In normotensive and hypertensive humans, prostaglandins, particularly PGE2 and PGI2, affect blood pressure through control of vascular resistance, salt excretion, cardiac output, and renin secretion.
Regulation (affect) of PGI2 in blood associated with hypertension
1) Confidence 0.19 Published 1985 Journal Adv. Prostaglandin Thromboxane Leukot. Res. Section Abstract Doc Link 3159200 Disease Relevance 0.38 Pain Relevance 0.05
Although the specific effects of PGI2 on its IP receptor are well documented, there are few data available in the literature about the distribution of IP receptors in human bone.
Regulation (effects) of IP receptor
2) Confidence 0.07 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2592809 Disease Relevance 0.69 Pain Relevance 0.31
The purpose of this study was to assess the curative and symptomatic efficacy of the prostacyclin analogue iloprost in BME and AVN patients.


Regulation (efficacy) of prostacyclin associated with aseptic necrosis of bone and pressure and volume under development
3) Confidence 0.06 Published 2008 Journal Arthritis Res Ther Section Abstract Doc Link PMC2592809 Disease Relevance 1.21 Pain Relevance 0.30
In our simulation, as aspirin strongly inhibited the production of TXA2, the value of PGI2/TXA2 was much larger than before the administration of medicine.
Regulation (value) of PGI2 associated with aspirin
4) Confidence 0.04 Published 2008 Journal Mol Syst Biol Section Body Doc Link PMC2673713 Disease Relevance 0.59 Pain Relevance 0.64
Specifically, we require that the desired state should satisfy the following conditions: (1) the cumulative production of LTB4 must be below 10% of that in the disease state; (2) the cumulative production of PGE2 must be below 10% of that in the disease state and (3) the change in the PGI2/TXA2 ratio between the desired and disease states must be smaller than a preset small value (here, we use 20%).
Regulation (change) of PGI2 associated with disease
5) Confidence 0.03 Published 2008 Journal Mol Syst Biol Section Body Doc Link PMC2673713 Disease Relevance 0.62 Pain Relevance 0.11
The value of PGI2/TXA2 became significantly smaller than that before the administration of medicine.
Regulation (value) of PGI2
6) Confidence 0.03 Published 2008 Journal Mol Syst Biol Section Body Doc Link PMC2673713 Disease Relevance 0.44 Pain Relevance 0.42
The effect of prostacyclin/cAMP and NO/cGMP on TP?
Regulation (effect) of prostacyclin
7) Confidence 0.03 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
Moreover, in view of the critical involvement of inhibitory agents including prostacyclin and NO, that largely signal through cAMP and cGMP second messengers, in regulating RhoA-dependent mechanisms [1,6,35,36] coupled to their role in differentially regulating TP?
Regulation (involvement) of prostacyclin
8) Confidence 0.03 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.50 Pain Relevance 0.07
is subject to regulation by both direct prostacyclin/PKA and NO/PKG-inhibition mediated through their respective phosphorylation of Ser329 and Ser331 within the unique C-tail domain of TP?
Regulation (regulation) of prostacyclin in tail
9) Confidence 0.02 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0
isoforms, respectively, suggest that such inhibitory responses of prostacyclin and NO are mediated, at least in part, at the interface of the stimulatory GPCR (i.e. the TP).
Regulation (responses) of prostacyclin
10) Confidence 0.02 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.03
is not as such a direct target of prostacyclin- or NO-mediated phosphorylation and inhibition, their effect on TP?
Regulation (target) of prostacyclin
11) Confidence 0.02 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0.06 Pain Relevance 0
isoforms suggest that such inhibitory responses of prostacyclin and NO are mediated, at least in part, directly at the level of TP?
Regulation (responses) of prostacyclin
12) Confidence 0.02 Published 2008 Journal Cellular Signalling Section Body Doc Link PMC2681257 Disease Relevance 0 Pain Relevance 0.08

General Comments

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