INT134902

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Context Info
Confidence 0.37
First Reported 2006
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 11
Total Number 12
Disease Relevance 3.06
Pain Relevance 0.53

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

molecular_function (Tymp) cellular_component (Tymp) biological_process (Tymp)
Anatomy Link Frequency
plasma 1
hematopoietic stem cell 1
smooth muscle 1
neurons 1
vessels 1
Tymp (Rattus norvegicus)
Pain Link Frequency Relevance Heat
cva 66 95.24 Very High Very High Very High
ischemia 8 94.44 High High
Glutamate 3 84.80 Quite High
agonist 26 71.36 Quite High
Clonidine 7 68.72 Quite High
antagonist 2 49.84 Quite Low
Pain 8 25.00 Low Low
Analgesic 3 25.00 Low Low
nociceptor 2 25.00 Low Low
Migraine 1 25.00 Low Low
Disease Link Frequency Relevance Heat
Mitochondrial Disorders 2 95.32 Very High Very High Very High
Cv General 4 Under Development 48 95.24 Very High Very High Very High
Cv Unclassified Under Development 8 94.44 High High
Hypertension 20 94.04 High High
Diabetes Mellitus 8 93.48 High High
Atherosclerosis 8 93.08 High High
Disease 29 91.60 High High
Parkinson's Disease 2 86.72 High High
Increased Venous Pressure Under Development 72 81.88 Quite High
Deafness 2 80.60 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To restore TP activity, allogeneic hematopoietic stem cell transplantation (HSCT) has been proposed as a treatment for patients with MNGIE obtaining encouraging results [15].
Positive_regulation (restore) of TP in hematopoietic stem cell
1) Confidence 0.37 Published 2010 Journal Int Arch Med Section Body Doc Link PMC3018369 Disease Relevance 0.46 Pain Relevance 0
While hemodialysis to reduce nucleoside levels does not seem to be effective, platelet infusions transiently provide TP activity and reduce plasma dThd and dUrd levels [13].
Positive_regulation (provide) of TP in plasma
2) Confidence 0.37 Published 2010 Journal Int Arch Med Section Body Doc Link PMC3018369 Disease Relevance 0.65 Pain Relevance 0
Compared with the group which received TP alone, the prostate organ quotient and the volume of the other groups (E2 ?
Positive_regulation (received) of TP
3) Confidence 0.32 Published 2010 Journal Indian Journal of Pharmacology Section Body Doc Link PMC2959216 Disease Relevance 0 Pain Relevance 0
Extracellular single-unit recordings were made from 38 C1 neurons responding to electrical stimulation of TP under pentobarbital-anesthetized rats.
Positive_regulation (stimulation) of TP in neurons
4) Confidence 0.25 Published 2006 Journal Exp Brain Res Section Abstract Doc Link 16604314 Disease Relevance 0 Pain Relevance 0.27
Since endothelium-derived nitric oxide (NO) suppresses constitutively the release and vascular effects of thromboxane A2 (TXA2), NO-deficiency is often associated with activation of thromboxane receptors (TP).
Positive_regulation (activation) of TP in endothelium
5) Confidence 0.24 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC3013104 Disease Relevance 0.17 Pain Relevance 0
Why is this TP-receptor mediated mechanism enhanced in NO-deficiency?
Neg (NO) Positive_regulation (enhanced) of TP-receptor
6) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3013104 Disease Relevance 0.14 Pain Relevance 0
Subsequent stimulation of the TP-receptors with 100 nM U-46619 induced significantly (P<0.001) stronger elevation of the mean vascular tone (by 77.2±6.2%) as compared to the control vessels.
Positive_regulation (stimulation) of TP in vessels
7) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3013104 Disease Relevance 0.08 Pain Relevance 0
Since NO suppresses platelet aggregation as well as vascular release of TXA2, NO-deficiency is often associated with activation of TP-receptors.
Positive_regulation (activation) of TP in platelet
8) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3013104 Disease Relevance 0.75 Pain Relevance 0.12
In the present study we hypothesized that in the absence of NO, overactivation of the TP-receptor mediated cerebrovascular signaling pathway contributes to the development of vasomotion and CBF oscillations.


Positive_regulation (overactivation) of TP-receptor
9) Confidence 0.17 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC3013104 Disease Relevance 0.16 Pain Relevance 0.03
Our results indicate that activation of TP-receptors increases cerebral vasomotion and CBF oscillations in NO-deficiency.
Positive_regulation (activation) of TP
10) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3013104 Disease Relevance 0.43 Pain Relevance 0.07
Effects of pharmacological modulation of TP-receptor activation and its downstream signaling pathway have been investigated on CBF oscillations (measured by laser-Doppler flowmetry in anesthetized rats) and vasomotion (measured by isometric tension recording in isolated rat middle cerebral arteries, MCAs) both under physiological conditions and after acute inhibition of NO synthesis.
Positive_regulation (activation) of TP-receptor
11) Confidence 0.16 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC3013104 Disease Relevance 0.15 Pain Relevance 0.04
Furthermore, NO also interferes with the signaling pathway coupling TP-receptor activation to vascular smooth muscle contraction.
Positive_regulation (activation) of TP-receptor in smooth muscle
12) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3013104 Disease Relevance 0.06 Pain Relevance 0

General Comments

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