INT89664

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Context Info
Confidence 0.59
First Reported 2000
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 11
Total Number 13
Disease Relevance 7.81
Pain Relevance 5.07

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 (Adora2a) plasma membrane (Adora2a) enzyme binding (Adora2a)
signal transducer activity (Adora2a)
Anatomy Link Frequency
granulocytes 1
striatum 1
lung 1
body 1
Adora2a (Mus musculus)
Pain Link Frequency Relevance Heat
adenocard 342 100.00 Very High Very High Very High
antagonist 125 100.00 Very High Very High Very High
agonist 117 100.00 Very High Very High Very High
Inflammation 396 99.84 Very High Very High Very High
Pain 1 99.36 Very High Very High Very High
Dopamine 69 99.20 Very High Very High Very High
Arthritis 4 99.02 Very High Very High Very High
Analgesic 1 98.60 Very High Very High Very High
methotrexate 50 97.32 Very High Very High Very High
MU agonist 1 96.92 Very High Very High Very High
Disease Link Frequency Relevance Heat
Hypoxia 330 99.88 Very High Very High Very High
INFLAMMATION 342 99.84 Very High Very High Very High
Pain 1 99.36 Very High Very High Very High
Lung Injury 175 99.32 Very High Very High Very High
Experimental Arthritis 2 99.02 Very High Very High Very High
Body Weight 35 98.80 Very High Very High Very High
Depression 2 94.60 High High
Disease 45 92.72 High High
Parkinson's Disease 6 90.64 High High
Pneumonia 65 88.84 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In agreement with the genetic evidence in Figure 5A, similar proinflammatory changes in numbers of granulocytes, levels of protein, and values of lung gas exchange were observed after pharmacological inactivation of A2AR with the antagonist ZM241385 (Figure 5B).
Negative_regulation (inactivation) of A2AR in granulocytes associated with antagonist
1) Confidence 0.59 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1088279 Disease Relevance 0.95 Pain Relevance 0.30
Mice lacking the adenosine A2A receptor are hypoalgesic, and have altered analgesic responses to receptor-selective opioid agonists.
Negative_regulation (lacking) of adenosine A2A receptor associated with mu agonist, adenocard and analgesic
2) Confidence 0.43 Published 2007 Journal Pain Section Abstract Doc Link 17134834 Disease Relevance 0.45 Pain Relevance 0.59
To distinguish between these two possibilities we tested the effects of genetic deficiency of the A2AR on inflammatory lung injury in hypoxic conditions.
Negative_regulation (deficiency) of A2AR in lung associated with lung injury, inflammation and hypoxia
3) Confidence 0.43 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1088279 Disease Relevance 1.16 Pain Relevance 0.26
concentrations between A2AR gene-deficient mice breathing either 10% or 100% oxygen.
Negative_regulation (deficient) of A2AR
4) Confidence 0.43 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1088279 Disease Relevance 1.07 Pain Relevance 0.24
A2AR pathway is nonredundant and would not be substituted by another hypoxia ?
Negative_regulation (nonredundant) of A2AR associated with hypoxia
5) Confidence 0.43 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1088279 Disease Relevance 0.89 Pain Relevance 0.07
Interestingly, blockade of A2AR rescues the behavioral parameters altered in D2R-/- mice.
Negative_regulation (blockade) of A2AR
6) Confidence 0.42 Published 2000 Journal J. Neurosci. Section Abstract Doc Link 10908627 Disease Relevance 0.41 Pain Relevance 0.60
Blockade of the adenosine A2a receptor abrogated the protective effect of OGT.
Negative_regulation (Blockade) of adenosine A2a receptor
7) Confidence 0.41 Published 2009 Journal J. Gastroenterol. Section Body Doc Link 19319464 Disease Relevance 0 Pain Relevance 0
This was associated with a 45% decrease in the striatal extracellular dopamine concentration, suggesting that chronic absence of A2A receptor results in a functional hypodopaminergic state in the striatum.
Negative_regulation (absence) of A2A in striatum associated with dopamine
8) Confidence 0.41 Published 2003 Journal Neurology Section Abstract Doc Link 14663005 Disease Relevance 0.36 Pain Relevance 0.37
The A2AR agonist CGS21680 was dissolved in PBS and administered by IT injection at 0,1 mg/kg body weight in a total volume of 50 ?
Negative_regulation (administered) of A2AR in body associated with body weight and agonist
9) Confidence 0.37 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1088279 Disease Relevance 0.57 Pain Relevance 0.34
We have previously demonstrated pharmacologically, using nonselective antagonists, that the anti-inflammatory effect of methotrexate is mediated by more than one subtype of adenosine receptor in the adjuvant arthritis model in the rat [16], and, using mice rendered deficient in A2A or A3 adenosine receptors, we found that both receptor subtypes are critical for the anti-inflammatory effects of methotrexate in the murine air pouch model of inflammation [17].
Negative_regulation (deficient) of A2A associated with adenocard, inflammation, antagonist, experimental arthritis, methotrexate and arthritis
10) Confidence 0.36 Published 2006 Journal Arthritis Res Ther Section Body Doc Link PMC1526598 Disease Relevance 1.53 Pain Relevance 1.25
Naïve wild-type and knockout mice were also examined for enkephalin and dynorphin mRNA expression by in situ hybridization and for mu-opiate receptor by ligand binding autoradiography to check for possible opiate receptor changes induced by A2A receptor inactivation.
Spec (possible) Negative_regulation (inactivation) of A2A receptor
11) Confidence 0.35 Published 2006 Journal Psychopharmacology (Berl.) Section Body Doc Link 16470403 Disease Relevance 0.07 Pain Relevance 0
It has been found that the psychomotor stimulant effect of low doses of caffeine is mediated by the inhibition of adenosine A2A receptors, involving dopamine-dependent as well as dopamine-independent mechanisms, whereas higher doses of caffeine elicit locomotor depression, most likely acting through antagonism at adenosine A1 receptors [8].
Negative_regulation (inhibition) of A2A associated with dopamine, adenocard and depression
12) Confidence 0.25 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2843608 Disease Relevance 0.24 Pain Relevance 0.66
We also demonstrated that chronic treatment of caffeine and a selective A2A antagonist enhance the phosphorylation level of tyrosine hydroxylase at Ser31.
Negative_regulation (antagonist) of A2A associated with antagonist
13) Confidence 0.25 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2843608 Disease Relevance 0.12 Pain Relevance 0.39

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