INT108063

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Context Info
Confidence 0.78
First Reported 2003
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 29
Total Number 32
Disease Relevance 13.11
Pain Relevance 13.78

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
central nervous system 3
lungs 2
neutrophils 2
granulocytes 2
macrophages 1
Adora2a (Mus musculus)
Pain Link Frequency Relevance Heat
adenocard 941 100.00 Very High Very High Very High
agonist 201 100.00 Very High Very High Very High
Dopamine 104 100.00 Very High Very High Very High
GABAergic 6 100.00 Very High Very High Very High
Neuropeptide 3 100.00 Very High Very High Very High
Cannabinoid receptor 1 100.00 Very High Very High Very High
Analgesic 7 99.96 Very High Very High Very High
Cannabinoid 4 99.90 Very High Very High Very High
withdrawal 20 99.82 Very High Very High Very High
Enkephalin 2 99.76 Very High Very High Very High
Disease Link Frequency Relevance Heat
Targeted Disruption 78 100.00 Very High Very High Very High
Lung Injury 205 99.64 Very High Very High Very High
INFLAMMATION 462 99.56 Very High Very High Very High
Pneumonia 167 99.04 Very High Very High Very High
Rheumatoid Arthritis 78 99.04 Very High Very High Very High
Ganglion Cysts 3 98.48 Very High Very High Very High
Drug Dependence 32 97.96 Very High Very High Very High
Cancer 21 96.80 Very High Very High Very High
Necrosis 14 96.56 Very High Very High Very High
Psychosis 48 96.24 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
When compared to the several-fold increase in A2AR mRNA expression levels in inflammatory granulocytes from mice exposed to 21% oxygen, these levels were up-regulated to a much lesser extent in mice breathing 100% oxygen.
Gene_expression (expression) of A2AR mRNA in granulocytes associated with inflammation
1) Confidence 0.78 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1088279 Disease Relevance 0.22 Pain Relevance 0.21
Results of parallel assays confirmed increased expression of A2AR on activated granulocytes, since CGS21680 inhibited the functional response of in vivo-activated granulocytes (i.e., as evidenced by the production of tissue-damaging reactive oxygen species) much more strongly than in naïve cells (Figure 4A, right graph).
Gene_expression (expression) of A2AR in granulocytes
2) Confidence 0.78 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1088279 Disease Relevance 0 Pain Relevance 0.16
Therefore it was important to test whether “in vivo-activated” granulocytes isolated from inflamed lungs of IT LPS-injected mice might have up-regulated their A2AR expression.
Gene_expression (expression) of A2AR in lungs
3) Confidence 0.78 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1088279 Disease Relevance 0.17 Pain Relevance 0.13
A2A receptor is highly coexpressed with enkephalin and D2 receptor in striatopallidal neurons.
Gene_expression (coexpressed) of A2A in neurons associated with enkephalin
4) Confidence 0.75 Published 2003 Journal Neurology Section Abstract Doc Link 14663005 Disease Relevance 0.26 Pain Relevance 0.24
Severe symptoms of opioid withdrawal observed in SWR/J mice were associated with strong transcriptional activation of cytotoxic T lymphocyte-associated protein 2 (Ctla2a) and methionine adenosyltransferase II (Mat2a) genes after acute administration of morphine, whereas changes in gene expression of adenosine A2a receptor (Adora2a) were negatively related to the level of morphine physical dependence across the four inbred mouse strains (Figure 7).
Gene_expression (expression) of Adora2a in cytotoxic T lymphocyte associated with adenocard, physical dependence, sprains and strains, withdrawal, opioid and morphine
5) Confidence 0.71 Published 2007 Journal Genome Biol Section Body Doc Link PMC2394777 Disease Relevance 0.67 Pain Relevance 1.31
A2A adenosine and CB1 cannabinoid receptors are highly expressed in the central nervous system, where they modulate numerous physiological processes including adaptive responses to drugs of abuse.
Gene_expression (expressed) of A2A in central nervous system associated with adenocard, cannabinoid receptor and central nervous system
6) Confidence 0.70 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15450100 Disease Relevance 0.13 Pain Relevance 0.44
Targeted disruption of the A2A adenosine receptor reduces in-vitro prostate contractility in mature mice.
Gene_expression (disruption) of A2A associated with targeted disruption and adenocard
7) Confidence 0.68 Published 2008 Journal Eur. J. Pharmacol. Section Title Doc Link 18655781 Disease Relevance 0.10 Pain Relevance 0.27
Disruption of the A2A adenosine receptor leads to reduced nerve mediated contractile responses of the prostate in mature mice.
Gene_expression (Disruption) of A2A in nerve associated with adenocard
8) Confidence 0.68 Published 2008 Journal Eur. J. Pharmacol. Section Abstract Doc Link 18655781 Disease Relevance 0.07 Pain Relevance 0.37
Defining variants of the ADORA2A gene
Gene_expression (variants) of ADORA2A gene
9) Confidence 0.67 Published 2010 Journal Behav Brain Funct Section Body Doc Link PMC2939586 Disease Relevance 0.47 Pain Relevance 0.07
These studies provide genetic evidence that even though the A2AAR, A2BAR or A3AR are expressed on cardiac tissues [11], [18], they do not mediate the heart-rate slowing effects of adenosine.


Gene_expression (expressed) of A2AAR in heart associated with adenocard
10) Confidence 0.66 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2727950 Disease Relevance 0.15 Pain Relevance 0.38
This conclusion is supported by (i) the strong increase in lung inflammation and mortality after short-term exposure of mice to high and even to moderately elevated concentrations of oxygen (see Figures 1 and 2); (ii) the causative pathogenic role of PMNs in inflammatory lung injury (see Figure 3) and the up-regulation of A2AR expression on alveolar PMNs (see Figures 4); (iii) the critical role of A2AR in lung protection from enhanced accumulation of PMNs as well as more pronounced vascular permeability and stronger impairment of lung gas exchange in A2AR genetically deficient mice (see Figure 5A) and in A2AR antagonist-treated wild-type mice (see Figure 5B); (iv) the strong lung-protective effects of hypoxia by suppression of PMN emigration, PMN activation, lung vascular permeability, and impairment of gas exchange in wild-type mice (see Figure 6); (v) the evidence that hypoxia is upstream of A2ARs in the same anti-inflammatory, lung tissue-protecting pathway, as shown by the failure of the adenosine-producing (see Figure 7A) hypoxia to protect A2AR-deficient mice from death and excessive pulmonary TNF-?
Gene_expression (expression) of A2AR in lung associated with lung injury, adenocard, inflammation, hypoxia, antagonist, pneumonia and death
11) Confidence 0.60 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1088279 Disease Relevance 1.37 Pain Relevance 0.35
A2AR pathway, which is hypothesized as being responsible for protecting inflamed lungs and down-regulating neutrophils, we (i) determined the role of neutrophils in inflammatory lung injury, (ii) tested for A2AR expression on these cells to demonstrate their susceptibility to modulation by endogenously produced adenosine, (iii) analyzed the degree of inflammatory lung tissue damage in A2AR gene-deficient mice or in wild-type mice treated with highly selective pharmacologic antagonists for A2ARs, and (iv) tested whether the hypoxia has a lung-protective role and whether there is a direct linkage between hypoxia (upstream) and A2ARs (downstream) in the proposed lung-protective hypoxia ?
Gene_expression (expression) of A2AR in neutrophils associated with lung injury, adenocard, inflammation, hypoxia and antagonist
12) Confidence 0.60 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1088279 Disease Relevance 1.01 Pain Relevance 0.28
CB1 cannabinoid and A2a adenosine receptors are highly expressed in the central nervous system where they modulate numerous physiological processes including emotional behaviour and the responses of several drugs of abuse.
Gene_expression (expressed) of A2a in central nervous system associated with adenocard, cannabinoid and central nervous system
13) Confidence 0.59 Published 2003 Journal Eur. J. Neurosci. Section Abstract Doc Link 12542668 Disease Relevance 0.28 Pain Relevance 0.42
It is of interest that the ADORA2a receptor is strongly expressed within the CNS, especially around the basal ganglia [19].
Gene_expression (expressed) of ADORA2a in CNS associated with central nervous system
14) Confidence 0.59 Published 2008 Journal Rheumatology (Oxford, England) Section Body Doc Link PMC2468887 Disease Relevance 0.62 Pain Relevance 0.68
Increase of morphine withdrawal in mice lacking A2a receptors and no changes in CB1/A2a double knockout mice.
Neg (lacking) Gene_expression (lacking) of A2a associated with targeted disruption, narcan, withdrawal and morphine
15) Confidence 0.59 Published 2003 Journal Eur. J. Neurosci. Section Title Doc Link 12542668 Disease Relevance 0.59 Pain Relevance 0.85
Adenosine's effect is also mediated by adenosine A2 receptors (ADORA2), which are present on neutrophils, monocytes, lymphocytes and basophils, generally suppressing the immune function of these cells [32].
Gene_expression (present) of ADORA2 in basophils associated with adenocard
16) Confidence 0.55 Published 2010 Journal Human Genomics and Proteomics : HGP Section Body Doc Link PMC2958653 Disease Relevance 0.26 Pain Relevance 0.47
It is well documented that microvascular endothelial cells, major players conducting the movement of leukocytes between tissue compartments, express adenosine A2A and A2B receptors [31,32].
Gene_expression (express) of A2A in endothelial cells associated with adenocard
17) Confidence 0.51 Published 2006 Journal Arthritis Res Ther Section Body Doc Link PMC1526598 Disease Relevance 0.60 Pain Relevance 0.75
Indeed, the expression of adenosine A2A receptors in the brain is mostly limited to the striatum [20].
Gene_expression (expression) of A2A in striatum associated with adenocard
18) Confidence 0.46 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2843608 Disease Relevance 0.28 Pain Relevance 0.65
In summary, we report a novel association between ADORA2a polymorphisms and AEs in MTX-treated RA patients.
Gene_expression (polymorphisms) of ADORA2a associated with rheumatoid arthritis and methotrexate
19) Confidence 0.45 Published 2008 Journal Rheumatology (Oxford, England) Section Body Doc Link PMC2468887 Disease Relevance 0.24 Pain Relevance 0.21
Adenosine A2A receptors colocalized with dopamine D2 receptors in the medium-sized spiny GABAergic neurons are highly and selectively expressed in areas receiving a rich dopamine innervation, i.e., the dorsal and ventral striatum and tuberculum olfactorium [27-29].
Gene_expression (expressed) of A2A in ventral associated with dopamine, adenocard and gabaergic
20) Confidence 0.36 Published 2010 Journal J Biomed Sci Section Body Doc Link PMC2843608 Disease Relevance 0 Pain Relevance 0.57

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