INT111385

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Context Info
Confidence 0.43
First Reported 2003
Last Reported 2007
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 12
Disease Relevance 3.91
Pain Relevance 2.80

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 (Adora3) plasma membrane (Adora3) signal transducer activity (Adora3)
Anatomy Link Frequency
respiratory 2
hindbrain 1
Adora3 (Mus musculus)
Pain Link Frequency Relevance Heat
adenocard 364 100.00 Very High Very High Very High
agonist 620 99.72 Very High Very High Very High
Pain 8 99.28 Very High Very High Very High
antagonist 104 97.56 Very High Very High Very High
antidepressant 4 93.76 High High
analgesia 2 90.92 High High
depression 2 89.20 High High
Opioid 4 88.80 High High
tail-flick 4 79.92 Quite High
Pyramidal cell 6 75.32 Quite High
Disease Link Frequency Relevance Heat
Hypoxia 40 99.32 Very High Very High Very High
Pain 2 97.40 Very High Very High Very High
Apnoea 68 95.80 Very High Very High Very High
Cancer 66 93.28 High High
Targeted Disruption 28 91.88 High High
Cognitive Disorder 8 89.40 High High
Depression 2 89.20 High High
Anxiety Disorder 12 88.60 High High
Wound Healing 6 86.32 High High
Death 10 80.36 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Behavioral characterization of mice lacking the A3 adenosine receptor: sensitivity to hypoxic neurodegeneration.
Negative_regulation (lacking) of A3 adenosine receptor associated with pain, adenocard and hypoxia
1) Confidence 0.43 Published 2003 Journal Cell. Mol. Neurobiol. Section Title Doc Link 12825837 Disease Relevance 0.67 Pain Relevance 0.69
These results indicate that pharmacologic or genetic suppression of A3AR function enhances some aspects of motor function and suppresses pain processing at supraspinal levels, while acting as a depressant in tests predictive of antidepressant action.
Negative_regulation (suppression) of A3AR associated with pain and antidepressant
2) Confidence 0.43 Published 2003 Journal Cell. Mol. Neurobiol. Section Abstract Doc Link 12825837 Disease Relevance 0.65 Pain Relevance 0.43
The fast desensitization of the A3R after agonist exposure may be therapeutically equivalent to antagonist occupancy of the receptor.



Negative_regulation (desensitization) of A3R associated with antagonist and agonist
3) Confidence 0.14 Published 2007 Journal Purinergic Signal Section Body Doc Link PMC2245999 Disease Relevance 0.17 Pain Relevance 0.30
The fast desensitization of the A3R after agonist exposure may be therapeutically equivalent to antagonist occupancy of the receptor.
Negative_regulation (desensitization) of A3R associated with antagonist and agonist
4) Confidence 0.14 Published 2007 Journal Purinergic Signal Section Abstract Doc Link PMC2245999 Disease Relevance 0.06 Pain Relevance 0.32
To circumvent the species differences mentioned in the introduction to the A3R section, Yamano et al. generated A3R humanized (A3ARh/h) mice in which the A3R was replaced by its human counterpart.
Negative_regulation (replaced) of A3R
5) Confidence 0.10 Published 2007 Journal Purinergic Signal Section Body Doc Link PMC2245999 Disease Relevance 0.78 Pain Relevance 0.20
Long-term agonist exposure (1–24 h) resulted in a marked downregulation of A3R to 22?
Negative_regulation (downregulation) of A3R associated with agonist
6) Confidence 0.10 Published 2007 Journal Purinergic Signal Section Body Doc Link PMC2245999 Disease Relevance 0.22 Pain Relevance 0.30
The A3R is subject to even faster downregulation, often a matter of minutes.
Negative_regulation (downregulation) of A3R
7) Confidence 0.10 Published 2007 Journal Purinergic Signal Section Abstract Doc Link PMC2245999 Disease Relevance 0.07 Pain Relevance 0.32
Palmer and Stiles as well as Ferguson et al. investigated which amino acid residues in the C terminus are responsible and crucial for the rapid desensitization of the A3R [96, 91].
Negative_regulation (desensitization) of A3R
8) Confidence 0.09 Published 2007 Journal Purinergic Signal Section Body Doc Link PMC2245999 Disease Relevance 0.35 Pain Relevance 0.16
The abnormal inspiratory control in Hoxa2 mutants might, therefore, originate from an adaptive respiratory behavior following compensation for the loss of Hoxa2 in r3, while Krox20 is still functional.
Negative_regulation (loss) of r3 in respiratory
9) Confidence 0.01 Published 2007 Journal Neural Develop Section Body Doc Link PMC2098766 Disease Relevance 0.08 Pain Relevance 0
Therefore, partial impairment of Krox20 function, resulting in a severe reduction of r3, is compatible with a normal control of the respiratory rhythm at birth and does not reproduce the Hoxa2 null phenotype characterized by the absence of a transient decrease in tidal volume around birth.
Negative_regulation (reduction) of r3 in respiratory
10) Confidence 0.01 Published 2007 Journal Neural Develop Section Body Doc Link PMC2098766 Disease Relevance 0.31 Pain Relevance 0
Compound heterozygous Krox20Cre/flox mutants express Krox20 only transiently and, in the hindbrain, this results in a severe reduction of r3 (Figure 4).
Negative_regulation (reduction) of r3 in hindbrain
11) Confidence 0.01 Published 2007 Journal Neural Develop Section Body Doc Link PMC2098766 Disease Relevance 0.17 Pain Relevance 0
Our results, therefore, suggest that the transient expression of Krox20 and the subsequent reduction of r3 size observed in hypomorphic Krox20 mutants do not prevent the development of the para-facial anti-apneic system.
Negative_regulation (reduction) of r3
12) Confidence 0.01 Published 2007 Journal Neural Develop Section Body Doc Link PMC2098766 Disease Relevance 0.39 Pain Relevance 0.09

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