INT115071

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Context Info
Confidence 0.70
First Reported 2003
Last Reported 2010
Negated 2
Speculated 1
Reported most in Body
Documents 14
Total Number 27
Disease Relevance 16.56
Pain Relevance 14.24

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

transport (Accn3) plasma membrane (Accn3) cytoplasm (Accn3)
Anatomy Link Frequency
muscle 2
neurons 2
paw 1
Ovary 1
intestine 1
Accn3 (Mus musculus)
Pain Link Frequency Relevance Heat
Pain 230 100.00 Very High Very High Very High
ASIC 248 99.96 Very High Very High Very High
Inflammation 710 99.90 Very High Very High Very High
wide dynamic range 6 99.68 Very High Very High Very High
tissue acidosis 16 99.66 Very High Very High Very High
trigeminal ganglion 75 99.34 Very High Very High Very High
Inflammatory mediators 22 98.92 Very High Very High Very High
Nav1.9 101 98.66 Very High Very High Very High
Hyperalgesia 205 97.48 Very High Very High Very High
central sensitization 4 96.80 Very High Very High Very High
Disease Link Frequency Relevance Heat
Pain 218 100.00 Very High Very High Very High
INFLAMMATION 747 99.90 Very High Very High Very High
Acidosis 215 99.66 Very High Very High Very High
Targeted Disruption 57 99.64 Very High Very High Very High
Ganglion Cysts 113 99.34 Very High Very High Very High
Aids-related Complex 112 97.60 Very High Very High Very High
Hyperalgesia 261 97.48 Very High Very High Very High
Inflammatory Pain 102 95.60 Very High Very High Very High
Nociception 36 94.24 High High
Cancer 28 92.20 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Thus, activation of ASIC3s on muscle afferents is required for development of mechanical hyperalgesia and central sensitization that normally occurs in response to repeated intramuscular acid.
Positive_regulation (activation) of ASIC3s in muscle associated with hyperalgesia and central sensitization
1) Confidence 0.70 Published 2003 Journal Pain Section Abstract Doc Link 14659506 Disease Relevance 0.51 Pain Relevance 0.96
It is, however, possible that AGM-induced ASIC3 channel activation was through the chelation of extracellular Ca2+ as observed with lactate [39,56] at neutral pH.
Spec (possible) Positive_regulation (activation) of ASIC3
2) Confidence 0.68 Published 2010 Journal Mol Pain Section Body Doc Link PMC3017031 Disease Relevance 0.18 Pain Relevance 0.09
Similar mRNA increases were observed after inflammation in knockout mice: ASIC2 mRNA increases in ASIC3-/- mice; ASIC2 and ASIC3 mRNAs increase in ASIC1-/- mice.
Positive_regulation (increase) of ASIC3 associated with targeted disruption and inflammation
3) Confidence 0.67 Published 2010 Journal J Pain Section Abstract Doc Link 20015700 Disease Relevance 1.46 Pain Relevance 0.84
Muscle inflammation causes bilateral increases of ASIC2 and ASIC3 but not ASIC1 (neither ASIC1a nor ASIC1b) mRNA, suggesting differential regulation of ASIC1 versus ASIC2 and ASIC3 mRNA.
Neg (not) Positive_regulation (increases) of ASIC3 in Muscle associated with inflammation
4) Confidence 0.67 Published 2010 Journal J Pain Section Abstract Doc Link 20015700 Disease Relevance 1.19 Pain Relevance 0.58
These changes in WDR neurons do not occur in ASIC3 knockouts.
Neg (not) Positive_regulation (occur) of ASIC3 in neurons associated with wide dynamic range
5) Confidence 0.50 Published 2003 Journal Pain Section Abstract Doc Link 14659506 Disease Relevance 0.51 Pain Relevance 0.99
That AGM activates ASIC3 channels independent of Ca2+ chelation is consistent with the notion that AGM modulates ASIC3 activation via novel mechanisms (Figure 2D, E).


Positive_regulation (activation) of ASIC3
6) Confidence 0.49 Published 2010 Journal Mol Pain Section Body Doc Link PMC3017031 Disease Relevance 0.15 Pain Relevance 0.07
While its critical role for GMQ was supported by the fact that covalently linking circular GMQ or TNB to C79 activated ASIC3E79C channels (with the GMQ-dimer or DTNB treatment) [10], the role of the same site for the linear AGM was not established.
Positive_regulation (activated) of ASIC3E79C
7) Confidence 0.49 Published 2010 Journal Mol Pain Section Body Doc Link PMC3017031 Disease Relevance 0.06 Pain Relevance 0
In addition, the emergence of new ASIC isoforms [60] adds an additional possibility underlying the ASIC3-dependent pain-behavior induced by AGM in vivo [10].


Positive_regulation (induced) of ASIC3 associated with pain and asic
8) Confidence 0.49 Published 2010 Journal Mol Pain Section Body Doc Link PMC3017031 Disease Relevance 0.48 Pain Relevance 0.39
At a concentration of 1 mM, only AGM and its analog ARC (Figure 1B), but not polyamines (including spermine, spermidine, and putrescine), nor L-arginine, nor L-ornithine, were able to activate the ASIC3 channel at pH 7.4.
Positive_regulation (activate) of ASIC3 associated with aids-related complex
9) Confidence 0.49 Published 2010 Journal Mol Pain Section Body Doc Link PMC3017031 Disease Relevance 0.74 Pain Relevance 0.26
Conventional whole-cell patch clamp recordings were performed in Chinese Hamster Ovary (CHO) cell lines transiently expressing ASIC3 tagged with GFP to measure the functional activation of ASIC3 channels under voltage clamp conditions.
Positive_regulation (activation) of ASIC3 in Ovary
10) Confidence 0.49 Published 2010 Journal Mol Pain Section Body Doc Link PMC3017031 Disease Relevance 0.94 Pain Relevance 0.34
In this study, we further showed that AGM-induced activation of ASIC3 is profoundly potentiated by mild acidosis, hyperosmolarity, increased arachidonic acid (AA), or reduced extracellular Ca2+, conditions that occur during inflammation and many other pathophysiological processes [8,33-39].
Positive_regulation (activation) of ASIC3 associated with acidosis and inflammation
11) Confidence 0.49 Published 2010 Journal Mol Pain Section Body Doc Link PMC3017031 Disease Relevance 0.98 Pain Relevance 0.42
Similar mRNA increases were observed after inflammation in knockout mice: ASIC2 mRNA increases in ASIC3-/- mice; ASIC2 and ASIC3 mRNAs increase in ASIC1-/- mice.
Positive_regulation (increases) of ASIC3 associated with targeted disruption and inflammation
12) Confidence 0.48 Published 2010 Journal J Pain Section Abstract Doc Link 20015700 Disease Relevance 1.44 Pain Relevance 0.83
In particular ASIC3, the least abundant in the general population, is the most abundant ASIC transcript in colonic neurons.
Positive_regulation (abundant) of ASIC3 in neurons associated with asic
13) Confidence 0.48 Published 2007 Journal J. Comp. Neurol. Section Abstract Doc Link 17177258 Disease Relevance 0 Pain Relevance 0.28
The similar phenotypes in the pain behavior for Nav1.9-/- and ASIC3-/- mice under inflammation and the ASIC3-dependent up-regulation of Nav1.9 suggest that inflammation induces tissue acidosis, which leads to activation of ASIC3 and subsequent ASIC3-dependent up-regulation of Nav1.9; the increased Nav1.9 level in turn contributes to thermal hyperalgesia.
Positive_regulation (activation) of ASIC3 associated with pain, acidosis, inflammation, thermal hyperalgesia, tissue acidosis and nav1.9
14) Confidence 0.47 Published 2009 Journal Mol Pain Section Body Doc Link PMC2632618 Disease Relevance 1.35 Pain Relevance 2.12
In contrast to up-regulation of Nav1.9 transcripts, increase of INav1.8 on day 2 with intraplantar carrageenan-induced inflammation was significant and ASIC3 dependent on electrophysiology (Fig. 11).
Positive_regulation (dependent) of ASIC3 associated with inflammation and nav1.9
15) Confidence 0.47 Published 2009 Journal Mol Pain Section Body Doc Link PMC2632618 Disease Relevance 1.11 Pain Relevance 1.78
Many studies have reported increased expression of acid-sensing ion channel 3 (ASIC3) in inflammation and enhanced ASIC3 channel activity with pro-inflammatory mediators.
Positive_regulation (enhanced) of ASIC3 associated with inflammatory mediators and inflammation
16) Confidence 0.47 Published 2009 Journal Mol Pain Section Abstract Doc Link PMC2632618 Disease Relevance 0.97 Pain Relevance 0.62
Up-regulation of ASIC3 is seen in inflamed human intestine [8] and dorsal root ganglia (DRG) of rodents with inflamed hind paws [9,10].
Positive_regulation (regulation) of ASIC3 in intestine
17) Confidence 0.47 Published 2009 Journal Mol Pain Section Body Doc Link PMC2632618 Disease Relevance 1.48 Pain Relevance 0.77
Concentration-response relationships for pH-dependent activation of ASIC3 channels were obtained by measuring currents in response to acidic solutions with graded pH values.
Positive_regulation (activation) of ASIC3
18) Confidence 0.46 Published 2010 Journal Mol Pain Section Body Doc Link PMC3017031 Disease Relevance 0.21 Pain Relevance 0.12
AGM-induced ASIC3 channel activation was not through the chelation of extracellular Ca2+ as occurs with increased lactate, but rather through a direct interaction with the newly identified nonproton ligand sensing domain.
Positive_regulation (activation) of ASIC3
19) Confidence 0.46 Published 2010 Journal Mol Pain Section Abstract Doc Link PMC3017031 Disease Relevance 0.48 Pain Relevance 0.25
In addition to protons, a synthetic compound, 2-guanidine-4-methylquinazoline (GMQ) has been found to activate ASIC3 channels at physiologically normal pH in a sustained manner [10].
Positive_regulation (activate) of ASIC3
20) Confidence 0.46 Published 2010 Journal Mol Pain Section Body Doc Link PMC3017031 Disease Relevance 0.15 Pain Relevance 0.39

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