INT146053

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Context Info
Confidence 0.61
First Reported 2007
Last Reported 2009
Negated 0
Speculated 1
Reported most in Body
Documents 2
Total Number 20
Disease Relevance 12.11
Pain Relevance 13.38

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 (Gpr65) plasma membrane (Gpr65) signal transducer activity (Gpr65)
Anatomy Link Frequency
neurons 6
IB4 2
Gpr65 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 951 99.80 Very High Very High Very High
qutenza 836 99.28 Very High Very High Very High
IPN 532 99.04 Very High Very High Very High
Kinase C 171 98.32 Very High Very High Very High
nociceptor 136 98.16 Very High Very High Very High
Thermal hyperalgesia 76 97.68 Very High Very High Very High
Hyperalgesia 437 96.40 Very High Very High Very High
Pain 271 92.64 High High
vanilloid receptor subtype 1 20 89.88 High High
withdrawal 190 89.80 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 970 99.80 Very High Very High Very High
Inflammatory Pain 532 99.04 Very High Very High Very High
Hyperalgesia 513 97.68 Very High Very High Very High
Pain 309 92.64 High High
Acidosis 40 92.16 High High
Pressure And Volume Under Development 399 84.16 Quite High
Ganglion Cysts 5 81.76 Quite High
Cv Unclassified Under Development 1 80.52 Quite High
Erythema 19 80.48 Quite High
Nociception 173 79.84 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Given that we found only an 11% increase in TDAG8-expressing neurons after inflammation and that DRG neurons are heterogeneous, our finding of no large increase in cAMP levels in DRG cultures after CFA injection is not surprising.
Positive_regulation (increase) of TDAG8 in neurons associated with inflammation
1) Confidence 0.61 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.63 Pain Relevance 0.73
TDAG8-expressing neurons were increased in number in small- and large-diameter neuron populations.
Positive_regulation (increased) of TDAG8 in neuron
2) Confidence 0.61 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.07 Pain Relevance 0.06
Accordingly, TDAG8-expressing neurons were increased in number in both IB4-positive and -negative populations after CFA injection.


Positive_regulation (increased) of TDAG8 in IB4
3) Confidence 0.61 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.16 Pain Relevance 0.16
TDAG8 activation sensitizes TRPV1 response to capsaicin
Positive_regulation (activation) of TDAG8 associated with qutenza
4) Confidence 0.61 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.13 Pain Relevance 0.56
Given that the number of neurons expressing both TDAG8 and TRPV1 genes was increased as well and that TDAG8 activation sensitized TRPV1 responses to capsaicin, TDAG8 is likely involved in long-term chronic inflammatory pain by sensitizing TRPV1 function.
Positive_regulation (activation) of TDAG8 in neurons associated with qutenza and ipn
5) Confidence 0.61 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.94 Pain Relevance 0.89
We further tested whether TDAG8 activation sensitizes the TRPV1 response to capsaicin.
Spec (whether) Positive_regulation (activation) of TDAG8 associated with qutenza
6) Confidence 0.61 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.07 Pain Relevance 0.54
The enhanced response of TRPV1 to capsaicin was possibly due to proton-induced TDAG8 activation.
Positive_regulation (activation) of TDAG8 associated with qutenza
7) Confidence 0.61 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.25 Pain Relevance 0.79
TDAG8 activation increases levels of intracellular cAMP
Positive_regulation (activation) of TDAG8
8) Confidence 0.61 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.21 Pain Relevance 0.15
TDAG8 activation elevates cAMP levels, activating PKA and PKC?.
Positive_regulation (activation) of TDAG8 associated with kinase c
9) Confidence 0.61 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.73 Pain Relevance 0.96
DRG neurons expressing TDAG8 increase in number with CFA-induced inflammation
Positive_regulation (increase) of TDAG8 in neurons associated with inflammation
10) Confidence 0.53 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.44 Pain Relevance 0.51
Proton-sensing GPCRs, including OGR1, GPR4, G2A, and TDAG8, are fully activated at pH 6.4-6.8 in vitro.
Positive_regulation (activated) of TDAG8
11) Confidence 0.52 Published 2007 Journal Mol. Cell. Neurosci. Section Abstract Doc Link 17720533 Disease Relevance 1.26 Pain Relevance 0.98
Whether increased TDAG8 expression enhances TDAG8 function after inflammation has remained unclear.
Positive_regulation (enhances) of TDAG8 associated with inflammation
12) Confidence 0.44 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.23 Pain Relevance 0.15
The total number of A-fiber neurons that expressed both TDAG8 and TRPV1 was largely increased after CFA injection.
Positive_regulation (increased) of TDAG8 in neurons
13) Confidence 0.44 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.69 Pain Relevance 0.48
As demonstrated here, TDAG8 activation can lead to TRPV1 sensitization, and TDAG8 expression increased after CFA-induced inflammation.
Positive_regulation (activation) of TDAG8 associated with inflammation
14) Confidence 0.41 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.69 Pain Relevance 0.71
In small-diameter neurons, TDAG8-expressing neurons were increased in number in both IB4-positive and -negative nociceptors.
Positive_regulation (increased) of TDAG8 in IB4 associated with nociceptor
15) Confidence 0.41 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.60 Pain Relevance 0.83
Given that TDAG8 and TRPV1 expression increased after CFA-induced inflammation and that TDAG8 activation can lead to TRPV1 sensitization, it suggests that high concentrations of protons after inflammation may not only directly activate proton-sensing ion channels (such as TRPV1) to cause pain but also act on proton-sensing GPCRs to regulate the development of hyperalgesia.



Positive_regulation (activation) of TDAG8 associated with pain, hyperalgesia and inflammation
16) Confidence 0.41 Published 2009 Journal Mol Pain Section Abstract Doc Link PMC2716309 Disease Relevance 0.92 Pain Relevance 0.85
Accordingly, peripheral inflammation induces a local increase of protons, leading to TDAG8 activation.
Positive_regulation (activation) of TDAG8 associated with inflammation
17) Confidence 0.41 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.73 Pain Relevance 0.97
Further studies revealed that TDAG8 activation sensitized the TRPV1 response to capsaicin, suggesting that TDAG8 could be involved in CFA-induced chronic inflammatory pain through regulation of TRPV1 function.


Positive_regulation (activation) of TDAG8 associated with qutenza and ipn
18) Confidence 0.41 Published 2009 Journal Mol Pain Section Abstract Doc Link PMC2716309 Disease Relevance 1.11 Pain Relevance 0.92
Further studies demonstrated that the number of DRG neurons expressing both TDAG8 and TRPV1 genes was increased as well, and TDAG8 activation sensitized TRPV1 response to capsaicin.
Positive_regulation (activation) of TDAG8 in neurons associated with qutenza
19) Confidence 0.41 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 1.24 Pain Relevance 1.19
GPR4, G2A, and TDAG8 transcripts were increased in levels 24 hours after carrageenan injection, but only TDAG8 expression was increased after CFA injection.
Positive_regulation (increased) of TDAG8
20) Confidence 0.27 Published 2009 Journal Mol Pain Section Body Doc Link PMC2716309 Disease Relevance 0.99 Pain Relevance 0.96

General Comments

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