INT86521

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Context Info
Confidence 0.78
First Reported 2000
Last Reported 2010
Negated 8
Speculated 0
Reported most in Body
Documents 167
Total Number 214
Disease Relevance 154.61
Pain Relevance 80.35

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 (Lpar1) plasma membrane (Lpar1) cytoplasm (Lpar1)
signal transducer activity (Lpar1)
Anatomy Link Frequency
nerve 27
dorsal root 11
platelets 7
spinal cord 7
dorsal horn 5
Lpar1 (Mus musculus)
Pain Link Frequency Relevance Heat
Spinal cord 2861 100.00 Very High Very High Very High
Sciatic nerve 1708 100.00 Very High Very High Very High
Pain 1329 100.00 Very High Very High Very High
agonist 744 100.00 Very High Very High Very High
fibrosis 453 100.00 Very High Very High Very High
Demyelination 2489 99.96 Very High Very High Very High
Neuropathic pain 2759 99.90 Very High Very High Very High
chemokine 96 99.84 Very High Very High Very High
Hyperalgesia 368 99.72 Very High Very High Very High
dorsal root ganglion 724 99.68 Very High Very High Very High
Disease Link Frequency Relevance Heat
Neuropathic Pain 3950 100.00 Very High Very High Very High
Cancer 2300 100.00 Very High Very High Very High
Nervous System Injury 1728 100.00 Very High Very High Very High
Pain 1436 100.00 Very High Very High Very High
Metastasis 1394 100.00 Very High Very High Very High
Infection 350 100.00 Very High Very High Very High
Pulmonary Fibrosis 152 100.00 Very High Very High Very High
Malignant Neoplastic Disease 96 100.00 Very High Very High Very High
Targeted Disruption 887 99.98 Very High Very High Very High
Demyelinating Disease 2796 99.96 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Experiments to evaluate LPA and LPC production following nerve injury and clarify the relationship of ATX to LPA production are the next important issues to be addressed.
Gene_expression (production) of LPA in nerve associated with nervous system injury
1) Confidence 0.78 Published 2008 Journal Mol Pain Section Body Doc Link PMC2277392 Disease Relevance 1.33 Pain Relevance 0.88
It is well known that LPA is mainly produced via two major pathways, namely LPC conversion mediated by activation of ATX and phosphatidic acid conversion mediated by activation of phospholipase A2 (PLA2) [6,7].
Gene_expression (produced) of LPA
2) Confidence 0.78 Published 2008 Journal Mol Pain Section Body Doc Link PMC2277392 Disease Relevance 0.98 Pain Relevance 0.58
Using RT-PCR analysis, however, we found that the LPA1 receptor is ubiquitously expressed in the dorsal root, spinal nerve, sciatic nerve and DRG (Figure 6a).
Gene_expression (expressed) of LPA1 receptor in dorsal root associated with dorsal root ganglion and sciatic nerve
3) Confidence 0.78 Published 2010 Journal Mol Pain Section Body Doc Link PMC2989310 Disease Relevance 1.29 Pain Relevance 0.62
The expression levels of LPA receptors in SC and DR were evaluated by reverse transcription polymerase chain reaction (RT-PCR), according to described method [31].
Gene_expression (expression) of LPA associated with spinal cord
4) Confidence 0.77 Published 2009 Journal Mol Pain Section Body Doc Link PMC2780384 Disease Relevance 0.21 Pain Relevance 0.25
B103 cells expressing LPA1 receptors and enhanced green fluorescence protein [B103 (+) cells] were used for the quantitative measurement of LPA, according to a method [22] modified from the earlier report [28].
Gene_expression (expressing) of LPA1
5) Confidence 0.77 Published 2009 Journal Mol Pain Section Body Doc Link PMC2780384 Disease Relevance 0.32 Pain Relevance 0.22
Therefore, the total synthesis of LPA is likely to have been at least 1.66 nmol (936 pmol + 724 pmol), which is higher than the original level of LPC at 1 nmol.
Gene_expression (synthesis) of LPA
6) Confidence 0.77 Published 2009 Journal Mol Pain Section Body Doc Link PMC2780384 Disease Relevance 0.15 Pain Relevance 0.33
Unlike sphingosine 1-phosphate, a structurally similar bio-active lysophospholipid to LPA and produced intracellularly, LPA is produced by multiple extracellular degradative routes.
Gene_expression (produced) of LPA
7) Confidence 0.76 Published 2010 Journal Biochimie Section Abstract Doc Link 20417246 Disease Relevance 0.36 Pain Relevance 0.14
LPA receptors and LPA receptor gene expression activates Rho in peripheral nerves [69-71], which suggests that LPA receptors might pathophysiologically activate Rho in neuropathic pain states of peripheral nerve injury.
Gene_expression (expression) of LPA receptor gene in peripheral nerve associated with nervous system injury, neuropathic pain and peripheral nerve injury
8) Confidence 0.76 Published 2008 Journal Mol Pain Section Body Doc Link PMC2365930 Disease Relevance 1.22 Pain Relevance 0.93
In summary, we have demonstrated that LPA biosynthesis by ATX is the source of LPA for LPA1 receptor-mediated neuropathic pain.
Gene_expression (source) of LPA associated with neuropathic pain
9) Confidence 0.68 Published 2008 Journal Mol Pain Section Body Doc Link PMC2277392 Disease Relevance 1.15 Pain Relevance 0.72
However, all the findings in the present report suggest that nerve injury-induced LPA production mainly occurs through LPC conversion mediated by activation of ATX.
Gene_expression (production) of LPA in nerve associated with nervous system injury
10) Confidence 0.68 Published 2008 Journal Mol Pain Section Body Doc Link PMC2277392 Disease Relevance 0.98 Pain Relevance 0.63
These findings suggest that the marked reduction of neuropathic pain in atx+/- mice can be attributed to a reduction in LPA production following nerve injury.
Gene_expression (production) of LPA in nerve associated with nervous system injury and neuropathic pain
11) Confidence 0.68 Published 2008 Journal Mol Pain Section Body Doc Link PMC2277392 Disease Relevance 1.17 Pain Relevance 0.73
In summary, we have demonstrated that LPA biosynthesis by ATX is the source of LPA for LPA1 receptor-mediated neuropathic pain.
Gene_expression (biosynthesis) of LPA associated with neuropathic pain
12) Confidence 0.68 Published 2008 Journal Mol Pain Section Body Doc Link PMC2277392 Disease Relevance 1.15 Pain Relevance 0.73
Therefore, nerve injury seems to cause LPA production in the spinal cord.
Gene_expression (production) of LPA in spinal cord associated with nervous system injury and spinal cord
13) Confidence 0.68 Published 2008 Journal Mol Pain Section Body Doc Link PMC2277392 Disease Relevance 1.28 Pain Relevance 0.82
Experiments to evaluate LPA and LPC production following nerve injury and clarify the relationship of ATX to LPA production are the next important issues to be addressed.
Gene_expression (production) of LPA in nerve associated with nervous system injury
14) Confidence 0.68 Published 2008 Journal Mol Pain Section Body Doc Link PMC2277392 Disease Relevance 1.40 Pain Relevance 0.96
Therefore, targeted inhibition of ATX-mediated LPA biosynthesis as well as LPA1 receptor and its downstream pathways may represent a novel way to prevent nerve injury-induced neuropathic pain.



Gene_expression (biosynthesis) of LPA in nerve associated with nervous system injury and neuropathic pain
15) Confidence 0.68 Published 2008 Journal Mol Pain Section Body Doc Link PMC2277392 Disease Relevance 1.02 Pain Relevance 0.65
Therefore, the dorsal root-specific LPA1-mediated demyelination would be explained by the speculation that LPA is produced in spinal cord and transferred to the dorsal root, where demyelination occurs.
Gene_expression (produced) of LPA in dorsal root associated with demyelination and spinal cord
16) Confidence 0.68 Published 2010 Journal Mol Pain Section Body Doc Link PMC2989310 Disease Relevance 1.06 Pain Relevance 0.78
Regarding the proposal that LPA involved in the dorsal root demyelination comes from the spinal dorsal horn, we have reported that the intense stimulation of spinal dorsal horn in vitro causes de novo production of LPA [29].
Gene_expression (production) of LPA in dorsal horn associated with demyelination and spinal dorsal horn
17) Confidence 0.68 Published 2010 Journal Mol Pain Section Body Doc Link PMC2989310 Disease Relevance 1.15 Pain Relevance 0.90
In the toluidine blue analysis, the injury-induced demyelination level in atx+/- mice was reduced to approximately half in WT mice (Figure 7), being consistent with the change of LPA production and neuropathic pain in atx+/- mice [10,11].
Gene_expression (production) of LPA associated with demyelination, injury and neuropathic pain
18) Confidence 0.68 Published 2010 Journal Mol Pain Section Body Doc Link PMC2989310 Disease Relevance 1.34 Pain Relevance 0.73
However, this activation is unlikely related to the action of LPA, since no significant LPA production in the sciatic nerve was observed by nerve injury [10].
Neg (no) Gene_expression (production) of LPA in nerve associated with nervous system injury and sciatic nerve
19) Confidence 0.68 Published 2010 Journal Mol Pain Section Body Doc Link PMC2989310 Disease Relevance 1.10 Pain Relevance 0.92
Western blot analysis also showed similar expression patterns of the LPA1 receptor (Figure 6b).


Gene_expression (expression) of LPA1 receptor
20) Confidence 0.68 Published 2010 Journal Mol Pain Section Body Doc Link PMC2989310 Disease Relevance 1.29 Pain Relevance 0.62

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