INT153913

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.70
First Reported 2002
Last Reported 2010
Negated 3
Speculated 1
Reported most in Body
Documents 31
Total Number 52
Disease Relevance 33.50
Pain Relevance 16.14

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 5
spinal cord 2
platelets 2
plasma 1
mammary gland 1
Lpar1 (Mus musculus)
Pain Link Frequency Relevance Heat
Spinal cord 551 100.00 Very High Very High Very High
antagonist 353 100.00 Very High Very High Very High
Pain 322 100.00 Very High Very High Very High
Demyelination 285 99.90 Very High Very High Very High
fibrosis 191 99.88 Very High Very High Very High
Thermal hyperalgesia 49 99.40 Very High Very High Very High
c fibre 161 99.34 Very High Very High Very High
alcohol 43 98.92 Very High Very High Very High
allodynia 196 98.90 Very High Very High Very High
Neuropathic pain 580 98.88 Very High Very High Very High
Disease Link Frequency Relevance Heat
Pain 343 100.00 Very High Very High Very High
Mycobacterial Infection 63 99.92 Very High Very High Very High
Demyelinating Disease 353 99.90 Very High Very High Very High
Breast Cancer 247 99.88 Very High Very High Very High
Pulmonary Fibrosis 63 99.88 Very High Very High Very High
Pressure And Volume Under Development 42 99.76 Very High Very High Very High
Cancer 788 99.68 Very High Very High Very High
Systemic Sclerosis 42 99.68 Very High Very High Very High
Ovarian Cancer 396 99.60 Very High Very High Very High
Nervous System Injury 273 99.56 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The major conclusion of the present study is that LPA1 receptor activation is also involved in this loss of function through type-1C fibers in mice with nerve injury, which causes neuropathic pain and underlying alterations of gene expressions and demyelination.
Positive_regulation (activation) of LPA1 in nerve associated with demyelination, nervous system injury and neuropathic pain
1) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1562366 Disease Relevance 1.20 Pain Relevance 1.42
In the present study, we sought to determine, whether activation of LPA1 receptor and the downstream RhoA pathway are required for abrogation of polymodal C-fiber signaling following nerve injury.
Spec (whether) Positive_regulation (activation) of LPA1 in nerve associated with c fibre and nervous system injury
2) Confidence 0.70 Published 2006 Journal Mol Pain Section Body Doc Link PMC1562366 Disease Relevance 1.36 Pain Relevance 0.98
In contrast, no significant increase in LPA levels was observed in the preparations of DRG, SPN or SCN, as shown in Fig. 1d.
Neg (no) Positive_regulation (increase) of LPA associated with ganglion cysts, urological neuroanatomy and sciatic nerve
3) Confidence 0.60 Published 2009 Journal Mol Pain Section Body Doc Link PMC2780384 Disease Relevance 0.20 Pain Relevance 0.35
An increase in LPC-induced LPA was observed with a similar time-course in dorsal root (DR) preparations.
Positive_regulation (increase) of LPA in dorsal root
4) Confidence 0.60 Published 2009 Journal Mol Pain Section Body Doc Link PMC2780384 Disease Relevance 0 Pain Relevance 0.29
A second important issue is the time-dependent increase in LPA levels caused by injections of LPA as well as LPC.
Positive_regulation (increase) of LPA
5) Confidence 0.60 Published 2009 Journal Mol Pain Section Body Doc Link PMC2780384 Disease Relevance 0.18 Pain Relevance 0.14
In conclusion, in addition to the predominant role of autotaxin/LPA track in the carcinogenesis of breast cancers our results demonstrated that activation of autotaxin/LPA axis in breast cancer cells controlled the progression of osteolytic bone metastases by stimulating directly both cancer cells and osteoclasts.
Positive_regulation (activation) of LPA in osteoclasts associated with cancer, breast cancer and metastasis
6) Confidence 0.57 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2840030 Disease Relevance 1.86 Pain Relevance 0
A recent study showed that transgenic overexpression of autotaxin or LPA1-3 receptors in the mouse mammary gland is sufficient to initiate breast cancers in mice, demonstrating that activation of the autotaxin/LPA track induces carcinogenesis [25].
Positive_regulation (activation) of LPA in mammary gland associated with targeted disruption and breast cancer
7) Confidence 0.57 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2840030 Disease Relevance 1.27 Pain Relevance 0
Although the nerve-injury alone also failed to induce pERK signals in Lpar1-/- mice, the A?
Neg (failed) Positive_regulation (induce) of Lpar1 in nerve associated with injury
8) Confidence 0.50 Published 2008 Journal Mol Pain Section Body Doc Link PMC2599895 Disease Relevance 0.30 Pain Relevance 0.20
A similarly high level of LPA was also observed at 5 h post-treatment.
Positive_regulation (level) of LPA
9) Confidence 0.50 Published 2009 Journal Mol Pain Section Body Doc Link PMC2780384 Disease Relevance 0.18 Pain Relevance 0.35
Inhibition of the RhoA downstream pathway of LPA1 receptor activation has shown that this pathway is essential for both nerve injury- and LPA-induced neuropathic pain.
Positive_regulation (activation) of LPA1 in nerve associated with nervous system injury and neuropathic pain
10) Confidence 0.47 Published 2006 Journal Mol Pain Section Body Doc Link PMC1562366 Disease Relevance 1.37 Pain Relevance 0.99
All these results suggest that the loss of pain transmission through polymodal C-fiber neurons is also mediated by the LPA1 activation following nerve injury.



Positive_regulation (activation) of LPA1 in neurons associated with c fibre, pain and nervous system injury
11) Confidence 0.47 Published 2006 Journal Mol Pain Section Abstract Doc Link PMC1562366 Disease Relevance 0.80 Pain Relevance 1.10
Autotaxin, a synthetic enzyme of lysophosphatidic acid (LPA), mediates the induction of nerve-injured neuropathic pain

Recently, we reported that lysophosphatidic acid (LPA) induces long-lasting mechanical allodynia and thermal hyperalgesia as well as demyelination and upregulation of pain-related proteins through one of its cognate receptors, LPA1.

Positive_regulation (upregulation) of LPA1 in nerve associated with pain, demyelination, allodynia, thermal hyperalgesia and neuropathic pain
12) Confidence 0.47 Published 2008 Journal Mol Pain Section Title Doc Link PMC2277392 Disease Relevance 1.65 Pain Relevance 1.04
These findings suggest that LPA1 receptor activation initiates the machineries of neuropathic pain.
Positive_regulation (activation) of LPA1 receptor associated with neuropathic pain
13) Confidence 0.47 Published 2008 Journal Mol Pain Section Body Doc Link PMC2277392 Disease Relevance 1.22 Pain Relevance 0.68
These investigators showed that patients with idiopathic pulmonary fibrosis, had increased LPA levels in bronchoalveolar lavage fluid and that inhibition of LPA1 reduced fibroblast responses to the chemotactic activity of the lavage fluid.
Positive_regulation (increased) of LPA in fibroblast associated with fibrosis and pulmonary fibrosis
14) Confidence 0.45 Published 2010 Journal British Journal of Pharmacology Section Body Doc Link PMC2989581 Disease Relevance 0.88 Pain Relevance 0.28
This similarity prompted us to confirm that farnesyl mono- and diphosphate activate various LPA GPCR targets (Liliom et al., 2006).
Positive_regulation (activate) of LPA
15) Confidence 0.45 Published 2010 Journal British Journal of Pharmacology Section Body Doc Link PMC2989581 Disease Relevance 0.15 Pain Relevance 0.28
Whereas LPA GPCR are activated by both saturated and unsaturated fatty acid-substituted LPAs, PPAR?
Positive_regulation (activated) of LPA
16) Confidence 0.45 Published 2010 Journal British Journal of Pharmacology Section Body Doc Link PMC2989581 Disease Relevance 0.54 Pain Relevance 0.16
In search of the minimal pharmacophore that activates LPA GPCR, we identified fatty alcohol phosphates that, depending on the length of the hydrocarbon chain and the headgroup (phosphate or thiophosphate), function as either antagonists or agonists (Durgam et al., 2005; Deng et al., 2007; Zhang et al., 2009a).
Positive_regulation (activates) of LPA associated with antagonist, agonist and alcohol
17) Confidence 0.45 Published 2010 Journal British Journal of Pharmacology Section Body Doc Link PMC2989581 Disease Relevance 0.18 Pain Relevance 0.26
We obtained evidence that LPA1 receptor activation mediates down-regulation of myelin proteins, such as peripheral myelin protein PMP22, myelin basic protein MBP, and myelin protein zero MP0, in in vivo injury models and ex vivo culture models [73,74].
Positive_regulation (activation) of LPA1 receptor associated with injury
18) Confidence 0.45 Published 2008 Journal Mol Pain Section Body Doc Link PMC2365930 Disease Relevance 1.33 Pain Relevance 0.68
LPA-induced ex vivo demyelination in whole regions of sensory fibers
Positive_regulation (induced) of LPA associated with demyelination
19) Confidence 0.44 Published 2010 Journal Mol Pain Section Body Doc Link PMC2989310 Disease Relevance 0.81 Pain Relevance 0.36
In the presence of rATX (30 ng/mL), the addition of LPA at 0.1 pmol increased the LPA level in a time-dependent manner from 30 to 60 min, followed by a slight decline (Fig. 4b).
Positive_regulation (increased) of LPA
20) Confidence 0.44 Published 2009 Journal Mol Pain Section Body Doc Link PMC2780384 Disease Relevance 0.11 Pain Relevance 0.26

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox