INT117497

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Context Info
Confidence 0.57
First Reported 2002
Last Reported 2010
Negated 2
Speculated 3
Reported most in Body
Documents 18
Total Number 29
Disease Relevance 14.45
Pain Relevance 8.13

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 (F2r) plasma membrane (F2r) signal transducer activity (F2r)
Anatomy Link Frequency
bladder 4
macrophages 2
nerve 2
neurons 2
urinary bladder 1
F2r (Mus musculus)
Pain Link Frequency Relevance Heat
Dopamine 4 99.76 Very High Very High Very High
Antinociceptive 41 99.66 Very High Very High Very High
agonist 155 99.62 Very High Very High Very High
Nicotine 4 99.28 Very High Very High Very High
Calcitonin gene-related peptide 200 99.26 Very High Very High Very High
Hyperalgesia 35 99.08 Very High Very High Very High
substance P 151 99.00 Very High Very High Very High
Inflammation 693 98.64 Very High Very High Very High
Visceral pain 5 98.56 Very High Very High Very High
nociceptor 160 98.32 Very High Very High Very High
Disease Link Frequency Relevance Heat
Stab Wounds 90 99.80 Very High Very High Very High
Brain Injury 60 99.72 Very High Very High Very High
Injury 411 99.36 Very High Very High Very High
Nociception 221 99.18 Very High Very High Very High
Hyperalgesia 35 99.08 Very High Very High Very High
Nervous System Injury 10 98.76 Very High Very High Very High
Hypertrophy 18 98.68 Very High Very High Very High
INFLAMMATION 806 98.64 Very High Very High Very High
Neurogenic Inflammation 20 98.56 Very High Very High Very High
Irritable Bowel Syndrome /

Irritable Bowel Syndrome Super / Visceral Pain

5 98.56 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Induction of protease-activated receptor-1 (PAR-1) by stab wound injury is ablated by the deletion of IL-1R1 (Fig. 3 and 4)
Positive_regulation (Induction) of PAR-1 associated with injury and stab wounds
1) Confidence 0.57 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.81 Pain Relevance 0.09
Induction of protease-activated receptor-1 (PAR-1) by stab wound injury is ablated by the deletion of IL-1R1 (Fig. 3 and 4)
Positive_regulation (Induction) of protease-activated receptor-1 associated with injury and stab wounds
2) Confidence 0.57 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.81 Pain Relevance 0.09
Our findings suggest that blocking IL-1 signaling via IL-1R1 may attenuate the activation of PAR-1 after brain injury.
Positive_regulation (activation) of PAR-1 in brain associated with brain injury
3) Confidence 0.57 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.66 Pain Relevance 0.08
In summary, this study on the effect of a penetrating brain injury in mice lacking IL-1R1 demonstrates that IL-1R1 deletion results in: 1) attenuated hypertrophy of astrocytes; 2) delayed cellular GFAP induction; 3) diminished induction of PAR1; 4) intact induction of extracellular matrix proteins and 5) intact induction of glutamate transporters, glutamine synthetase and S-100B.
Positive_regulation (induction) of PAR1 in extracellular matrix associated with hypertrophy, glutamate and penetrating head injuries
4) Confidence 0.57 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.96 Pain Relevance 0.17
By contrast, PAR-1 protein was not induced and remained undetectable in the IL-1R1-null mice.
Neg (not) Positive_regulation (induced) of PAR-1 protein
5) Confidence 0.57 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.77 Pain Relevance 0.08
We are aware of a single publication investigating genes downstream of PAR1 activation.
Spec (investigating) Positive_regulation (activation) of PAR1
6) Confidence 0.44 Published 2007 Journal BMC Physiol Section Body Doc Link PMC1853107 Disease Relevance 0.41 Pain Relevance 0.09
To test this more conclusively it would be desirable to activate PAR3 alone, but specific activation of PAR3 in neurons coexpressing PAR1 and PAR4 is not possible because PAR3 peptides also activate PAR1 and PAR4 [45,46].
Neg (not) Spec (possible) Positive_regulation (activate) of PAR1 in neurons
7) Confidence 0.38 Published 2010 Journal Mol Pain Section Body Doc Link PMC2956715 Disease Relevance 0 Pain Relevance 0
The peptide agonist TFLLR was used to activate PAR1 apart from in experiments on intact rat skin, where the more effective rat agonist SFLLRN was used.
Positive_regulation (activate) of PAR1 in skin associated with agonist
8) Confidence 0.38 Published 2010 Journal Mol Pain Section Body Doc Link PMC2956715 Disease Relevance 0 Pain Relevance 0.22
Other proteases known to activate PAR1 and PAR4 were also effective in causing translocation of PKC?
Positive_regulation (activate) of PAR1
9) Confidence 0.38 Published 2010 Journal Mol Pain Section Body Doc Link PMC2956715 Disease Relevance 0.06 Pain Relevance 0.22
Activation of PAR1 may be involved in peripheral nerve damage [24,25].
Positive_regulation (Activation) of PAR1 in peripheral nerve associated with nervous system injury
10) Confidence 0.38 Published 2010 Journal Mol Pain Section Body Doc Link PMC2956715 Disease Relevance 0.63 Pain Relevance 0.29
The induced levels of the protease-activated receptor, PAR-1, were significantly attenuated in IL-1R1-null mice.
Positive_regulation (induced) of PAR-1
11) Confidence 0.38 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.90 Pain Relevance 0.17
Genes downstream of PAR1 activation
Positive_regulation (activation) of PAR1
12) Confidence 0.29 Published 2007 Journal BMC Physiol Section Body Doc Link PMC1853107 Disease Relevance 0.71 Pain Relevance 0.19
The combination of cDNA arrays and in silico genomics network analysis reveals an overriding participation of PAR1 receptors in bladder inflammation, provides a working model for the involvement of downstream transcripts, and evokes testable hypotheses regarding the transcriptome downstream of PAR1 activation.


Positive_regulation (activation) of PAR1 in bladder associated with inflammation
13) Confidence 0.29 Published 2007 Journal BMC Physiol Section Body Doc Link PMC1853107 Disease Relevance 0.73 Pain Relevance 0.20
The combination of cDNA array results and genomic networks reveals an overriding participation of PAR1 in bladder inflammation, provides a working model for the involvement of downstream signaling, and evokes testable hypotheses regarding the transcriptome downstream of PAR1 activation.
Positive_regulation (activation) of PAR1 in bladder associated with inflammation
14) Confidence 0.29 Published 2007 Journal BMC Physiol Section Abstract Doc Link PMC1853107 Disease Relevance 0.62 Pain Relevance 0.32
Since PAR1 is well represented in the urinary bladder [24] and its expression is altered in bladder inflammation [24], we set forth to determine the molecular pathways downstream of PAR1 activation.
Positive_regulation (activation) of PAR1 in urinary bladder associated with inflammation
15) Confidence 0.29 Published 2007 Journal BMC Physiol Section Body Doc Link PMC1853107 Disease Relevance 0.72 Pain Relevance 0.38
The present results indicated fundamental alterations elicited by pro-inflammatory substances (LPS and SP) in bladder gene-regulation that are mediated by activation of PAR1.
Positive_regulation (activation) of PAR1 in bladder associated with inflammation and substance p
16) Confidence 0.29 Published 2007 Journal BMC Physiol Section Body Doc Link PMC1853107 Disease Relevance 0.53 Pain Relevance 0.27
Here, we used an approach involving the combination of cDNA arrays, CHIP assay, and in silico querying of knowledge databases in order to identify functions dependent of PAR1 activation that are modified during bladder inflammation.
Positive_regulation (activation) of PAR1 in bladder associated with inflammation
17) Confidence 0.29 Published 2007 Journal BMC Physiol Section Body Doc Link PMC1853107 Disease Relevance 0.32 Pain Relevance 0.16
Given the possible cross talk between PAR-2 and capsaicin receptors, we investigated if PAR-2 activation could facilitate capsaicin-evoked visceral pain and referred hyperalgesia in the mouse and also examined the effect of PAR-1 activation in this model.
Spec (examined) Positive_regulation (activation) of PAR-1 in visceral associated with hyperalgesia, visceral pain and qutenza
18) Confidence 0.28 Published 2004 Journal J. Pharmacol. Sci. Section Abstract Doc Link 15037813 Disease Relevance 0.64 Pain Relevance 1.24
To test this more conclusively it would be desirable to activate PAR3 alone, but specific activation of PAR3 in neurons coexpressing PAR1 and PAR4 is not possible because PAR3 peptides also activate PAR1 and PAR4 [45,46].
Positive_regulation (activation) of PAR1 in neurons
19) Confidence 0.27 Published 2010 Journal Mol Pain Section Body Doc Link PMC2956715 Disease Relevance 0 Pain Relevance 0
Out of 345 TFs present in this array, only TFEB was shared by PAR1-, PAR2-, and PAR4 activation.
Positive_regulation (activation) of PAR1
20) Confidence 0.27 Published 2007 Journal BMC Immunol Section Body Doc Link PMC2000913 Disease Relevance 0.35 Pain Relevance 0.17

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