INT90848

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Context Info
Confidence 0.80
First Reported 2000
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 23
Total Number 24
Disease Relevance 3.15
Pain Relevance 5.20

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

plasma membrane (F2rl1) signal transducer activity (F2rl1)
Anatomy Link Frequency
sensory neurons 3
parotid gland 3
tear 3
pancreas 3
LSM 1
F2rl1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
agonist 30 100.00 Very High Very High Very High
antagonist 9 99.92 Very High Very High Very High
qutenza 40 99.84 Very High Very High Very High
Opioid 6 99.48 Very High Very High Very High
dorsal root ganglion 64 99.00 Very High Very High Very High
Inflammation 93 98.92 Very High Very High Very High
Potency 1 98.60 Very High Very High Very High
Pain 13 95.44 Very High Very High Very High
Enkephalin 2 95.00 High High
Calcitonin gene-related peptide 4 94.28 High High
Disease Link Frequency Relevance Heat
Ganglion Cysts 67 99.00 Very High Very High Very High
INFLAMMATION 96 98.92 Very High Very High Very High
Nociception 27 98.60 Very High Very High Very High
Increased Venous Pressure Under Development 6 97.16 Very High Very High Very High
Pain 16 95.44 Very High Very High Very High
Injury 11 90.00 High High
Reperfusion Injury 1 75.00 Quite High
Cv Unclassified Under Development 1 75.00 Quite High
Coronary Artery Disease 1 71.76 Quite High
Inflammatory Pain 1 68.80 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Our findings suggest that the PAR-2-APs SLIGRL-NH(2) and SLIGKV-NH(2) cause tear secretion, most likely via PAR-2 and that LSIGRL-NH(2), a PAR-2-inactive peptide, and IGRL-NH(2), its key structure, trigger tear secretion by stimulating parasympathetic nerves via an unidentified target molecule.
Localization (secretion) of PAR-2 in tear
1) Confidence 0.80 Published 2005 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 15331653 Disease Relevance 0 Pain Relevance 0
The present findings demonstrate that activation of the PAR-2 localized on capsaicin-sensitive trigeminal nociceptive afferent nerves induces vasodilatation in the dural vascular bed by mechanisms involving NO and CGRP release.
Localization (localized) of PAR-2 in nerves associated with nociception, qutenza, increased venous pressure under development and calcitonin gene-related peptide
2) Confidence 0.78 Published 2009 Journal Neuroscience Section Abstract Doc Link 19362118 Disease Relevance 0.34 Pain Relevance 0.97
Confocal microscopy revealed colocalization of PAR2 to 4 with protein gene product 9.5 and VR1, suggesting that PARs are distributed in C-fiber bladder nerves.
Localization (colocalization) of PAR2 in bladder
3) Confidence 0.77 Published 2005 Journal J. Urol. Section Body Doc Link 15643279 Disease Relevance 0.13 Pain Relevance 0
SLIGRL-NH(2), a PAR-2-activating peptide (PAR-2-AP) derived from mouse/rat PAR-2, when administered i.v. in combination with amastatin, an aminopeptidase inhibitor, evoked tear secretion, whereas LRGILS-NH(2), a PAR-2-inactive reversed peptide, had no such effect.
Localization (secretion) of PAR-2-activating peptide in tear
4) Confidence 0.75 Published 2005 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 15331653 Disease Relevance 0 Pain Relevance 0
In the present study, we investigated whether PAR-2 could modulate gastric acid secretion in rats.
Localization (secretion) of PAR-2
5) Confidence 0.75 Published 2002 Journal Eur. J. Pharmacol. Section Abstract Doc Link 12106807 Disease Relevance 0 Pain Relevance 0.06
Moreover, protein kinase A does not participate in the inhibition of P2X3 currents caused by PAR2 activation.
Localization (caused) of PAR2
6) Confidence 0.75 Published 2010 Journal Neuroreport Section Abstract Doc Link 20118742 Disease Relevance 0.46 Pain Relevance 0.39
Desensitization of PAR2 receptors indicated that the high potency phase was mediated by PAR2.
Localization (Desensitization) of PAR2 associated with potency
7) Confidence 0.72 Published 2002 Journal Circ. Res. Section Abstract Doc Link 11884377 Disease Relevance 0.55 Pain Relevance 0.30
Activation of protease-activated receptor-2 (PAR-2), a receptor activated by trypsin/tryptase, induces neurally mediated gastric mucus secretion accompanied by mucosal cytoprotection.
Localization (secretion) of PAR-2
8) Confidence 0.70 Published 2002 Journal Eur. J. Pharmacol. Section Abstract Doc Link 12106807 Disease Relevance 0 Pain Relevance 0.05
In conclusion, our study demonstrates expression of PAR-2 in rat pancreatic acini as well as parotid acini and indicates that nitric oxide participates in the PAR-2-mediated in vivo secretion of pancreatic amylase, and, to a certain extent, of salivary amylase, although capsaicin-sensitive sensory neurons, known to be activated by PAR-2, are not involved in the evoked pancreatic or salivary amylase secretion.
Localization (secretion) of PAR-2 in sensory neurons associated with qutenza
9) Confidence 0.64 Published 2002 Journal Life Sci. Section Abstract Doc Link 12231404 Disease Relevance 0 Pain Relevance 0.25
Protease-activated receptor-2 (PAR-2) in the pancreas and parotid gland: Immunolocalization and involvement of nitric oxide in the evoked amylase secretion.
Localization (secretion) of Protease-activated receptor-2 in parotid gland
10) Confidence 0.64 Published 2002 Journal Life Sci. Section Title Doc Link 12231404 Disease Relevance 0 Pain Relevance 0.12
Protease-activated receptor-2 (PAR-2) in the pancreas and parotid gland: Immunolocalization and involvement of nitric oxide in the evoked amylase secretion.
Localization (secretion) of PAR-2 in parotid gland
11) Confidence 0.64 Published 2002 Journal Life Sci. Section Title Doc Link 12231404 Disease Relevance 0 Pain Relevance 0.12
Furthermore, the co-localization of DiI with the PAR2 receptor appeared to decrease by approximately 50% following inflammation (P < 0.0003) (Fig 6a, b).
Localization (localization) of PAR2 associated with inflammation
12) Confidence 0.63 Published 2009 Journal Mol Pain Section Body Doc Link PMC2758842 Disease Relevance 0.58 Pain Relevance 0.34
Our findings suggest that the PAR-2-APs SLIGRL-NH(2) and SLIGKV-NH(2) cause tear secretion, most likely via PAR-2 and that LSIGRL-NH(2), a PAR-2-inactive peptide, and IGRL-NH(2), its key structure, trigger tear secretion by stimulating parasympathetic nerves via an unidentified target molecule.
Localization (secretion) of PAR-2-inactive in tear
13) Confidence 0.61 Published 2005 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 15331653 Disease Relevance 0 Pain Relevance 0
In the present study, we examined the distribution of PAR-2 in the pancreas and parotid gland, and characterized the PAR-2-mediated secretion of amylase by these tissues in vivo.
Localization (secretion) of PAR-2-mediated in parotid gland
14) Confidence 0.60 Published 2002 Journal Life Sci. Section Abstract Doc Link 12231404 Disease Relevance 0 Pain Relevance 0.04
The PAR-2-mediated secretion of pancreatic amylase was abolished by pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor.
Localization (secretion) of PAR-2-mediated
15) Confidence 0.60 Published 2002 Journal Life Sci. Section Abstract Doc Link 12231404 Disease Relevance 0 Pain Relevance 0.16
In conclusion, our study demonstrates expression of PAR-2 in rat pancreatic acini as well as parotid acini and indicates that nitric oxide participates in the PAR-2-mediated in vivo secretion of pancreatic amylase, and, to a certain extent, of salivary amylase, although capsaicin-sensitive sensory neurons, known to be activated by PAR-2, are not involved in the evoked pancreatic or salivary amylase secretion.
Localization (secretion) of PAR-2-mediated in sensory neurons associated with qutenza
16) Confidence 0.60 Published 2002 Journal Life Sci. Section Abstract Doc Link 12231404 Disease Relevance 0 Pain Relevance 0.26
Pretreatment with capsaicin for ablation of the sensory neurons did not modify the PAR-2-mediated secretion of pancreatic and salivary amylase in the mouse.
Localization (secretion) of PAR-2-mediated in sensory neurons associated with qutenza
17) Confidence 0.60 Published 2002 Journal Life Sci. Section Abstract Doc Link 12231404 Disease Relevance 0 Pain Relevance 0.26
This finding is in agreement with data from Amadesi et al. [24] which demonstrated that the PAR2 receptor co-localized with TRPV1 receptors in DRG neurons.
Localization (localized) of PAR2 in neurons associated with dorsal root ganglion
18) Confidence 0.59 Published 2009 Journal Mol Pain Section Body Doc Link PMC2758842 Disease Relevance 1.08 Pain Relevance 0.51
Immunohistochemistry revealed co-localization of SP, calcitonin gene-related peptide and PAR-2 in axons of opossum oesophageal LSM.
Localization (localization) of PAR-2 in LSM
19) Confidence 0.24 Published 2010 Journal Neurogastroenterol. Motil. Section Body Doc Link 19740117 Disease Relevance 0 Pain Relevance 0
PAR-2 agonists stimulate active anion secretion by a neurogenic mechanism that is modulated by prostanoids and opioids.
Localization (secretion) of PAR-2 associated with agonist and opioid
20) Confidence 0.22 Published 2000 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 10992008 Disease Relevance 0 Pain Relevance 0.53

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