INT112037

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Context Info
Confidence 0.59
First Reported 2003
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 19
Total Number 19
Disease Relevance 8.90
Pain Relevance 10.55

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

cytosol (Trpv1) transport (Trpv1) plasma membrane (Trpv1)
transmembrane transport (Trpv1) lipid metabolic process (Trpv1)
Anatomy Link Frequency
body 12
HEK 2
Trpv1 (Mus musculus)
Pain Link Frequency Relevance Heat
calcitonin gene related peptide 28 100.00 Very High Very High Very High
Hyperalgesia 66 99.90 Very High Very High Very High
qutenza 469 99.76 Very High Very High Very High
bradykinin 40 99.36 Very High Very High Very High
IPN 29 98.60 Very High Very High Very High
Pain 134 97.52 Very High Very High Very High
dorsal root ganglion 184 97.12 Very High Very High Very High
Kinase C 15 96.88 Very High Very High Very High
cOX1 10 96.08 Very High Very High Very High
Spontaneous pain 4 94.96 High High
Disease Link Frequency Relevance Heat
Hyperalgesia 142 99.90 Very High Very High Very High
Cancer 17 99.84 Very High Very High Very High
Inflammatory Pain 30 98.60 Very High Very High Very High
Necrosis 8 98.60 Very High Very High Very High
Ganglion Cysts 189 97.12 Very High Very High Very High
Targeted Disruption 45 94.56 High High
Pain 149 94.48 High High
Diabetes Mellitus 17 94.24 High High
Nociception 144 93.60 High High
INFLAMMATION 189 92.84 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In the presence of ATP, the temperature threshold for TRPV1 activation was reduced from 42 degrees C to 35 degrees C, such that normal body temperature could activate TRPV1.
Negative_regulation (reduced) of Positive_regulation (activation) of TRPV1 in body
1) Confidence 0.59 Published 2004 Journal Novartis Found. Symp. Section Abstract Doc Link 15469041 Disease Relevance 0.25 Pain Relevance 0.51
In the presence of PGE2 or PGI2, the temperature threshold for TRPV1 activation was reduced below 35°C, so that temperatures near body temperature are sufficient to activate TRPV1.
Negative_regulation (reduced) of Positive_regulation (activation) of TRPV1 in body
2) Confidence 0.57 Published 2005 Journal Mol Pain Section Abstract Doc Link PMC1074353 Disease Relevance 0.68 Pain Relevance 0.50
In contrast, the temperature threshold for TRPV1 activation was significantly reduced to 30.6 ± 1.1°C in the presence of PGE2 (n = 8, p < 0.05) (Figure 2D) implying that under these conditions, TRPV1 could be activated at normal body temperature.
Negative_regulation (reduced) of Positive_regulation (activation) of TRPV1 in body
3) Confidence 0.57 Published 2005 Journal Mol Pain Section Body Doc Link PMC1074353 Disease Relevance 0 Pain Relevance 0.35
Deletion of the tumor necrosis factor receptor type 2 (TNFR2) gene attenuated heat hyperalgesia and prevented TRPV1 upregulation in tumor-bearing mice, whereas TNFR1 gene deletion played a minor role.
Negative_regulation (prevented) of Positive_regulation (upregulation) of TRPV1 associated with necrosis, hyperalgesia and cancer
4) Confidence 0.57 Published 2008 Journal J. Neurosci. Section Abstract Doc Link 18463260 Disease Relevance 1.57 Pain Relevance 1.02
In the presence of ATP or bradykinin, the temperature threshold for VR1 activation was reduced from 42 degrees C to 30-35 degrees C, such that normally non-painful normal body temperatures were capable of activating TRPV1, thereby leading to the sensation of pain.
Negative_regulation (reduced) of Positive_regulation (activation) of VR1 in body associated with pain and bradykinin
5) Confidence 0.43 Published 2003 Journal Nihon Shinkei Seishin Yakurigaku Zasshi Section Abstract Doc Link 12884755 Disease Relevance 0.64 Pain Relevance 1.33
Capsazepine inhibits acid-induced activation of human TRPV1 (hTRPV1), but has no inhibitory effect on acid-induced activation of rat TRPV1 (rTRPV1) [190]; however, it can inhibit heat-mediated responses in both hTRPV1 and rTRPV1.
Negative_regulation (inhibits) of Positive_regulation (activation) of TRPV1
6) Confidence 0.43 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2647151 Disease Relevance 0 Pain Relevance 0.48
Downstream signaling required G-protein activation and phosphorylation as intracellularly administered GDP-beta-S [guanosine 5'-O-(2-thiodiphosphate], protein kinase A inhibitors, and an A-kinase anchoring protein inhibitor significantly blocked serotonergic facilitation of TRPV1 function; 5-HT2 receptor-mediated facilitation was also inhibited by a PKC inhibitor.
Negative_regulation (blocked) of Positive_regulation (facilitation) of TRPV1
7) Confidence 0.43 Published 2004 Journal J. Neurosci. Section Abstract Doc Link 15509739 Disease Relevance 0.07 Pain Relevance 0.35
Furthermore, in stably TRPV1-expressing HEK 293T cells, STZ treatment induced an increase in TRPV1 protein content and p-p38 MAPK levels, which was abolished with concomitant treatment with catalase or p38 MAPK inhibitor.
Negative_regulation (abolished) of Positive_regulation (increase) of TRPV1 protein in HEK
8) Confidence 0.42 Published 2008 Journal Mol. Pharmacol. Section Abstract Doc Link 18089839 Disease Relevance 0.95 Pain Relevance 0.56
This effect is TRPV1 specific as it was inhibited by capsazepine and suggested to occur as a result of CGRP and tachykinin release upon TRPV1 activation [86].
Negative_regulation (result) of Positive_regulation (activation) of TRPV1 associated with calcitonin gene related peptide
9) Confidence 0.42 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2647151 Disease Relevance 0.65 Pain Relevance 0.59
The fact that only PKC activation leads to the reduction of temperature threshold for TRPV1 activation might be pertinent to this issue.
Negative_regulation (reduction) of Positive_regulation (activation) of TRPV1
10) Confidence 0.42 Published 2005 Journal Mol Pain Section Body Doc Link PMC1074353 Disease Relevance 0.20 Pain Relevance 0.36
The temperature threshold for TRPV1 activation is reduced below 35°C in the presence of prostaglandins, so that TRPV1 can be activated at normal body temperature, possibly leading to spontaneous pain sensation.
Negative_regulation (reduced) of Positive_regulation (activation) of TRPV1 in body associated with pain and spontaneous pain
11) Confidence 0.42 Published 2005 Journal Mol Pain Section Body Doc Link PMC1074353 Disease Relevance 0.73 Pain Relevance 0.46
Comparable results were achieved with rat TRPV1, while capsazepine blocked all modes of human TRPV1 activation.
Negative_regulation (blocked) of Positive_regulation (activation) of TRPV1
12) Confidence 0.42 Published 2004 Journal Neurosci. Lett. Section Abstract Doc Link 15489017 Disease Relevance 0 Pain Relevance 0.84
Reduction of the temperature threshold for TRPV1 activation is thought to be one mechanism of inflammatory pain.
Negative_regulation (Reduction) of Positive_regulation (activation) of TRPV1 associated with ipn
13) Confidence 0.42 Published 2004 Journal Nippon Yakurigaku Zasshi Section Abstract Doc Link 15467255 Disease Relevance 0.26 Pain Relevance 0.21
PBN was used to block ROS production after TRPV1 activation with capsaicin.
Negative_regulation (block) of Positive_regulation (activation) of TRPV1 associated with qutenza
14) Confidence 0.42 Published 2009 Journal Mol Pain Section Body Doc Link PMC2706230 Disease Relevance 0.51 Pain Relevance 0.82
The increase of TRPV1 protein level after TNF?
Negative_regulation (level) of Positive_regulation (increase) of TRPV1 protein
15) Confidence 0.36 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2936303 Disease Relevance 1.41 Pain Relevance 1.04
Although BAA activated TRPV4 channels with an EC(50) of 790-950 nm, it did not activate or block activation of TRPV1, TRPV2, or TRPV3 channels.
Negative_regulation (block) of Positive_regulation (activation) of TRPV1
16) Confidence 0.36 Published 2006 Journal J. Biol. Chem. Section Abstract Doc Link 16899456 Disease Relevance 0 Pain Relevance 0.15
Importantly, in the phosphorylated state, the activation threshold of TRPV1 is reduced below body temperature rendering the channel constitutively active [20].
Negative_regulation (reduced) of Positive_regulation (activation) of TRPV1 in body
17) Confidence 0.29 Published 2006 Journal Mol Pain Section Body Doc Link PMC1563450 Disease Relevance 0.33 Pain Relevance 0.39
M, AP18 was unable to appreciably block activation of TRPV1, TRPV2, TRPV3, TRPV4, or TRPM8 (Figure 2).
Negative_regulation (block) of Positive_regulation (activation) of TRPV1
18) Confidence 0.28 Published 2007 Journal Mol Pain Section Body Doc Link PMC2222610 Disease Relevance 0.20 Pain Relevance 0.37
Sensitisation of TRPV1 was significantly reduced by PKC inhibitors.
Negative_regulation (reduced) of Positive_regulation (Sensitisation) of TRPV1
19) Confidence 0.27 Published 2010 Journal Mol Pain Section Abstract Doc Link PMC2956715 Disease Relevance 0.45 Pain Relevance 0.23

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