INT95787

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Context Info
Confidence 0.70
First Reported 2001
Last Reported 2010
Negated 10
Speculated 22
Reported most in Abstract
Documents 568
Total Number 590
Disease Relevance 226.51
Pain Relevance 220.94

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

nucleoplasm (Mapk1) mitochondrion (Mapk1) protein complex (Mapk1)
cytoplasm (Mapk1) cytosol (Mapk1) signal transduction (Mapk1)
Anatomy Link Frequency
neurons 25
amygdala 25
spinal cord 21
neuronal 17
brain 15
Mapk1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 3467 100.00 Very High Very High Very High
Pain 1414 100.00 Very High Very High Very High
nMDA receptor 996 100.00 Very High Very High Very High
Kinase C 845 100.00 Very High Very High Very High
nociceptor 138 100.00 Very High Very High Very High
adenocard 78 100.00 Very High Very High Very High
Anterior cingulate cortex 2317 99.98 Very High Very High Very High
amygdala 2084 99.98 Very High Very High Very High
cocaine 2043 99.98 Very High Very High Very High
Opioid 377 99.98 Very High Very High Very High
Disease Link Frequency Relevance Heat
Stress 1260 100.00 Very High Very High Very High
Injury 435 99.96 Very High Very High Very High
INFLAMMATION 3574 99.92 Very High Very High Very High
Diabetes Mellitus 2492 99.92 Very High Very High Very High
Pain 1781 99.92 Very High Very High Very High
Appetite Loss 478 99.92 Very High Very High Very High
Nociception 1140 99.90 Very High Very High Very High
Neuropathic Pain 579 99.90 Very High Very High Very High
Cancer 4381 99.84 Very High Very High Very High
Obesity 1687 99.84 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Furthermore, we found an acid-induced, Ca(v)3.2 T-channel-dependent activation of ERK (extracellular signal-regulated kinase) in the anterior nucleus of paraventricular thalamus (PVA), and prevention of the ERK activation abolished the chronic mechanical hyperalgesia.
Positive_regulation (activation) of ERK in PVA associated with hyperalgesia and thalamus
1) Confidence 0.70 Published 2010 Journal J. Neurosci. Section Abstract Doc Link 20685979 Disease Relevance 0.84 Pain Relevance 1.06
Our findings suggest that Ca(v)3.2 T-channel-dependent activation of ERK in PVA is required for the development of acid-induced chronic mechanical hyperalgesia.
Positive_regulation (activation) of ERK in PVA associated with hyperalgesia and thalamus
2) Confidence 0.70 Published 2010 Journal J. Neurosci. Section Abstract Doc Link 20685979 Disease Relevance 0.85 Pain Relevance 1.01
Furthermore, we found an acid-induced, Ca(v)3.2 T-channel-dependent activation of ERK (extracellular signal-regulated kinase) in the anterior nucleus of paraventricular thalamus (PVA), and prevention of the ERK activation abolished the chronic mechanical hyperalgesia.
Positive_regulation (activation) of extracellular signal-regulated kinase in PVA associated with hyperalgesia and thalamus
3) Confidence 0.70 Published 2010 Journal J. Neurosci. Section Abstract Doc Link 20685979 Disease Relevance 0.84 Pain Relevance 1.06
Using the formalin test as a mouse model of persistent inflammatory pain, we show that activation of ERK in the amygdala is both necessary for and sufficient to induce long-lasting peripheral hypersensitivity to tactile stimulation.
Positive_regulation (activation) of ERK in amygdala associated with ipn, hypersensitivity and amygdala
4) Confidence 0.70 Published 2007 Journal J. Neurosci. Section Abstract Doc Link 17301163 Disease Relevance 1.17 Pain Relevance 0.88
Activation of the extracellular signal-regulated kinase in the amygdala modulates pain perception.
Positive_regulation (Activation) of extracellular signal-regulated kinase in amygdala associated with pain and amygdala
5) Confidence 0.70 Published 2007 Journal J. Neurosci. Section Title Doc Link 17301163 Disease Relevance 0.72 Pain Relevance 0.98
Our results outline a subset of structures in which ERK activation might specifically contribute to the long-term effects of drugs of abuse, and suggest mapping ERK activation in brain as a way to identify potential sites of action of psychoactive drugs.
Positive_regulation (activation) of ERK in brain
6) Confidence 0.70 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15078556 Disease Relevance 0 Pain Relevance 0.49
Each drug generated a distinct regional pattern of ERK activation.
Positive_regulation (activation) of ERK
7) Confidence 0.70 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15078556 Disease Relevance 0 Pain Relevance 0.66
Typical antipsychotics mildly activated ERK in dorsal striatum and superficial prefrontal cortex, whereas clozapine had no effect in the striatum, but more widespread effects in cortex and amygdala.
Positive_regulation (activated) of ERK in amygdala associated with amygdala
8) Confidence 0.70 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15078556 Disease Relevance 0 Pain Relevance 0.63
Antidepressants and caffeine activated ERK in hippocampus and cerebral cortex.
Positive_regulation (activated) of ERK in cerebral cortex associated with antidepressant, hippocampus and cerebral cortex
9) Confidence 0.70 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15078556 Disease Relevance 0 Pain Relevance 0.67
Addictive and non-addictive drugs induce distinct and specific patterns of ERK activation in mouse brain.
Positive_regulation (activation) of ERK in brain
10) Confidence 0.70 Published 2004 Journal Eur. J. Neurosci. Section Title Doc Link 15078556 Disease Relevance 0 Pain Relevance 0.52
Our results outline a subset of structures in which ERK activation might specifically contribute to the long-term effects of drugs of abuse, and suggest mapping ERK activation in brain as a way to identify potential sites of action of psychoactive drugs.
Positive_regulation (activation) of ERK in brain
11) Confidence 0.70 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15078556 Disease Relevance 0 Pain Relevance 0.47
Although some non-addictive drugs moderately activated ERK in a few of these areas, they never induced this combined pattern of strong activation.
Positive_regulation (activated) of ERK
12) Confidence 0.70 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15078556 Disease Relevance 0 Pain Relevance 0.68
However, it is not known whether activation of ERK in the striatum is specific for these two drugs and/or this brain region.
Spec (whether) Positive_regulation (activation) of ERK in brain
13) Confidence 0.70 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15078556 Disease Relevance 0 Pain Relevance 0.50
Our data show that ERK activation plays a specific role in maintaining prolonged referred (secondary) hyperalgesia in visceral pain.
Positive_regulation (activation) of ERK in visceral associated with visceral pain and hyperalgesia
14) Confidence 0.70 Published 2003 Journal Brain Res. Mol. Brain Res. Section Abstract Doc Link 12941468 Disease Relevance 0.61 Pain Relevance 1.31
We hypothesized that activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and the expression of c-Fos, prodynorphin (mRNA), and dynorphin in the spinal cord could participate in the molecular mechanisms underlying postoperative opioid-induced sensitization.
Positive_regulation (activation) of extracellular signal-regulated kinases 1 and 2 in spinal cord associated with dynorphin, opioid and spinal cord
15) Confidence 0.70 Published 2010 Journal Mol. Pharmacol. Section Abstract Doc Link 19917879 Disease Relevance 0.26 Pain Relevance 0.89
These data suggest that the sustained activation of ERK activity be associated with the development of antinociceptive tolerance to morphine in mice.
Positive_regulation (activation) of ERK associated with tolerance, antinociceptive and morphine
16) Confidence 0.69 Published 2002 Journal Neurosci. Lett. Section Abstract Doc Link 11988336 Disease Relevance 0 Pain Relevance 1.54
These results show that mGluR1 and mGluR5 are activated in dorsal horn neurons in response to peripheral inflammation and that activation of these group I mGluRs leads to activation of ERK1 and ERK2, resulting in enhanced pain sensitivity.
Positive_regulation (activation) of ERK2 in neurons associated with pain, inflammation and dorsal horn neuron
17) Confidence 0.69 Published 2001 Journal J. Neurosci. Section Abstract Doc Link 11356865 Disease Relevance 0.71 Pain Relevance 0.65
Furthermore, we find that inflammation-evoked ERK activation, which is required for nociceptive plasticity, is downstream of mGluR1 and mGluR5.
Positive_regulation (activation) of ERK associated with nociception and inflammation
18) Confidence 0.69 Published 2001 Journal J. Neurosci. Section Abstract Doc Link 11356865 Disease Relevance 0.59 Pain Relevance 0.72
We show that activation of mGluR1 and mGluR5 leads to activation of ERK1 and ERK2 in the spinal cord.
Positive_regulation (activation) of ERK2 in spinal cord associated with spinal cord
19) Confidence 0.69 Published 2001 Journal J. Neurosci. Section Abstract Doc Link 11356865 Disease Relevance 0.60 Pain Relevance 0.71
Capsaicin decreased the activation of extracellular signal-regulated kinases (ERK) without markedly affecting p38 kinases.
Positive_regulation (activation) of ERK associated with qutenza
20) Confidence 0.69 Published 2010 Journal J. Toxicol. Environ. Health Part A Section Abstract Doc Link 20954075 Disease Relevance 0.50 Pain Relevance 0.86

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