INT111998

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Context Info
Confidence 0.69
First Reported 2003
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 23
Total Number 25
Disease Relevance 9.33
Pain Relevance 8.97

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

cytosol (Mapk8) signal transduction (Mapk8) mitochondrion (Mapk8)
nucleus (Mapk8) kinase activity (Mapk8) cytoplasm (Mapk8)
Anatomy Link Frequency
brain 6
spinal cord 4
neurons 4
PSCs 4
spinal 2
Mapk8 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Dopamine 340 99.98 Very High Very High Very High
dorsal root ganglion 4 99.84 Very High Very High Very High
Morphine 31 99.78 Very High Very High Very High
Spinal cord 10 99.68 Very High Very High Very High
Root ganglion neuron 1 99.58 Very High Very High Very High
Sciatic nerve 2 99.50 Very High Very High Very High
tolerance 27 99.00 Very High Very High Very High
Antinociceptive 16 98.70 Very High Very High Very High
Pain 13 98.44 Very High Very High Very High
lidocaine 2 98.06 Very High Very High Very High
Disease Link Frequency Relevance Heat
Infection 82 100.00 Very High Very High Very High
Hypoxia 58 99.98 Very High Very High Very High
Ganglion Cysts 13 99.84 Very High Very High Very High
Apoptosis 184 99.80 Very High Very High Very High
Sepsis 103 99.76 Very High Very High Very High
Injury 53 98.78 Very High Very High Very High
Pain 11 98.44 Very High Very High Very High
Hyperalgesia 15 97.56 Very High Very High Very High
INFLAMMATION 137 96.48 Very High Very High Very High
Lung Injury 13 96.16 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
An intra-plantar (i.pl.) injection of complete Freund's adjuvant induced the activation of JNK in DRG neurons within 30 min.
Positive_regulation (induced) of Positive_regulation (activation) of JNK in DRG associated with dorsal root ganglion
1) Confidence 0.69 Published 2005 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 16055088 Disease Relevance 1.34 Pain Relevance 0.88
Fifteen days after injury, the analysis in the sciatic nerves highlighted a bilateral increase of the activated forms of PKCgamma, ERK 1,2 and SAP/JNK, whereas c-Jun showed an increase only ipsilaterally.
Positive_regulation (increase) of Positive_regulation (activated) of JNK in sciatic nerves associated with injury and sciatic nerve
2) Confidence 0.49 Published 2010 Journal Neuroscience Section Abstract Doc Link 19925851 Disease Relevance 0.57 Pain Relevance 0.60
Taken together, we conclude that activation of peripheral MAPKs, including ERK, JNK and p38, might contribute to the induction and maintenance of persistent ongoing pain and primary heat hyperalgesia in the melittin test.
Spec (might) Positive_regulation (induction) of Positive_regulation (activation) of JNK associated with pain and hyperalgesia
3) Confidence 0.46 Published 2008 Journal Neuroscience Section Abstract Doc Link 18329815 Disease Relevance 1.02 Pain Relevance 0.94
Our results showed that chronic morphine treatment induced upregulation of the NR2B expression and activation of JNK in the spinal cord.
Positive_regulation (induced) of Positive_regulation (activation) of JNK in spinal cord associated with spinal cord and morphine
4) Confidence 0.46 Published 2009 Journal Neurosci. Lett. Section Abstract Doc Link 19818835 Disease Relevance 0 Pain Relevance 1.34
MK-801, a noncompetitive NMDA receptor antagonist, not only suppressed morphine antinociceptive tolerance and the increase in NR2B, but also reduced the spinal JNK activation induced by chronic morphine treatment.
Positive_regulation (induced) of Positive_regulation (activation) of JNK in spinal associated with nmda receptor antagonist, tolerance, antinociceptive and morphine
5) Confidence 0.46 Published 2009 Journal Neurosci. Lett. Section Abstract Doc Link 19818835 Disease Relevance 0 Pain Relevance 1.64
Our results showed that chronic morphine treatment induced upregulation of the NR2B expression and activation of JNK in the spinal cord.
Positive_regulation (upregulation) of Positive_regulation (activation) of JNK in spinal cord associated with spinal cord and morphine
6) Confidence 0.46 Published 2009 Journal Neurosci. Lett. Section Abstract Doc Link 19818835 Disease Relevance 0 Pain Relevance 1.34
Sepsis induced an increase in the expression/activation of TLR4 and its downstream signaling JNK and IKK/NF-?
Positive_regulation (increase) of Positive_regulation (activation) of JNK associated with sepsis
7) Confidence 0.35 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2997789 Disease Relevance 0.73 Pain Relevance 0.21
The time course of JNK activation (progressive increase up to 24 hours after LPS treatment) appears to occur in parallel with those of the biochemical lung injury variables and neutrophil influx into the lungs after intratracheal treatment with LPS [14].
Positive_regulation (increase) of Positive_regulation (activation) of JNK in neutrophil associated with lung injury
8) Confidence 0.33 Published 2004 Journal Respir Res Section Body Doc Link PMC538282 Disease Relevance 0.62 Pain Relevance 0.17
METHODS: Rat PSCs were incubated with ethanol (50 mM) or acetaldehyde (200 microM) for 15 min, 30 min, 60 min, and 24 h; and activities of ERK 1/2, JNK, and p38 kinase were assessed in cell lysates using kinase assays and Western blot.
Positive_regulation (assessed) of Positive_regulation (activities) of JNK in PSCs
9) Confidence 0.31 Published 2003 Journal Pancreas Section Body Doc Link 12883264 Disease Relevance 0 Pain Relevance 0
RESULTS: Ethanol and acetaldehyde increased the activation of all 3 subfamilies (ERK 1/2, JNK and p38 kinase) of the MAPK pathway in PSCs.
Positive_regulation (increased) of Positive_regulation (activation) of JNK in PSCs
10) Confidence 0.31 Published 2003 Journal Pancreas Section Body Doc Link 12883264 Disease Relevance 0 Pain Relevance 0
Expression of claudin 4, claudin 18, and occludin was significantly lower, and activation of JNK and ERK signaling pathways was significantly increased in 2CLP monolayers, relative to sham monolayers.
Positive_regulation (increased) of Positive_regulation (activation) of JNK
11) Confidence 0.31 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2892473 Disease Relevance 0.20 Pain Relevance 0
Agmatine suppressed the hypoxia-induced activation of JNK and NF-?
Positive_regulation (induced) of Positive_regulation (activation) of JNK associated with hypoxia
12) Confidence 0.27 Published 2007 Journal BMC Neurosci Section Body Doc Link PMC2089075 Disease Relevance 0.77 Pain Relevance 0
inhibitor blocked the As-induced JNK activation with a similar trend to the results of taurine treatment.
Positive_regulation (induced) of Positive_regulation (activation) of JNK
13) Confidence 0.25 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2935368 Disease Relevance 0.23 Pain Relevance 0
Thus, these results suggest that taurine inhibits NaAsO2-induced JNK activation and apoptosis by suppressing the activation of PKC?.


Positive_regulation (induced) of Positive_regulation (activation) of JNK associated with apoptosis
14) Confidence 0.24 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2935368 Disease Relevance 0.25 Pain Relevance 0
is involved in As-induced JNK activation and mitochondrial dependent apoptosis.
Positive_regulation (induced) of Positive_regulation (activation) of JNK associated with apoptosis
15) Confidence 0.24 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2935368 Disease Relevance 0.90 Pain Relevance 0
Finally, these data show the increased activation of ERK, not JNK, signaling plays a role in barrier dysfunction in 2CLP monolayers.


Positive_regulation (increased) of Positive_regulation (activation) of JNK
16) Confidence 0.22 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2892473 Disease Relevance 0.10 Pain Relevance 0
In contrast to p44/42 MAPK, increased phosphorylation and activation of p38 and c-Jun N-terminal kinase (JNK) members of MAPK promote the apoptosis of cerebella neurons [28-31].
Positive_regulation (increased) of Positive_regulation (activation) of JNK in neurons associated with apoptosis
17) Confidence 0.20 Published 2010 Journal BMC Neurol Section Body Doc Link PMC3020671 Disease Relevance 0.63 Pain Relevance 0.06
Analogous to its effects on P-MEK1/2, but much more dramatically, forced swimming enhanced the levels of P-MKK4, the immediate upstream activator of JNK, in all brain areas tested (Fig. 3, top).
Positive_regulation (enhanced) of Positive_regulation (immediate upstream activator) of JNK in brain
18) Confidence 0.20 Published 2004 Journal BMC Neurosci Section Body Doc Link PMC526203 Disease Relevance 0.16 Pain Relevance 0.24
Co-application of NMDA and dopamine induced a significant activation of JNK compared to control (1.54±0.19, p<0.05, n?
Positive_regulation (induced) of Positive_regulation (activation) of JNK associated with dopamine
19) Confidence 0.09 Published 2006 Journal PLoS ONE Section Body Doc Link PMC1762427 Disease Relevance 0 Pain Relevance 0.36
We investigated the hypotheses that these drugs (A) are less neurotoxic than the prototype local anesthetic, lidocaine (B) are selectively toxic for subcategories of dorsal root ganglion neurons and (C) induce activation of either p38 MAPK or related enzymes, such as the c-jun terminal N-kinase (JNK) and extracellular signal-regulated kinase (ERK).
Positive_regulation (induce) of Positive_regulation (activation) of c-jun terminal N-kinase in neurons associated with ganglion cysts, root ganglion neuron, lidocaine and local anesthetic
20) Confidence 0.09 Published 2008 Journal Anesth. Analg. Section Abstract Doc Link 18420860 Disease Relevance 0.26 Pain Relevance 0.42

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