INT80690

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Context Info
Confidence 0.68
First Reported 1999
Last Reported 2011
Negated 2
Speculated 7
Reported most in Abstract
Documents 223
Total Number 248
Disease Relevance 125.63
Pain Relevance 36.75

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) nucleoplasm (MAPK8) mitochondrion (MAPK8)
nucleus (MAPK8) response to stress (MAPK8) cytoplasm (MAPK8)
Anatomy Link Frequency
fibroblasts 15
epithelial cells 10
Caco-2 5
T cells 4
macrophages 3
MAPK8 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 2178 100.00 Very High Very High Very High
Osteoarthritis 458 100.00 Very High Very High Very High
Kappa opioid receptor 32 99.98 Very High Very High Very High
Spinal nerve ligature 10 99.98 Very High Very High Very High
agonist 475 99.92 Very High Very High Very High
aspirin 58 99.92 Very High Very High Very High
Nicotine 873 99.84 Very High Very High Very High
Morphine 32 99.84 Very High Very High Very High
Bile 217 99.78 Very High Very High Very High
cINOD 122 99.76 Very High Very High Very High
Disease Link Frequency Relevance Heat
Stress 3527 100.00 Very High Very High Very High
Apoptosis 2730 100.00 Very High Very High Very High
INFLAMMATION 2552 100.00 Very High Very High Very High
Osteoarthritis 419 100.00 Very High Very High Very High
Injury 616 99.96 Very High Very High Very High
Metabolic Syndrome 41 99.92 Very High Very High Very High
Disease 3565 99.84 Very High Very High Very High
Obesity 300 99.84 Very High Very High Very High
Nerve Sheath Neoplasms 132 99.76 Very High Very High Very High
Infection 443 99.68 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Activation of JNK by morphine led to reactive oxygen species (ROS) generation via the mitochondrial permeability transition pore, because the mPTP inhibitor cyclosporin A significantly inhibited ROS generation.
Positive_regulation (Activation) of JNK in pore associated with morphine
1) Confidence 0.68 Published 2009 Journal FEBS J. Section Abstract Doc Link 19292871 Disease Relevance 0.35 Pain Relevance 0.52
Activation of JNK or p38 MAPK by NaSal (or aspirin) was not due to a nonspecific hyperosmotic effect because much higher molar concentrations of sorbitol or NaCl were required to produce a similar activation.
Positive_regulation (Activation) of JNK in molar associated with aspirin
2) Confidence 0.68 Published 1999 Journal J. Cell. Physiol. Section Abstract Doc Link 10082138 Disease Relevance 0.25 Pain Relevance 0.13
Cell-type-specific activation of c-Jun N-terminal kinase by salicylates.
Positive_regulation (activation) of c-Jun N-terminal kinase associated with aspirin
3) Confidence 0.68 Published 1999 Journal J. Cell. Physiol. Section Title Doc Link 10082138 Disease Relevance 0.27 Pain Relevance 0.16
On the other hand, we recently showed that in normal human diploid fibroblasts sodium salicylate (NaSal) elicits activation of p38 MAPK but not activation of c-Jun N-terminal kinase (JNK).
Neg (not) Positive_regulation (activation) of JNK in fibroblasts
4) Confidence 0.68 Published 1999 Journal J. Cell. Physiol. Section Abstract Doc Link 10082138 Disease Relevance 0.25 Pain Relevance 0.11
Activation of JNK and p38 MAPKs may be relevant for some antiinflammatory actions of salicylates.
Positive_regulation (Activation) of JNK associated with inflammation
5) Confidence 0.68 Published 1999 Journal J. Cell. Physiol. Section Abstract Doc Link 10082138 Disease Relevance 0.32 Pain Relevance 0.13
On the other hand, we recently showed that in normal human diploid fibroblasts sodium salicylate (NaSal) elicits activation of p38 MAPK but not activation of c-Jun N-terminal kinase (JNK).
Neg (not) Positive_regulation (activation) of c-Jun N-terminal kinase in fibroblasts
6) Confidence 0.68 Published 1999 Journal J. Cell. Physiol. Section Abstract Doc Link 10082138 Disease Relevance 0.25 Pain Relevance 0.11
Three structurally unrelated nonsteroidal antiinflammatory drugs (ibuprofen, acetaminophen, and indomethacin) failed to induce significant activation of JNK or p38 MAPK, suggesting that cyclooxygenase inhibition is not the underlying mechanism whereby salicylates induce p38 MAPK and JNK activation.
Positive_regulation (activation) of JNK associated with paracetamol and inflammation
7) Confidence 0.68 Published 1999 Journal J. Cell. Physiol. Section Abstract Doc Link 10082138 Disease Relevance 0.22 Pain Relevance 0.14
Three structurally unrelated nonsteroidal antiinflammatory drugs (ibuprofen, acetaminophen, and indomethacin) failed to induce significant activation of JNK or p38 MAPK, suggesting that cyclooxygenase inhibition is not the underlying mechanism whereby salicylates induce p38 MAPK and JNK activation.
Positive_regulation (activation) of JNK associated with paracetamol and inflammation
8) Confidence 0.68 Published 1999 Journal J. Cell. Physiol. Section Abstract Doc Link 10082138 Disease Relevance 0.24 Pain Relevance 0.14
It has been shown to specifically activate MAPK8/JNK and mediate the TNF-alpha signaling pathway [31,32].
Positive_regulation (activate) of JNK
9) Confidence 0.67 Published 2008 Journal BMC Genomics Section Body Doc Link PMC2529314 Disease Relevance 0.82 Pain Relevance 0.03
Sodium salicylate-induced apoptosis of human peripheral blood eosinophils is independent of the activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase.
Positive_regulation (activation) of c-Jun N-terminal kinase in eosinophils associated with apoptosis
10) Confidence 0.66 Published 2000 Journal Int. Arch. Allergy Immunol. Section Title Doc Link 10686508 Disease Relevance 0.66 Pain Relevance 0.08
It could also activate c-Jun N-terminal kinase (JNK) and p38 MAPK but not extracellular signal-regulated protein kinase (ERK) activity within 1 h.
Positive_regulation (activate) of JNK
11) Confidence 0.66 Published 2000 Journal Int. Arch. Allergy Immunol. Section Body Doc Link 10686508 Disease Relevance 0.16 Pain Relevance 0
It could also activate c-Jun N-terminal kinase (JNK) and p38 MAPK but not extracellular signal-regulated protein kinase (ERK) activity within 1 h.
Positive_regulation (activate) of c-Jun N-terminal kinase
12) Confidence 0.66 Published 2000 Journal Int. Arch. Allergy Immunol. Section Body Doc Link 10686508 Disease Relevance 0.16 Pain Relevance 0
Taken together, these data show that activation of JNK is required for H2O2 to promote ?
Positive_regulation (activation) of JNK
13) Confidence 0.64 Published 2008 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2427353 Disease Relevance 0.09 Pain Relevance 0
-secretase activity through activation of JNK.
Positive_regulation (activation) of JNK
14) Confidence 0.64 Published 2008 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2427353 Disease Relevance 0.42 Pain Relevance 0.04
Furthermore, the JNK activation in response to kappa-opioid receptor was suppressed by an autophosphorylation-resistant mutant of focal adhesion kinase (FAK).
Positive_regulation (activation) of JNK associated with kappa opioid receptor and adhesions
15) Confidence 0.56 Published 2004 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 14996948 Disease Relevance 0.17 Pain Relevance 0.47
The participation of small GTPases as well as a guanine nucleotide exchange factor was also implicated because dominant-negative mutants of Rac, Cdc42, and Son-of-sevenless (Sos) attenuated the agonist-induced activation of JNK.
Positive_regulation (activation) of JNK associated with agonist
16) Confidence 0.56 Published 2004 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 14996948 Disease Relevance 0.16 Pain Relevance 0.33
The activation of JNK and p38 was accompanied by large increases in the phosphorylation of the downstream transcription factors cJun and activating transcription factor 2 (ATF-2).
Positive_regulation (activation) of JNK
17) Confidence 0.54 Published 2006 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 16169935 Disease Relevance 0.52 Pain Relevance 0.49
Activation of stress kinase pathways ERK, JNK, and p38 MAPK is a typical feature of chronic synovitis during RA, and several proinflammatory mediators use the signaling of these stress kinase pathways [82].
Positive_regulation (Activation) of JNK associated with stress, synovitis and arthritis
18) Confidence 0.53 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2855702 Disease Relevance 1.49 Pain Relevance 0.55
MAPK8 activation in adipose tissue can cause insulin resistance in the liver [75].


Positive_regulation (activation) of MAPK8 in liver associated with obesity and insulin resistance
19) Confidence 0.53 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2855702 Disease Relevance 0.96 Pain Relevance 0
Cell cycle inhibition has been explained by activation of the c-Jun-N-terminal kinase (JNK) and downregulation of cyclin D1 expression.
Positive_regulation (activation) of c-Jun-N-terminal kinase
20) Confidence 0.53 Published 2005 Journal Biochem. Pharmacol. Section Abstract Doc Link 15710360 Disease Relevance 0.67 Pain Relevance 0.14

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