INT80686

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Context Info
Confidence 0.68
First Reported 1999
Last Reported 2010
Negated 4
Speculated 3
Reported most in Abstract
Documents 42
Total Number 48
Disease Relevance 26.95
Pain Relevance 7.63

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 12
epithelial cells 6
chondrocytes 2
skeletal muscle 2
nucleus 2
MAPK8 (Homo sapiens)
Pain Link Frequency Relevance Heat
agonist 92 100.00 Very High Very High Very High
Nicotine 192 99.98 Very High Very High Very High
Sciatic nerve 8 99.42 Very High Very High Very High
Paracetamol 10 99.40 Very High Very High Very High
rheumatoid arthritis 133 99.20 Very High Very High Very High
bradykinin 457 99.06 Very High Very High Very High
chemokine 57 98.96 Very High Very High Very High
Spinal cord 9 98.56 Very High Very High Very High
Osteoarthritis 78 98.20 Very High Very High Very High
cytokine 209 98.04 Very High Very High Very High
Disease Link Frequency Relevance Heat
Death 260 100.00 Very High Very High Very High
Insulin Resistance 41 100.00 Very High Very High Very High
Stress 814 99.98 Very High Very High Very High
Disease 1088 99.84 Very High Very High Very High
Colorectal Cancer 8 99.42 Very High Very High Very High
Rheumatoid Arthritis 178 99.20 Very High Very High Very High
INFLAMMATION 640 98.76 Very High Very High Very High
Osteoarthritis 46 98.20 Very High Very High Very High
Osteoporosis 42 98.10 Very High Very High Very High
Obesity 247 97.68 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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).
Positive_regulation (activation) of Neg (not) Positive_regulation (activation) of c-Jun N-terminal kinase in fibroblasts
1) Confidence 0.68 Published 1999 Journal J. Cell. Physiol. Section Abstract Doc Link 10082138 Disease Relevance 0.25 Pain Relevance 0.11
To further validate whether the increased activation of JNK-mediated downregulation of VEGF-C is dependent on podoplanin, the levels of phosphorylated JNK and VEGF-C mRNA were examined using siRNA methods.
Spec (whether) Positive_regulation (increased) of Spec (whether) Positive_regulation (activation) of JNK
2) Confidence 0.50 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2987985 Disease Relevance 0 Pain Relevance 0
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).
Positive_regulation (activation) of Neg (not) Positive_regulation (activation) of JNK in fibroblasts
3) Confidence 0.49 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.
Neg (failed) Positive_regulation (induce) of Positive_regulation (activation) of JNK associated with paracetamol and inflammation
4) Confidence 0.49 Published 1999 Journal J. Cell. Physiol. Section Abstract Doc Link 10082138 Disease Relevance 0.24 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 (induce) of Positive_regulation (activation) of JNK associated with paracetamol and inflammation
5) Confidence 0.49 Published 1999 Journal J. Cell. Physiol. Section Abstract Doc Link 10082138 Disease Relevance 0.23 Pain Relevance 0.14
The similarity of proteolytic process between wild type APP and APP(T668A) mutant suggests that H2O2-induced, JNK-dependent augmentation of ?
Positive_regulation (augmentation) of Positive_regulation (induced) of JNK
6) Confidence 0.46 Published 2008 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2427353 Disease Relevance 0.09 Pain Relevance 0
Next, we wondered whether JNK activation is required for H2O2 to promote ?
Spec (whether) Positive_regulation (required) of Spec (whether) Positive_regulation (activation) of JNK
7) Confidence 0.46 Published 2008 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2427353 Disease Relevance 0.19 Pain Relevance 0
Taken together, these data show that activation of JNK is required for H2O2 to promote ?
Positive_regulation (required) of Positive_regulation (activation) of JNK
8) Confidence 0.46 Published 2008 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2427353 Disease Relevance 0.09 Pain Relevance 0
Sciatic nerve transection in rats rapidly induced JNK1 activation and
                       upregulation of mRNA and protein expression of WOX1 in the injured DRG
                       neurons in 30 min. 
Positive_regulation (induced) of Positive_regulation (activation) of JNK1 in neurons associated with sciatic nerve
9) Confidence 0.45 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2771921 Disease Relevance 0.38 Pain Relevance 0.05
In the PS-1 M146L AD human skin fibroblasts whose aberrant BK signaling was the strongest, oxidative stress induced a massive enhancement of JNK activation concomitant with lagging p38 and ERK activation.
Positive_regulation (induced) of Positive_regulation (activation) of JNK in fibroblasts associated with stress, disease and bradykinin
10) Confidence 0.41 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2644820 Disease Relevance 1.83 Pain Relevance 0.28
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 (agonist-induced) of Positive_regulation (activation) of JNK associated with agonist
11) Confidence 0.40 Published 2004 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 14996948 Disease Relevance 0.16 Pain Relevance 0.33
Western blotting revealed the activation of extracellular signal-regulated kinase (ERK), p38 MAPK, and c-Jun N-terminal kinase (JNK) with indomethacin treatment.
Positive_regulation (revealed) of Positive_regulation (activation) of c-Jun N-terminal kinase
12) Confidence 0.38 Published 2007 Journal Eur. J. Pharmacol. Section Abstract Doc Link 17341418 Disease Relevance 1.02 Pain Relevance 0.18
Western blotting revealed the activation of extracellular signal-regulated kinase (ERK), p38 MAPK, and c-Jun N-terminal kinase (JNK) with indomethacin treatment.
Positive_regulation (revealed) of Positive_regulation (activation) of JNK
13) Confidence 0.38 Published 2007 Journal Eur. J. Pharmacol. Section Abstract Doc Link 17341418 Disease Relevance 1.02 Pain Relevance 0.18
Taken together, these findings suggested that the podoplanin-mediated increase in the level of activated JNK was a downregulation signal for the VEGF-C gene in EBC-1 cells.
Positive_regulation (increase) of Positive_regulation (increase) of JNK
14) Confidence 0.36 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2987985 Disease Relevance 0.08 Pain Relevance 0
Podoplanin-induced VEGF-C downregulation is mediated by an increase in the level of activated JNK in LSCCs
Positive_regulation (increase) of Positive_regulation (activated) of JNK
15) Confidence 0.36 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2987985 Disease Relevance 0.38 Pain Relevance 0
Podoplanin-induced VEGF-C downregulation is mediated by an increase in the level of activated JNK in LSCCs
Positive_regulation (mediated) of Positive_regulation (increase) of JNK
16) Confidence 0.36 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2987985 Disease Relevance 0.39 Pain Relevance 0
Intracellular Ca(2+) triggered the activation of mitogen-activated protein kinase (MAPK) in HMC-1, especially p42 and p44 isoforms of extracellular signal-regulated kinase (ERK) and p38 MAPK, but not c-Jun N-terminal kinase (JNK).
Positive_regulation (triggered) of Positive_regulation (activation) of c-Jun N-terminal kinase
17) Confidence 0.36 Published 2005 Journal Cytokine Section Abstract Doc Link 16343928 Disease Relevance 0.17 Pain Relevance 0.21
Intracellular Ca(2+) triggered the activation of mitogen-activated protein kinase (MAPK) in HMC-1, especially p42 and p44 isoforms of extracellular signal-regulated kinase (ERK) and p38 MAPK, but not c-Jun N-terminal kinase (JNK).
Positive_regulation (triggered) of Positive_regulation (activation) of JNK
18) Confidence 0.36 Published 2005 Journal Cytokine Section Abstract Doc Link 16343928 Disease Relevance 0.17 Pain Relevance 0.21
Treatment of HT29 colorectal carcinoma cells with 75 microM NS-398 caused activation of ERK-1/-2 but not of the p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinases.
Positive_regulation (caused) of Positive_regulation (activation) of JNK associated with colorectal cancer
19) Confidence 0.36 Published 2002 Journal Int. J. Cancer Section Abstract Doc Link 11992399 Disease Relevance 0.65 Pain Relevance 0.20
Treatment of HT29 colorectal carcinoma cells with 75 microM NS-398 caused activation of ERK-1/-2 but not of the p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinases.
Positive_regulation (caused) of Positive_regulation (activation) of c-Jun N-terminal kinase associated with colorectal cancer
20) Confidence 0.36 Published 2002 Journal Int. J. Cancer Section Abstract Doc Link 11992399 Disease Relevance 0.65 Pain Relevance 0.20

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