INT109928

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Context Info
Confidence 0.42
First Reported 2003
Last Reported 2010
Negated 1
Speculated 2
Reported most in Body
Documents 19
Total Number 21
Disease Relevance 10.42
Pain Relevance 5.23

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
macrophages 2
THP-1 2
fibroblasts 2
MAPK8 (Homo sapiens)
Pain Link Frequency Relevance Heat
agonist 41 100.00 Very High Very High Very High
Paracetamol 8 100.00 Very High Very High Very High
cINOD 16 99.88 Very High Very High Very High
Morphine 10 99.84 Very High Very High Very High
Leflunomide 8 99.74 Very High Very High Very High
dexamethasone 15 99.38 Very High Very High Very High
Nicotine 96 98.90 Very High Very High Very High
adenocard 3 98.24 Very High Very High Very High
Inflammation 103 97.72 Very High Very High Very High
Kappa opioid receptor 16 95.36 Very High Very High Very High
Disease Link Frequency Relevance Heat
Stress 139 100.00 Very High Very High Very High
Vibrio Infection 1 99.44 Very High Very High Very High
Apoptosis 227 99.12 Very High Very High Very High
INFLAMMATION 121 98.88 Very High Very High Very High
Disease 213 98.48 Very High Very High Very High
Death 76 97.96 Very High Very High Very High
Shock 10 96.90 Very High Very High Very High
Injury 11 93.40 High High
Infection 20 91.20 High High
Colon Cancer 5 89.88 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
ROS in turn exerted feedback regulation on JNK activation, as shown by the observations that cyclosporin A and the antioxidant N-acetylcysteine significantly inhibited the phosphorylation of JNK induced by morphine.
Negative_regulation (inhibited) of Positive_regulation (induced) of JNK associated with morphine
1) Confidence 0.42 Published 2009 Journal FEBS J. Section Abstract Doc Link 19292871 Disease Relevance 0.38 Pain Relevance 0.75
In addition, anti-inflammatory drugs dexamethasone (DEX) and cyclosporin A (CSA) both blocked activation of JNKS/SAPK and the cell-cell contact induced production of hRPE IL-8 and MCP-1, while activation of p38 and ERK was only inhibited by DEX, but not by CSA.
Negative_regulation (blocked) of Positive_regulation (activation) of JNK associated with inflammation, cinod and dexamethasone
2) Confidence 0.41 Published 2003 Journal Exp. Eye Res. Section Abstract Doc Link 12697421 Disease Relevance 0.15 Pain Relevance 0.40
Instead, we demonstrate that leflunomide (20 microM) inhibited the APAP-induced early (3 h) activation (phosphorylation) of JNK1/2, thus inhibiting phosphorylation of the anti-apoptotic protein Bcl-2 and preventing P-Bcl-2-mediated induction of the mPT.
Negative_regulation (inhibited) of Positive_regulation (activation) of JNK associated with paracetamol, leflunomide and apoptosis
3) Confidence 0.41 Published 2006 Journal Toxicol. Appl. Pharmacol. Section Abstract Doc Link 16979204 Disease Relevance 0.75 Pain Relevance 0.97
Consistently, pretreatment with JNK inhibitor SP600125 also decreased JNK activation (Fig. 5B, lane 4).
Negative_regulation (decreased) of Positive_regulation (activation) of JNK
4) Confidence 0.39 Published 2008 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2427353 Disease Relevance 0.20 Pain Relevance 0
The Pa-PDT induced apoptosis is started by the collapse of mitochondria which is facilitated by JNK, according to Figure 4B, the degree of mitochondrial membrane potential change was reduced significantly when activation of JNK was inhibited.
Negative_regulation (inhibited) of Positive_regulation (activation) of JNK associated with shock and apoptosis
5) Confidence 0.36 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2731730 Disease Relevance 0.99 Pain Relevance 0
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.
Negative_regulation (attenuated) of Positive_regulation (activation) of JNK associated with agonist
6) Confidence 0.35 Published 2004 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 14996948 Disease Relevance 0.16 Pain Relevance 0.34
Thus we pre-treated both cell types with the JNK inhibitor SP 600125 to test whether blocking JNK activation by oxidative stress would rescue the AD fibroblasts.
Spec (whether) Negative_regulation (blocking) of Spec (whether) Positive_regulation (activation) of JNK in fibroblasts associated with stress and disease
7) Confidence 0.34 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2644820 Disease Relevance 1.93 Pain Relevance 0
In both THP-1 and transfected COS-7 cells, pretreatment of the selective Src family kinase inhibitor pyrazolopyrimidine PP1 abolished the JNK activation, whereas the epidermal growth factor receptor inhibitor AG1478 [N-(3-chlorophenyl)-6,7-dimethoxy-4-quinazolinanine] failed to do that.
Negative_regulation (abolished) of Positive_regulation (activation) of JNK in THP-1
8) Confidence 0.34 Published 2004 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 14996948 Disease Relevance 0.15 Pain Relevance 0.42
Thus, Pa treatment is able to inhibit the P-glycoprotein mediated MDR via JNK activation when PDT illumination was applied in R-HepG2 cells.


Negative_regulation (inhibit) of Positive_regulation (activation) of JNK
9) Confidence 0.27 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2731730 Disease Relevance 0.59 Pain Relevance 0
This is associated with phosphorylation of the protein VASP, a marker of PKG activation, activation of JNK1 and a decrease in cellular levels of cyclin D1; effects seen with other agents that cause activation of PKG in these cells.
Negative_regulation (decrease) of Positive_regulation (activation) of JNK1
10) Confidence 0.26 Published 2008 Journal Mol. Carcinog. Section Abstract Doc Link 18163459 Disease Relevance 0.39 Pain Relevance 0.22
Studies assessing JNK activation in response to GPCRs are limited; however, it has been shown that free ??
Negative_regulation (limited) of Positive_regulation (activation) of JNK
11) Confidence 0.21 Published 2010 Journal Cellular Signalling Section Body Doc Link PMC2806525 Disease Relevance 0 Pain Relevance 0.28
B [29], the overall outcome of PAR2/TNFR1 is a loss in JNK activation only.
Negative_regulation (loss) of Positive_regulation (activation) of JNK
12) Confidence 0.21 Published 2010 Journal Cellular Signalling Section Body Doc Link PMC2806525 Disease Relevance 0.06 Pain Relevance 0
No decrease was observed in interleukin-1beta-induced p38 mitogen-activated protein kinase, extracellular signal-related kinase or cJun N-terminal kinase activation.
Neg (No) Negative_regulation (decrease) of Positive_regulation (activation) of cJun N-terminal kinase
13) Confidence 0.21 Published 2003 Journal Eur. Respir. J. Section Abstract Doc Link 12952251 Disease Relevance 0 Pain Relevance 0.22
In order to link the activation of JNK to nicotine-induced up-regulation of kinin B1 and B2 receptors, a specific JNK inhibitor SP600125 (10 ?
Negative_regulation (inhibitor) of Positive_regulation (specific) of JNK associated with nicotine
14) Confidence 0.19 Published 2010 Journal Respir Res Section Body Doc Link PMC2845563 Disease Relevance 0.07 Pain Relevance 0.63
However, when cells were treated with a combination of SP600125 (1 hour) and TJ-41 (47 hours), the percentage of cells undergoing apoptosis was dramatically lower than those with TJ-41alone, indicating that inhibition of JNK activation protects against the apoptotic effects of TJ-41.
Negative_regulation (inhibition) of Positive_regulation (activation) of JNK associated with apoptosis
15) Confidence 0.19 Published 2009 Journal Journal of Oncology Section Body Doc Link PMC2730474 Disease Relevance 0.98 Pain Relevance 0
In more precise investigation with specific JNK inhibitor SP600215, we further showed that the combination treatment of JNK inhibitor with bee venom and melittin suppressed inhibitory effects of melittin and bee venom on the LPS and SNP-induced NO and PGE2 release with the suppressed effect on the inhibitory effect of melittin and bee venom on the NF-?
Negative_regulation (inhibitor) of Positive_regulation (specific) of JNK
16) Confidence 0.11 Published 2008 Journal J Inflamm (Lond) Section Body Doc Link PMC2442592 Disease Relevance 0.33 Pain Relevance 0.16
The same inhibitors were then used to determine the functional role of p38 and JNK in TNF-?
Spec (determine) Negative_regulation (determine) of Spec (determine) Positive_regulation (role) of JNK
17) Confidence 0.08 Published 2010 Journal Molecular Vision Section Body Doc Link PMC2838737 Disease Relevance 1.27 Pain Relevance 0
To examine the functional role of parthenolide induced surface protein thiol modification, we pretreated Granta cells with cell impermeable glutathione (GSH), prior to exposure to parthenolide, and showed that GSH pretreatment; (a) inhibited the interaction of parthenolide with exofacial thiols; (b) inhibited parthenolide mediated activation of JNK and inhibition of NF?
Negative_regulation (inhibition) of Positive_regulation (activation) of JNK
18) Confidence 0.08 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2780735 Disease Relevance 0.38 Pain Relevance 0
To examine the functional role of parthenolide induced surface protein thiol modification, we pretreated Granta cells with cell impermeable glutathione (GSH), prior to exposure to parthenolide, and showed that GSH pretreatment; (a) inhibited the interaction of parthenolide with exofacial thiols; (b) inhibited parthenolide mediated activation of JNK and inhibition of NF?
Negative_regulation (inhibited) of Positive_regulation (activation) of JNK
19) Confidence 0.08 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2780735 Disease Relevance 0.39 Pain Relevance 0
The results show that nonselective and COX-1-selective NSAIDs also block activation of the stress kinase c-Jun N-terminal kinase (JNK) and that prostaglandin-E2 (PGE2) reverses this block and enhances TCR-dependent JNK activation.
Negative_regulation (block) of Positive_regulation (activation) of c-Jun N-terminal kinase associated with stress and cinod
20) Confidence 0.07 Published 2005 Journal Blood Section Abstract Doc Link 15514010 Disease Relevance 0.59 Pain Relevance 0.70

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