INT110755

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Context Info
Confidence 0.46
First Reported 2003
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 15
Total Number 15
Disease Relevance 9.91
Pain Relevance 2.98

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
liver 2
skin 2
PGE2 2
hippocampus 2
Mapk8 (Mus musculus)
Pain Link Frequency Relevance Heat
Paracetamol 23 100.00 Very High Very High Very High
Leflunomide 10 99.98 Very High Very High Very High
antagonist 7 98.76 Very High Very High Very High
Hippocampus 31 97.00 Very High Very High Very High
Inflammatory response 14 93.28 High High
Neuropathic pain 2 87.52 High High
Glutamate 17 84.96 Quite High
ischemia 9 84.24 Quite High
Kinase C 41 81.76 Quite High
Inflammation 88 78.72 Quite High
Disease Link Frequency Relevance Heat
Stress 88 99.32 Very High Very High Very High
Apoptosis 239 99.28 Very High Very High Very High
Toxicity 21 98.90 Very High Very High Very High
Skin Cancer 2 98.52 Very High Very High Very High
Pressure And Volume Under Development 19 97.88 Very High Very High Very High
Brain Injury 5 97.32 Very High Very High Very High
Disease 251 96.52 Very High Very High Very High
Reprotox - General 1 117 96.46 Very High Very High Very High
Death 114 96.44 Very High Very High Very High
Insulin Resistance 40 95.36 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Another study showed that over expression of MKP-1 and DU145 cells blocked the activation of JNK [69].
Negative_regulation (blocked) of Positive_regulation (activation) of JNK
1) Confidence 0.46 Published 2004 Journal Cell Commun Signal Section Body Doc Link PMC449737 Disease Relevance 0.50 Pain Relevance 0
In conclusion, these findings suggest that extramitochondrial glutathione depletion alters the thiol-disulfide redox state, leading to inhibition of NF-kappaB transactivation of survival genes and to sustained activation of JNK, both of which contribute to the sensitization to TNF-induced apoptosis.
Negative_regulation (inhibition) of Positive_regulation (activation) of JNK associated with apoptosis
2) Confidence 0.40 Published 2003 Journal Hepatology Section Abstract Doc Link 12774022 Disease Relevance 0.73 Pain Relevance 0.14
Ras causes activation of a Raf-independent MAPK cascade, which leads to JNK activation [57], and inhibition of JNK activation also inhibits Ras transformation in NIH3T3 cells [58].
Negative_regulation (inhibition) of Positive_regulation (activation) of JNK
3) Confidence 0.40 Published 2010 Journal Gastroenterology Research and Practice Section Body Doc Link PMC2995932 Disease Relevance 0.91 Pain Relevance 0.05
As mentioned previously, arachidonate 5-lipoxygenase which converts arachidonic acid to 5-HETE provides a substrate that appears to prevent JNK activation [59].
Negative_regulation (prevent) of Positive_regulation (activation) of JNK
4) Confidence 0.34 Published 2004 Journal Cell Commun Signal Section Body Doc Link PMC449737 Disease Relevance 0.59 Pain Relevance 0
Numerous other agents have been studied regarding JNK activation in prostate cancer cell lines and these include the following: Ghosh et al showed that inhibition of arachidonate 5-lipoxygenase (an enzyme that converts arachidonic acid to 5-HETE) caused rapid depletion of 5-HETE and activation of JNK, which triggered apoptosis in LNCaP and PC3 cells [59].
Negative_regulation (depletion) of Positive_regulation (activation) of JNK associated with apoptosis and reprotox - general 1
5) Confidence 0.34 Published 2004 Journal Cell Commun Signal Section Body Doc Link PMC449737 Disease Relevance 0.81 Pain Relevance 0.07
RESULTS: In ASK1(-/-) mouse liver, APAP toxicity was attenuated significantly and the prolonged activation of JNK was inhibited.
Negative_regulation (inhibited) of Positive_regulation (activation) of JNK in liver
6) Confidence 0.34 Published 2008 Journal Gastroenterology Section Body Doc Link 18700144 Disease Relevance 0.16 Pain Relevance 0
The i.pl. injection of PGE2 (3 nmol/paw) induced a significant activation of MAPKs, namely, JNK and p38, an effect that was largely prevented by the selective EP3 receptor antagonist L826266 (10 nmol/paw).
Negative_regulation (prevented) of Positive_regulation (induced) of JNK in PGE2 associated with antagonist
7) Confidence 0.33 Published 2006 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 16644903 Disease Relevance 0.39 Pain Relevance 0.48
These results suggest that the KD suppresses KA-induced activation of JNK signaling pathways, followed by a decrease of PENK gene expression in the hippocampus, thereby resulting in antiepileptic effects.
Negative_regulation (suppresses) of Positive_regulation (activation) of JNK in hippocampus associated with hippocampus
8) Confidence 0.29 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16300887 Disease Relevance 0.06 Pain Relevance 0.24
Instead, leflunomide inhibited APAP-induced activation (phosphorylation) of c-jun NH2-terminal protein kinase (JNK), thus preventing downstream Bcl-2 and Bcl-XL inactivation and protecting from mitochondrial permeabilization and cytochrome c release.
Negative_regulation (inhibited) of Positive_regulation (activation) of JNK associated with paracetamol and leflunomide
9) Confidence 0.28 Published 2007 Journal Hepatology Section Abstract Doc Link 17366662 Disease Relevance 0.51 Pain Relevance 1.37
It is now known that the activation of JNK is prevented by cellular protective actions of Hsp72 [20], [21], [22] and this implies a possible role of Hsp72 in ameliorating insulin resistance (reviewed in [23]).
Negative_regulation (prevented) of Positive_regulation (activation) of JNK associated with insulin resistance
10) Confidence 0.25 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2603588 Disease Relevance 1.02 Pain Relevance 0
This is mediated by its inhibition of JNK activation [15, 108, 109].
Negative_regulation (inhibition) of Positive_regulation (activation) of JNK
11) Confidence 0.18 Published 2011 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2992819 Disease Relevance 0.90 Pain Relevance 0.36
It has been shown in rats that rosiglitazone inhibits the activation of JNK and AP-1 after myocardial IR [62].
Negative_regulation (inhibits) of Positive_regulation (activation) of JNK
12) Confidence 0.10 Published 2010 Journal PPAR Research Section Body Doc Link PMC2931381 Disease Relevance 1.60 Pain Relevance 0.21
In addition to suppressing TNF-induced activation of AP-1 in a variety of cells, inhibiting TPA-induced expression of c-Fos and c-Jun in mouse skin, and inhibiting anchorage-independent growth of melanoma cells [18-20], resveratrol suppressed TPA-induced expression of MMP-9 by inhibition of AP-1 activation through c-Jun N-terminal kinase (JNK) and PKC-delta pathways [26] and protected against 4-hydroxynonenal-induced apoptosis by blocking AP-1 signaling through JNK [27].
Negative_regulation (inhibition) of Positive_regulation (activation) of JNK in skin associated with apoptosis and skin cancer
13) Confidence 0.09 Published 2008 Journal BMC Pharmacol Section Body Doc Link PMC2632638 Disease Relevance 0.28 Pain Relevance 0
toxicity occurs through the activation of ERK and AKT/PKB and the prevention of c-Jun N-terminal kinase (JNK) activation in a PI3K-dependent manner [74, 83].
Negative_regulation (prevention) of Positive_regulation (activation) of JNK associated with toxicity
14) Confidence 0.07 Published 2010 Journal The Open Biochemistry Journal Section Body Doc Link PMC2864432 Disease Relevance 0.73 Pain Relevance 0.03
- toxicity and oxidative stress [152] by a mechanism mediated by reduced PI3K/Akt signaling and JNK/p53 activation, thus providing a link between NGF deprivation and the two pathological components of AD.
Negative_regulation (reduced) of Positive_regulation (activation) of JNK associated with stress, toxicity and disease
15) Confidence 0.03 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1775042 Disease Relevance 0.72 Pain Relevance 0.04

General Comments

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