INT135291

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Context Info
Confidence 0.64
First Reported 2004
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 24
Total Number 26
Disease Relevance 19.37
Pain Relevance 5.16

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
macrophages 4
PGE2 2
Mapk8 (Mus musculus)
Pain Link Frequency Relevance Heat
cytokine 83 100.00 Very High Very High Very High
Paracetamol 48 100.00 Very High Very High Very High
Taxol 3 100.00 Very High Very High Very High
long-term potentiation 114 99.12 Very High Very High Very High
Anterior cingulate cortex 34 98.68 Very High Very High Very High
antagonist 11 96.92 Very High Very High Very High
psoriasis 63 88.80 High High
Inflammation 199 87.00 High High
Pyramidal cell 5 84.08 Quite High
Kinase C 41 79.40 Quite High
Disease Link Frequency Relevance Heat
Stress 161 100.00 Very High Very High Very High
Insulin Resistance 132 100.00 Very High Very High Very High
Death 210 99.92 Very High Very High Very High
Diabetes Mellitus 79 99.68 Very High Very High Very High
Apoptosis 861 99.32 Very High Very High Very High
Toxicity 58 99.28 Very High Very High Very High
Retinoblastoma 5 99.18 Very High Very High Very High
Hepatocellular Cancer 208 98.84 Very High Very High Very High
Cancer 270 98.44 Very High Very High Very High
Hyperplasia 16 98.40 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
were correlated with increased ROS accumulation, which led to JNK and STAT3 activation.
Positive_regulation (led) of Positive_regulation (activation) of JNK
1) Confidence 0.64 Published 2010 Journal Gastroenterology Research and Practice Section Body Doc Link PMC2995932 Disease Relevance 1.22 Pain Relevance 0.07
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).
Positive_regulation (induced) of Positive_regulation (activation) of JNK in PGE2 associated with antagonist
2) Confidence 0.54 Published 2006 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 16644903 Disease Relevance 0.39 Pain Relevance 0.47
In our mouse model of smoke inhalation injury, we found that smoke inhalation induced the mucus overproduction was associated with an increase in epithelial MUC5AC protein expression, and this was dependent on the activation of the JNK pathway.
Positive_regulation (dependent) of Positive_regulation (activation) of JNK associated with smoke inhalation injury
3) Confidence 0.47 Published 2010 Journal Respir Res Section Body Doc Link PMC3014901 Disease Relevance 0.50 Pain Relevance 0.07
Enhanced JNK activation in the absence of IKK?
Positive_regulation (Enhanced) of Positive_regulation (activation) of JNK
4) Confidence 0.46 Published 2010 Journal Gastroenterology Research and Practice Section Body Doc Link PMC2995932 Disease Relevance 1.19 Pain Relevance 0.11
These results suggest that increased ROS and ROS-mediated JNK activation is a critical regulator for HCC development (Figure 3).
Positive_regulation (increased) of Positive_regulation (activation) of JNK associated with hepatocellular cancer
5) Confidence 0.46 Published 2010 Journal Gastroenterology Research and Practice Section Body Doc Link PMC2995932 Disease Relevance 1.30 Pain Relevance 0.10
In fact, enhanced JNK activation in IKK?
Positive_regulation (enhanced) of Positive_regulation (activation) of JNK
6) Confidence 0.46 Published 2010 Journal Gastroenterology Research and Practice Section Body Doc Link PMC2995932 Disease Relevance 0.92 Pain Relevance 0.04
Transfection with JNK siRNA attenuated APAP toxicity after 24 h, suggesting that higher levels of APAP-induced activation of JNK were related to higher rates of cell death.
Positive_regulation (induced) of Positive_regulation (activation) of JNK associated with toxicity, paracetamol and death
7) Confidence 0.45 Published 2010 Journal Toxicol. Sci. Section Abstract Doc Link 20363829 Disease Relevance 0.31 Pain Relevance 0.84
Transfection with JNK siRNA attenuated APAP toxicity after 24 h, suggesting that higher levels of APAP-induced activation of JNK were related to higher rates of cell death.
Positive_regulation (levels) of Positive_regulation (activation) of JNK associated with toxicity, paracetamol and death
8) Confidence 0.45 Published 2010 Journal Toxicol. Sci. Section Abstract Doc Link 20363829 Disease Relevance 0.31 Pain Relevance 0.84
Pre-treatment with TNF-alpha resulted in prolonged activation of JNK (upto 2 hr) in the presence of APAP or CPZ.
Positive_regulation (resulted) of Positive_regulation (activation) of JNK associated with paracetamol
9) Confidence 0.45 Published 2010 Journal J Toxicol Sci Section Abstract Doc Link 20371967 Disease Relevance 0.95 Pain Relevance 1.04
In DU145 cells normally deficient of the Retinoblastoma (Rb) gene, reactivation of this gene is required for gamma irradiation induced JNK phosphorylation.
Positive_regulation (required) of Positive_regulation (induced) of JNK associated with retinoblastoma
10) Confidence 0.40 Published 2004 Journal Cell Commun Signal Section Body Doc Link PMC449737 Disease Relevance 0.76 Pain Relevance 0.03
JNK is generally activated by cellular stress, however, numerous molecules are able to phosphorylate the enzyme [Table 3]. 2-methoxyestradiol (ME), an endogenous metabolite of estradiol, can synergize with taxol to increase JNK activation and enhance the apoptotic effect of this chemotherapeutic agent [56].
Positive_regulation (synergize) of Positive_regulation (activation) of JNK associated with stress, apoptosis and taxol
11) Confidence 0.37 Published 2004 Journal Cell Commun Signal Section Body Doc Link PMC449737 Disease Relevance 0.90 Pain Relevance 0.05
JNK is generally activated by cellular stress, however, numerous molecules are able to phosphorylate the enzyme [Table 3]. 2-methoxyestradiol (ME), an endogenous metabolite of estradiol, can synergize with taxol to increase JNK activation and enhance the apoptotic effect of this chemotherapeutic agent [56].
Positive_regulation (increase) of Positive_regulation (activation) of JNK associated with stress, apoptosis and taxol
12) Confidence 0.37 Published 2004 Journal Cell Commun Signal Section Body Doc Link PMC449737 Disease Relevance 0.89 Pain Relevance 0.05
Excessive FFAs induce hepatic insulin resistance by activation of c-Jun N-terminal protein kinase (JNK), which is known to be activated by oxidative stress and cytokines, and is abnormally elevated in the diabetics [7, 65].
Positive_regulation (induce) of Positive_regulation (activated) of JNK associated with stress, diabetes mellitus, insulin resistance and cytokine
13) Confidence 0.37 Published 2009 Journal PPAR Research Section Body Doc Link PMC2840373 Disease Relevance 0.61 Pain Relevance 0.08
Excessive FFAs induce hepatic insulin resistance by activation of c-Jun N-terminal protein kinase (JNK), which is known to be activated by oxidative stress and cytokines, and is abnormally elevated in the diabetics [7, 65].
Positive_regulation (induce) of Positive_regulation (activation) of c-Jun N-terminal protein kinase associated with stress, diabetes mellitus, insulin resistance and cytokine
14) Confidence 0.37 Published 2009 Journal PPAR Research Section Body Doc Link PMC2840373 Disease Relevance 0.60 Pain Relevance 0.08
Excessive FFAs induce hepatic insulin resistance by activation of c-Jun N-terminal protein kinase (JNK), which is known to be activated by oxidative stress and cytokines, and is abnormally elevated in the diabetics [7, 65].
Positive_regulation (elevated) of Positive_regulation (activated) of JNK associated with stress, diabetes mellitus, insulin resistance and cytokine
15) Confidence 0.37 Published 2009 Journal PPAR Research Section Body Doc Link PMC2840373 Disease Relevance 0.67 Pain Relevance 0.08
Excessive FFAs induce hepatic insulin resistance by activation of c-Jun N-terminal protein kinase (JNK), which is known to be activated by oxidative stress and cytokines, and is abnormally elevated in the diabetics [7, 65].
Positive_regulation (elevated) of Positive_regulation (activation) of c-Jun N-terminal protein kinase associated with stress, diabetes mellitus, insulin resistance and cytokine
16) Confidence 0.37 Published 2009 Journal PPAR Research Section Body Doc Link PMC2840373 Disease Relevance 0.67 Pain Relevance 0.08
Apoptosis signal-regulating kinase 1 (ASK1) is a member of the mitogen-activated protein kinase kinase kinase family and is important for stress-induced JNK activation.
Positive_regulation (important) of Positive_regulation (activation) of JNK associated with stress
17) Confidence 0.36 Published 2008 Journal Gastroenterology Section Abstract Doc Link 18700144 Disease Relevance 0.61 Pain Relevance 0.43
These results suggest that the activation of MAPK including ERK, JNK and p38, is critical for the induction of LTP in the ACC.


Positive_regulation (critical) of Positive_regulation (activation) of JNK associated with long-term potentiation and anterior cingulate cortex
18) Confidence 0.31 Published 2007 Journal Mol Pain Section Body Doc Link PMC2245920 Disease Relevance 0 Pain Relevance 0.39
These results indicate that ROS-induced JNK activation is at least in part involved in the pathogenesis of hepatic insulin resistance, through the activation of CREB.


Positive_regulation (induced) of Positive_regulation (activation) of JNK associated with insulin resistance
19) Confidence 0.24 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.46 Pain Relevance 0
Our further analysis of the PB-mediated sensitizing effects demonstrated that PB significantly enhanced the gemcitabine-mediated activation of JNK.
Positive_regulation (enhanced) of Positive_regulation (activation) of JNK
20) Confidence 0.22 Published 2006 Journal J Carcinog Section Body Doc Link PMC1665446 Disease Relevance 0.99 Pain Relevance 0

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