INT125079

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Context Info
Confidence 0.39
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 9
Total Number 9
Disease Relevance 4.87
Pain Relevance 1.25

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
brains 4
MAPK8 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammatory stimuli 7 99.26 Very High Very High Very High
rheumatoid arthritis 70 93.84 High High
Inflammation 115 92.16 High High
cINOD 4 89.32 High High
Inflammatory response 7 86.08 High High
Osteoarthritis 86 84.00 Quite High
Hippocampus 3 83.00 Quite High
Arthritis 47 67.20 Quite High
Rheumatism 3 66.40 Quite High
Inflammatory mediators 11 65.68 Quite High
Disease Link Frequency Relevance Heat
Amyloid Plaque 105 100.00 Very High Very High Very High
INFLAMMATION 143 99.10 Very High Very High Very High
Alzheimer's Dementia 108 98.98 Very High Very High Very High
Malaria 3 98.16 Very High Very High Very High
Apoptosis 26 96.44 Very High Very High Very High
Rheumatoid Arthritis 70 93.84 High High
Colon Cancer 2 91.20 High High
Cancer 16 90.68 High High
Renal Disease 3 87.80 High High
Disease 30 85.52 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To determine the link between amyloid deposits and JNK activation, we performed an immunostaining in brains of the AD animal model (Tg2576 mice) and found that phospho-JNK immunoreactivity was localized in the surrounding region of senile plaques, which was positive with A?
Negative_regulation (deposits) of Gene_expression (activation) of JNK in brains associated with alzheimer's dementia and amyloid plaque
1) Confidence 0.39 Published 2008 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2427353 Disease Relevance 0.84 Pain Relevance 0.04
To determine the link between amyloid deposits and JNK activation, we performed an immunostaining in brains of the AD animal model (Tg2576 mice) and found that phospho-JNK immunoreactivity was localized in the surrounding region of senile plaques, which was positive with A?
Negative_regulation (localized) of Gene_expression (immunoreactivity) of JNK in brains associated with alzheimer's dementia and amyloid plaque
2) Confidence 0.39 Published 2008 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2427353 Disease Relevance 0.89 Pain Relevance 0.04
Furthermore, silencing of JNK expression by siJNKs (24), which efficiently reduced the endogenous JNK protein level (Fig. 5E) but not the control siRNA, decreased H2O2-induced AICD level (Fig. 5E, compare lanes 4 and 6 to lane 2).
Neg (not) Negative_regulation (reduced) of Gene_expression (expression) of JNK
3) Confidence 0.39 Published 2008 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2427353 Disease Relevance 0.10 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.
Negative_regulation (downregulation) of Gene_expression (expression) of JNK
4) Confidence 0.32 Published 2005 Journal Biochem. Pharmacol. Section Abstract Doc Link 15710360 Disease Relevance 0.67 Pain Relevance 0.13
We found that SB203580 and SP600125 – specific inhibitors of the MAPKs p38 and JNK, respectively – almost completely abolished the IL-1-mediated downregulation of PPAR?
Negative_regulation (inhibitors) of Gene_expression (respectively) of JNK
5) Confidence 0.19 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC1906809 Disease Relevance 0.17 Pain Relevance 0.09
, Singh and colleagues showed that EGCG selectively inhibited the p46 isoform of c-Jun-N-terminal kinase induced by IL-1?
Negative_regulation (inhibited) of Gene_expression (isoform) of c-Jun-N-terminal kinase
6) Confidence 0.14 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2888220 Disease Relevance 0.42 Pain Relevance 0.26
These data show that specific inhibition of JNK pathway may be important for inactivation of NF-?
Negative_regulation (inhibition) of Gene_expression (pathway) of JNK
7) Confidence 0.11 Published 2008 Journal J Inflamm (Lond) Section Body Doc Link PMC2442592 Disease Relevance 0.14 Pain Relevance 0.04
Taken together, our data indicate that inhibition of JNK signal is the most involved in the inhibitory effect of melittin and bee venom on the LPS and SNP-induced activation of NF-?
Negative_regulation (inhibition) of Gene_expression (signal) of JNK
8) Confidence 0.11 Published 2008 Journal J Inflamm (Lond) Section Body Doc Link PMC2442592 Disease Relevance 0.79 Pain Relevance 0.23
In the present study, we further found that melittin and bee venom significantly reduced inflammatory stimuli (LPS and SNP)-induced activation of JNK signal, and the JNK signal specific inhibitor SP600215 suppressed the inhibitory effect of melittin and bee venom on the NF-?
Negative_regulation (inhibitor) of Gene_expression (signal) of JNK associated with inflammatory stimuli
9) Confidence 0.11 Published 2008 Journal J Inflamm (Lond) Section Body Doc Link PMC2442592 Disease Relevance 0.85 Pain Relevance 0.43

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