INT173647

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Context Info
Confidence 0.39
First Reported 2003
Last Reported 2011
Negated 2
Speculated 0
Reported most in Body
Documents 15
Total Number 16
Disease Relevance 7.54
Pain Relevance 2.05

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

cytosol (MAPK14) nucleoplasm (MAPK14) signal transduction (MAPK14)
nucleus (MAPK14) response to stress (MAPK14) cytoplasm (MAPK14)
Anatomy Link Frequency
cartilage 4
central nervous system 2
MAPK14 (Homo sapiens)
Pain Link Frequency Relevance Heat
Central nervous system 65 99.98 Very High Very High Very High
COX2 2 98.80 Very High Very High Very High
agonist 82 98.24 Very High Very High Very High
Nicotine 96 98.16 Very High Very High Very High
cytokine 199 95.84 Very High Very High Very High
Inflammation 92 94.56 High High
metalloproteinase 4 92.16 High High
Inflammatory response 16 85.20 High High
b2 receptor 29 69.20 Quite High
Arthritis 106 58.56 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 212 100.00 Very High Very High Very High
Stress 63 100.00 Very High Very High Very High
Brain Hemorrhage 4 98.44 Very High Very High Very High
Disease Progression 16 97.84 Very High Very High Very High
Infection 1 97.64 Very High Very High Very High
Arthritis 7 96.32 Very High Very High Very High
Central Nervous System Disease 3 95.24 Very High Very High Very High
INFLAMMATION 118 94.56 High High
Hepatocellular Cancer 17 92.16 High High
Nerve Sheath Neoplasms 66 91.92 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In the decomposition of the interaction map, FOS appears in Module 2 only and MAPK14 catalyzes the activation of FOS.
Positive_regulation (activation) of Gene_expression (catalyzes) of MAPK14
1) Confidence 0.39 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2855702 Disease Relevance 0.48 Pain Relevance 0.17
Results showed a high expression of p38 MAPK (ATF-2) at 4 ?
Positive_regulation (high) of Gene_expression (expression) of p38
2) Confidence 0.24 Published 2010 Journal International Journal of Environmental Research and Public Health Section Body Doc Link PMC2864039 Disease Relevance 0.13 Pain Relevance 0
Currently, novel p38?
Positive_regulation (novel) of Gene_expression (novel) of p38
3) Confidence 0.17 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2604896 Disease Relevance 0.53 Pain Relevance 0.28
Development of bioavailable, central nervous system-penetrant p38?
Positive_regulation (penetrant) of Gene_expression (penetrant) of p38 in central nervous system associated with central nervous system
4) Confidence 0.15 Published 2008 Journal BMC Neurosci Section Abstract Doc Link PMC2604896 Disease Relevance 0.34 Pain Relevance 0.36
Oral administration of a CNS-penetrant p38?
Positive_regulation (penetrant) of Gene_expression (penetrant) of p38 associated with central nervous system
5) Confidence 0.15 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2604896 Disease Relevance 0.44 Pain Relevance 0.20
The MAPK family, comprising of ERKs, JNK, and p38, is activated in response to the various stress stimuli caused by virus infections or chemical exposures.
Positive_regulation (activated) of Gene_expression (comprising) of p38 associated with stress and infection
6) Confidence 0.11 Published 2011 Journal Evidence-based Complementary and Alternative Medicine : eCAM Section Body Doc Link PMC2952314 Disease Relevance 0.58 Pain Relevance 0
However, in contrast to JNK, no significant differences in ERK1/2 (Fig. 6C, D, H) or p38 (Fig. 6E, F, I) activities were found between the specimen treated with nicotine (10 ?
Neg (no) Positive_regulation (differences) of Gene_expression (activities) of p38 associated with nicotine
7) Confidence 0.11 Published 2010 Journal Respir Res Section Body Doc Link PMC2845563 Disease Relevance 0 Pain Relevance 0.49
Inhibition of the individual MAP kinase pathways with specific chemical inhibitors either completely abolished or significantly reduced expression levels of cartilage-specific genes in a pattern distinct to each pathway, thus indicating that p38, ERK, and JNK are independently essential for the TGF-?
Positive_regulation (for) of Gene_expression (essential) of p38 in cartilage
8) Confidence 0.07 Published 2003 Journal Arthritis Res Ther Section Body Doc Link PMC154434 Disease Relevance 0.23 Pain Relevance 0
Inhibition of the individual MAP kinase pathways with specific chemical inhibitors either completely abolished or significantly reduced expression levels of cartilage-specific genes in a pattern distinct to each pathway, thus indicating that p38, ERK, and JNK are independently essential for the TGF-?
Neg (independently) Positive_regulation (independently) of Gene_expression (essential) of p38 in cartilage
9) Confidence 0.07 Published 2003 Journal Arthritis Res Ther Section Body Doc Link PMC154434 Disease Relevance 0.23 Pain Relevance 0
I/R increased the expression of all three MAPKs, with significantly greater expression of JNK and p38.
Positive_regulation (increased) of Gene_expression (expression) of p38
10) Confidence 0.07 Published 2007 Journal Crit Care Section Body Doc Link PMC2206506 Disease Relevance 1.44 Pain Relevance 0.32
plus epinephrine effect on IL-6, IL-8, and IL-13 expression suggesting that p38 plays an important role in signaling from both IL-1?
Positive_regulation (role) of Gene_expression (plays) of p38
11) Confidence 0.06 Published 2004 Journal BMC Immunol Section Body Doc Link PMC521685 Disease Relevance 0.12 Pain Relevance 0.14
The stress-activated protein kinase/ Jun-terminal kinase SAPK/JNK, a mediator of apoptosis, was activated (phosphorylated) 16 h after treatment with either of the Sulindac metabolites (not shown), and increased further after 24 h and 48 h (Fig. 6).
Positive_regulation (activated) of Gene_expression (/) of stress-activated protein kinase associated with stress and apoptosis
12) Confidence 0.05 Published 2004 Journal Cancer Cell Int Section Body Doc Link PMC425591 Disease Relevance 0.46 Pain Relevance 0
The stress-activated protein kinase/ Jun-terminal kinase SAPK/JNK, a mediator of apoptosis, was activated (phosphorylated) 16 h after treatment with either of the Sulindac metabolites (not shown), and increased further after 24 h and 48 h (Fig. 6).
Positive_regulation (increased) of Gene_expression (/) of stress-activated protein kinase associated with stress and apoptosis
13) Confidence 0.05 Published 2004 Journal Cancer Cell Int Section Body Doc Link PMC425591 Disease Relevance 0.48 Pain Relevance 0
The stress-activated protein kinase/ Jun-terminal kinase SAPK/JNK, a mediator of apoptosis, was activated (phosphorylated) 16 h after treatment with either of the Sulindac metabolites (not shown), and increased further after 24 h and 48 h (Fig. 6).
Positive_regulation (-) of Gene_expression (/) of stress-activated protein kinase associated with stress and apoptosis
14) Confidence 0.05 Published 2004 Journal Cancer Cell Int Section Body Doc Link PMC425591 Disease Relevance 0.45 Pain Relevance 0
Apoptosis was associated with activation of both c-Jun N-terminal protein kinase and p38 kinase and overexpression of proapoptotic proteins and cyclooxygenase 2 (COX-2) [77, 83].
Positive_regulation (overexpression) of Gene_expression (overexpression) of p38 kinase associated with cox2 and apoptosis
15) Confidence 0.04 Published 2010 Journal PPAR Research Section Body Doc Link PMC2963138 Disease Relevance 0.81 Pain Relevance 0.05
Apoptosis was associated with activation of both c-Jun N-terminal protein kinase and p38 kinase and overexpression of proapoptotic proteins and cyclooxygenase 2 (COX-2) [77, 83].
Positive_regulation (overexpression) of Gene_expression (overexpression) of p38 kinase associated with cox2 and apoptosis
16) Confidence 0.03 Published 2010 Journal PPAR Research Section Body Doc Link PMC2963138 Disease Relevance 0.81 Pain Relevance 0.05

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