INT173647

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

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 COX2 2 98.80 agonist 82 98.24 Nicotine 96 98.16 cytokine 199 95.84 Inflammation 92 94.56 metalloproteinase 4 92.16 Inflammatory response 16 85.20 b2 receptor 29 69.20 Arthritis 106 58.56

Disease Link Frequency Relevance Heat Apoptosis 212 100.00 Stress 63 100.00 Brain Hemorrhage 4 98.44 Disease Progression 16 97.84 Infection 1 97.64 Arthritis 7 96.32 Central Nervous System Disease 3 95.24 INFLAMMATION 118 94.56 Hepatocellular Cancer 17 92.16 Nerve Sheath Neoplasms 66 91.92

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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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