INT177935

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Context Info
Confidence 0.14
First Reported 2004
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 3
Disease Relevance 1.03
Pain Relevance 0.03

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

cytosol (MAPK9) nucleoplasm (MAPK9) mitochondrion (MAPK9)
nucleus (MAPK9) transcription factor binding (MAPK9) response to stress (MAPK9)
MAPK9 (Homo sapiens)
Pain Link Frequency Relevance Heat
COX-2 inhibitor 5 58.52 Quite High
Inflammation 23 5.00 Very Low Very Low Very Low
cINOD 15 5.00 Very Low Very Low Very Low
cytokine 4 5.00 Very Low Very Low Very Low
Pain 2 5.00 Very Low Very Low Very Low
rheumatoid arthritis 2 5.00 Very Low Very Low Very Low
psoriasis 1 5.00 Very Low Very Low Very Low
Kinase C 1 5.00 Very Low Very Low Very Low
antagonist 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 75 100.00 Very High Very High Very High
Stress 8 100.00 Very High Very High Very High
Nerve Sheath Neoplasms 44 91.92 High High
Necrosis 3 41.36 Quite Low
Toxicity 2 17.60 Low Low
Cancer 48 5.00 Very Low Very Low Very Low
Watson Syndrome 38 5.00 Very Low Very Low Very Low
INFLAMMATION 25 5.00 Very Low Very Low Very Low
Inflammatory Bowel Disease 15 5.00 Very Low Very Low Very Low
Malignant Neoplastic Disease 12 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Previously we have shown that VEGF stimulation of HIMECs leads to a marked phosphorylation and activation of all three MAPK family members (p44/42 MAPK, stress-activated protein kinase (SAPK)/JNK and p38 MAPK).25 To investigate whether MAPK pathways play a role in VEGF induction of COX-2, HIMECs were pretreated with specific MAPK inhibitors then activated with VEGF.
Positive_regulation (leads) of Positive_regulation (activation) of SAPK associated with stress
1) Confidence 0.14 Published 2008 Journal Gut Section Body Doc Link PMC2582343 Disease Relevance 0.10 Pain Relevance 0.03
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 Positive_regulation (kinase) of SAPK associated with stress and apoptosis
2) Confidence 0.11 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 Positive_regulation (kinase) of SAPK associated with stress and apoptosis
3) Confidence 0.11 Published 2004 Journal Cancer Cell Int Section Body Doc Link PMC425591 Disease Relevance 0.47 Pain Relevance 0

General Comments

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