INT184475

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Context Info
Confidence 0.30
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 6
Disease Relevance 1.85
Pain Relevance 0.57

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

signal transduction (Ptger2) plasma membrane (Ptger2) signal transducer activity (Ptger2)
Ptger2 (Mus musculus)
Pain Link Frequency Relevance Heat
COX-2 inhibitor 16 99.44 Very High Very High Very High
antagonist 103 96.08 Very High Very High Very High
cINOD 18 90.16 High High
agonist 15 62.96 Quite High
Inflammation 13 5.00 Very Low Very Low Very Low
withdrawal 4 5.00 Very Low Very Low Very Low
aspirin 3 5.00 Very Low Very Low Very Low
cerebral cortex 2 5.00 Very Low Very Low Very Low
Kinase C 2 5.00 Very Low Very Low Very Low
cytokine 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 83 97.88 Very High Very High Very High
Colon Cancer 78 96.44 Very High Very High Very High
Hypoxia 1 95.20 Very High Very High Very High
Cancer 172 94.08 High High
Reprotox - General 1 6 93.12 High High
Breast Cancer 45 82.52 Quite High
INFLAMMATION 16 81.24 Quite High
Endometriosis (extended) 16 70.08 Quite High
Carcinoma In Situ 2 64.96 Quite High
Adenoma 10 60.56 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This would most likely be due to PGE2 preventing proteolysis
Protein_catabolism (proteolysis) of PGE2
1) Confidence 0.30 Published 2009 Journal PPAR Research Section Body Doc Link PMC2651001 Disease Relevance 0.24 Pain Relevance 0.03
Mutation of the CRE region of this construct resulted in complete loss of COX-2 promoter activity in response to administration of either PGE2 or PGF2?
Protein_catabolism (administration) of PGE2
2) Confidence 0.17 Published 2008 Journal Molecular and Cellular Endocrinology Section Body Doc Link PMC2694994 Disease Relevance 0 Pain Relevance 0.03
cAMP accumulation was determined in response to administration of vehicle, PGE2 or PGF2?
Protein_catabolism (administration) of PGE2
3) Confidence 0.17 Published 2008 Journal Molecular and Cellular Endocrinology Section Body Doc Link PMC2694994 Disease Relevance 0.07 Pain Relevance 0.15
Varying amounts of PGE2 (12.5–200 pg/ml) were added to the medium in order to take into account the fact that some of the PGE2 may degrade or be internalized into cells.
Protein_catabolism (degrade) of PGE2
4) Confidence 0.06 Published 2005 Journal Breast Cancer Res Section Body Doc Link PMC1175053 Disease Relevance 0.20 Pain Relevance 0
Most of the PGE2 synthesized by cPLA2, COX-2, and mPGES-1 are degraded by 15-PGDH, which catalyzes the NAD+-dependent oxidation of the 15-OH group of prostaglandin to a 15-keto group.23 Accordingly, 15-PGDH is a normal physiologic antagonist of COX-2.
Protein_catabolism (degraded) of PGE2 associated with antagonist
5) Confidence 0.06 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2908865 Disease Relevance 0.93 Pain Relevance 0.35
The expressions of these entities are known to be related closely to the synthesis and degradation of PGE2, which is known to be associated with resistance to programmed cell death, cell migration, cell proliferation, and angiogenesis.
Protein_catabolism (degradation) of PGE2 associated with apoptosis
6) Confidence 0.05 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2908865 Disease Relevance 0.41 Pain Relevance 0

General Comments

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