INT224740

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.58
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 5
Disease Relevance 2.46
Pain Relevance 0.79

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

plasma membrane (PTGER2) signal transducer activity (PTGER2)
Anatomy Link Frequency
epithelium 1
PGE2 1
PTGER2 (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 41 93.92 High High
agonist 64 92.80 High High
COX-2 inhibitor 12 86.12 High High
Bioavailability 4 75.48 Quite High
Inflammation 15 12.36 Low Low
Osteoarthritis 19 5.00 Very Low Very Low Very Low
corticosteroid 4 5.00 Very Low Very Low Very Low
sSRI 4 5.00 Very Low Very Low Very Low
fibrosis 4 5.00 Very Low Very Low Very Low
Pain 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Colorectal Cancer 144 99.84 Very High Very High Very High
Apoptosis 48 99.56 Very High Very High Very High
Colon Cancer 4 95.76 Very High Very High Very High
INFLAMMATION 21 93.72 High High
Death 6 74.20 Quite High
Injury 14 50.12 Quite High
Cancer 58 44.76 Quite Low
Osteoarthritis 19 5.00 Very Low Very Low Very Low
Disease 5 5.00 Very Low Very Low Very Low
Obesity 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Thus, the combined effects of increased synthesis and export together with reduced elimination and degradation of extracellular PGE2 in CRC point to a maintained higher level of PGE2 in the auto-/paracrine milieu in the CRC colonic epithelium, Figure 1.
Protein_catabolism (degradation) of PGE2 in epithelium associated with colorectal cancer
1) Confidence 0.58 Published 2010 Journal BMC Gastroenterol Section Body Doc Link PMC2824707 Disease Relevance 0.72 Pain Relevance 0.07
We speculate that the observed increased sensitivity to indomethacin in the N-patients is due to a higher baseline production of prostaglandins in N-patients following an increased expression/activity of the COX-2 enzyme and export of PGE2 [27,38] and/or a lowered removal and degradation of PGE2, Figure 1[38,39].
Protein_catabolism (degradation) of PGE2
2) Confidence 0.58 Published 2010 Journal BMC Gastroenterol Section Body Doc Link PMC2824707 Disease Relevance 0.42 Pain Relevance 0.25
We speculate that the observed increased sensitivity to indomethacin in the N-patients is due to a higher baseline production of prostaglandins in N-patients following an increased expression/activity of the COX-2 enzyme and export of PGE2 [27,38] and/or a lowered removal and degradation of PGE2, Figure 1[38,39].
Protein_catabolism (degradation) of PGE2
3) Confidence 0.51 Published 2010 Journal BMC Gastroenterol Section Body Doc Link PMC2824707 Disease Relevance 0.43 Pain Relevance 0.25
Removal of extracellular PGE2 is partially performed by a specific prostaglandin transporter, PGT, and further degradation of PGE2 is by the enzymes 15-prostaglandin-dehydrogenase, 15-PGDH, and carbonyl reductase, CBR, of which, both the activity by PGT and 15-PGDH are reduced in CRC cells, Figure 1[3,38,39].
Protein_catabolism (degradation) of PGE2 associated with colorectal cancer
4) Confidence 0.44 Published 2010 Journal BMC Gastroenterol Section Body Doc Link PMC2824707 Disease Relevance 0.50 Pain Relevance 0
Cyclooxygenase inhibition lowers prostaglandin E2 release from articular cartilage and reduces apoptosis but not proteoglycan degradation following an impact load in vitro

This study investigated the release of prostaglandin E2 (PGE2) from cartilage following an impact load in vitro and the possible chondroprotective effect of cyclooxygenase-2 (COX-2) inhibition using non-steroidal anti-inflammatory drugs (NSAIDs).

Protein_catabolism (degradation) of PGE2 in PGE2 associated with inflammation, cinod and apoptosis
5) Confidence 0.07 Published 2007 Journal Arthritis Res Ther Section Title Doc Link PMC2246251 Disease Relevance 0.39 Pain Relevance 0.23

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox