INT58393

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Context Info
Confidence 0.25
First Reported 1993
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 37
Total Number 37
Disease Relevance 16.80
Pain Relevance 6.00

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
d cells 8
epithelial cell 4
HFF 4
HGF 4
PGE2 4
PTGER2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 755 100.00 Very High Very High Very High
agonist 78 100.00 Very High Very High Very High
MU agonist 2 99.84 Very High Very High Very High
dexamethasone 15 98.80 Very High Very High Very High
Osteoarthritis 187 98.76 Very High Very High Very High
substance P 12 96.68 Very High Very High Very High
antagonist 25 95.56 Very High Very High Very High
Opioid 2 94.48 High High
Neuropeptide 4 90.84 High High
cytokine 872 90.32 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 957 100.00 Very High Very High Very High
Infection 864 100.00 Very High Very High Very High
Fever 41 100.00 Very High Very High Very High
Herpes Simplex Virus 1904 99.84 Very High Very High Very High
Apoptosis 391 99.36 Very High Very High Very High
Adhesions 367 98.88 Very High Very High Very High
Osteoarthritis 197 98.76 Very High Very High Very High
Colon Cancer 160 98.64 Very High Very High Very High
Skin Cancer 5 92.96 High High
Influenza Virus Infection 44 92.92 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
LPS-induced IL-6 and PGE2 release was only slightly inhibited at high doses, whereas LPS-induced release of IL-8 and matrix metalloprotease (MMP)-9 was not affected.
Positive_regulation (LPS-induced) of Localization (release) of PGE2
1) Confidence 0.25 Published 2004 Journal Scand. J. Rheumatol. Suppl. Section Abstract Doc Link 15515409 Disease Relevance 0.50 Pain Relevance 0.19
Palmitoyl trifluormethyl ketone, an inhibitor of Ca(2+) independent phospholipase A2 (iPLA2) and a less potent inhibitor of cytosolic PLA2, dose-dependently reduced the IL-1beta induced PGE2 secretion.
Positive_regulation (induced) of Localization (secretion) of PGE2
2) Confidence 0.20 Published 2001 Journal Exp. Gerontol. Section Abstract Doc Link 11250126 Disease Relevance 0.69 Pain Relevance 0.41
COX inhibitors indomethacin and BF389, as well as the glucocorticoid dexamethasone (DEX) and pyrrolidinedithiocarbamate, which is an inhibitor of nuclear factor kappaB as well as a potent antioxidant, inhibited IL-1beta induced PGE2 secretion.
Positive_regulation (induced) of Localization (secretion) of PGE2 associated with dexamethasone
3) Confidence 0.20 Published 2001 Journal Exp. Gerontol. Section Abstract Doc Link 11250126 Disease Relevance 0.79 Pain Relevance 0.48
This suggests that the IL-1beta induced PGE2 secretion may depend on the availability of arachidonic acid.
Positive_regulation (induced) of Localization (secretion) of PGE2
4) Confidence 0.20 Published 2001 Journal Exp. Gerontol. Section Abstract Doc Link 11250126 Disease Relevance 0.67 Pain Relevance 0.40
EP1/3 agonist stimulates and EP2/4 agonists compromise proliferation of Lovo cells
Positive_regulation (stimulates) of Localization (proliferation) of EP2 associated with agonist
5) Confidence 0.19 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2615781 Disease Relevance 0.08 Pain Relevance 0.39
This shows that Gi-protein dependent signals elicit CRC cell proliferation, as corroborated by the ability of PTX to block PGE2 or LPA induced proliferation (Fig. 4B and data not shown).
Positive_regulation (induced) of Localization (proliferation) of PGE2 associated with colon cancer
6) Confidence 0.19 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2615781 Disease Relevance 0.16 Pain Relevance 0.09
B can be upregulated due to reactive oxygen species release and inflammation (i.e., PGE2).
Positive_regulation (upregulated) of Localization (release) of PGE2 associated with inflammation and fever
7) Confidence 0.16 Published 2010 Journal International Journal of Cell Biology Section Body Doc Link PMC2841246 Disease Relevance 0.95 Pain Relevance 0.09
IND significantly reduced both basal and IL-1 beta-induced PGE2 release and HGF production.
Positive_regulation (induced) of Localization (release) of PGE2 in HGF
8) Confidence 0.09 Published 1998 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 9571196 Disease Relevance 0.23 Pain Relevance 0.36
IND significantly reduced both basal and IL-1 beta-induced PGE2 release and HGF production.
Positive_regulation (-) of Localization (release) of PGE2 in HGF
9) Confidence 0.09 Published 1998 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 9571196 Disease Relevance 0.23 Pain Relevance 0.36
M HNE, however, PGE2 release and COX-2 protein expression were enhanced after 4 hours of incubation, with maximum values obtained at 24 hours (Figure 1c, d).
Positive_regulation (enhanced) of Localization (release) of PGE2
10) Confidence 0.08 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2875653 Disease Relevance 0.08 Pain Relevance 0
The explants were allowed to equilibrate for 72 h as Fermor et al. showed that there was an initial increase in PGE2 release from harvested cartilage explants, and that this stabilised after 72 h in culture and remained stable for up to 7 days [32].
Positive_regulation (increase) of Localization (release) of PGE2 in cartilage
11) Confidence 0.08 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2246251 Disease Relevance 0 Pain Relevance 0
induced PGE2 secretion was reduced drastically in si-COX-2- HMVEC-d cells (Figure 3B) suggesting that COX-2 silencing could effectively abrogate KSHV infection induced PGE2 secretion in endothelial cells.
Positive_regulation (induced) of Localization (secretion) of PGE2 in d cells associated with herpes simplex virus and infection
12) Confidence 0.06 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 1.16 Pain Relevance 0
In si-C-HMVEC-d cells, PGE2 secretion levels dramatically increased upon KSHV infection.
Positive_regulation (increased) of Localization (secretion) of PGE2 in d cells associated with herpes simplex virus and infection
13) Confidence 0.06 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 1.03 Pain Relevance 0
This requirement for a higher dose of inhibitors to block COX-2 function and PGE2 secretion could be due to the continuous loop of COX activation leading to the maintenance of a constant level of PGE2 in latently infected cells.
Positive_regulation (requirement) of Localization (secretion) of PGE2
14) Confidence 0.06 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 0.49 Pain Relevance 0
Silencing of COX-2 reduces KSHV infection induced COX-2 gene expression and PGE2 secretion in HMVEC-d cells
Positive_regulation (induced) of Localization (secretion) of PGE2 in d cells associated with herpes simplex virus and infection
15) Confidence 0.06 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 0.34 Pain Relevance 0
KSHV infection induced PGE2 secretion regulates endothelial cell adhesion
Positive_regulation (induced) of Localization (secretion) of PGE2 in endothelial cell associated with herpes simplex virus, adhesions and infection
16) Confidence 0.06 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 1.15 Pain Relevance 0
induced PGE2 secretion was reduced drastically in si-COX-2- HMVEC-d cells (Figure 3B) suggesting that COX-2 silencing could effectively abrogate KSHV infection induced PGE2 secretion in endothelial cells.
Positive_regulation (induced) of Localization (secretion) of PGE2 in d cells associated with herpes simplex virus and infection
17) Confidence 0.06 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 1.24 Pain Relevance 0
In our earlier studies, we demonstrated robust COX-2 gene expression and high levels of PGE2 secretion by KSHV during primary infection of HMVEC-d and HFF cells [26].
Positive_regulation (levels) of Localization (secretion) of PGE2 in HFF associated with herpes simplex virus and infection
18) Confidence 0.06 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2820536 Disease Relevance 0.84 Pain Relevance 0.11
Activation of the TRPV1 results in an increased release of IL-8 and PGE2 by epidermal keratinocytes [49], IL-6 [53] and IL-8 [54] by human bronchial epithelial cells and IL-6 by dental pulp fibroblast [52].
Positive_regulation (increased) of Localization (release) of PGE2 in keratinocytes
19) Confidence 0.06 Published 2010 Journal Mol Pain Section Body Doc Link PMC2834653 Disease Relevance 0.76 Pain Relevance 0.88
A single impact load resulted in a marked increase in PGE2 release, the number of apoptotic cells, and the concentration of GAGs in the culture medium.
Positive_regulation (increase) of Localization (release) of PGE2 in apoptotic cells associated with apoptosis
20) Confidence 0.05 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2246251 Disease Relevance 0.44 Pain Relevance 0.04

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