INT308962

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Context Info
Confidence 0.16
First Reported 2010
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 3
Total Number 7
Disease Relevance 1.20
Pain Relevance 0.18

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

transport (SLC7A7) plasma membrane (SLC7A7) protein complex assembly (SLC7A7)
transmembrane transport (SLC7A7) cellular amino acid metabolic process (SLC7A7)
Anatomy Link Frequency
endothelial cells 2
blood 1
SLC7A7 (Homo sapiens)
Pain Link Frequency Relevance Heat
Potency 5 89.64 High High
agonist 53 80.72 Quite High
fibrosis 8 55.36 Quite High
antagonist 14 46.48 Quite Low
Endocannabinoid 9 19.76 Low Low
Cannabinoid receptor 13 9.12 Low Low
Inflammation 13 5.00 Very Low Very Low Very Low
Cannabinoid 9 5.00 Very Low Very Low Very Low
member 8 5 5.00 Very Low Very Low Very Low
withdrawal 5 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Injury 1 99.24 Very High Very High Very High
Sickle Cell Anemia 86 98.84 Very High Very High Very High
Iron Overload 48 97.64 Very High Very High Very High
Infection 5 87.56 High High
Hypersplenism 2 81.40 Quite High
Increased Venous Pressure Under Development 7 80.16 Quite High
Hypertension 7 65.24 Quite High
Atherosclerosis 5 63.60 Quite High
Thalassemia 36 62.32 Quite High
Cirrhosis 8 56.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Moreover, because LPI-triggered sustained membrane depolarization and inward current were not affected by inhibition of GPR55 by rimonabant or the molecular manipulation of GPR55 expression, LPI obviously exhibited its sustained effects independently of this orphan receptor.
Neg (not) Regulation (affected) of LPI
1) Confidence 0.16 Published 2010 Journal British Journal of Pharmacology Section Body Doc Link PMC2931756 Disease Relevance 0 Pain Relevance 0.03
Thus, LPI is a potent signalling molecule affecting endothelial cells by modulating multiple electrical responses.
Regulation (affecting) of LPI in endothelial cells
2) Confidence 0.16 Published 2010 Journal British Journal of Pharmacology Section Body Doc Link PMC2931756 Disease Relevance 0 Pain Relevance 0.08
As LPI-evoked depolarization was not affected by the Cl- channel blocker DIDS, the involvement of Cl- channels (Nilius and Droogmans, 2001) in the membrane depolarization to LPI is unlikely.
Neg (not) Regulation (affected) of LPI
3) Confidence 0.16 Published 2010 Journal British Journal of Pharmacology Section Body Doc Link PMC2931756 Disease Relevance 0 Pain Relevance 0
Because other LPs including LPC and sphingosine exhibit inhibitory properties on the Na/K-ATPase (Oishi et al., 1990), we also evaluated the Na/K-ATPase as a putative target of LPI.
Regulation (target) of LPI
4) Confidence 0.10 Published 2010 Journal British Journal of Pharmacology Section Body Doc Link PMC2931756 Disease Relevance 0 Pain Relevance 0
This observation indicates that vascular endothelial cells are targets of LPI and might further point to LPI as an important modulator of endothelial functions under physiological and pathological conditions.
Regulation (targets) of LPI in endothelial cells
5) Confidence 0.10 Published 2010 Journal British Journal of Pharmacology Section Body Doc Link PMC2931756 Disease Relevance 0.21 Pain Relevance 0
Chelators work by targeting the unbound iron in the blood, including NTBI and LPI that cause tissue injury [80].
Regulation (targeting) of LPI in blood associated with injury
6) Confidence 0.01 Published 2010 Journal Advances in Hematology Section Body Doc Link PMC2872757 Disease Relevance 0.94 Pain Relevance 0.03
Here we report, NAGly > O-1602 > 2-AG > Abn-CBD > AEA, and the effects of PEA, LPI and PALGly were weak and concentration-independent (Figure 2A).
Regulation (effects) of LPI
7) Confidence 0.01 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2865488 Disease Relevance 0.05 Pain Relevance 0.04

General Comments

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