INT297577

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Context Info
Confidence 0.65
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 12
Total Number 12
Disease Relevance 4.58
Pain Relevance 0.15

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

extracellular space (APOA1) small molecule metabolic process (APOA1) extracellular region (APOA1)
plasma membrane (APOA1) enzyme binding (APOA1) transmembrane transport (APOA1)
Anatomy Link Frequency
BFA 3
APOA1 (Homo sapiens)
Pain Link Frequency Relevance Heat
agonist 30 96.32 Very High Very High Very High
Bile 9 93.00 High High
Inflammation 59 5.00 Very Low Very Low Very Low
cytokine 14 5.00 Very Low Very Low Very Low
anesthesia 9 5.00 Very Low Very Low Very Low
Inflammatory response 6 5.00 Very Low Very Low Very Low
Angina 3 5.00 Very Low Very Low Very Low
Central nervous system 2 5.00 Very Low Very Low Very Low
Endocannabinoid 2 5.00 Very Low Very Low Very Low
COX2 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Disorder Of Lipid Metabolism 478 99.88 Very High Very High Very High
Obesity 473 90.88 High High
Coronary Artery Disease 15 35.92 Quite Low
Hypoglycemia 2 34.64 Quite Low
Atherosclerosis 63 22.88 Low Low
Hyperlipidemia 5 9.12 Low Low
Targeted Disruption 3 7.84 Low Low
INFLAMMATION 65 5.00 Very Low Very Low Very Low
Infection 53 5.00 Very Low Very Low Very Low
Cardiovascular Disease 41 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However, our results prove that neither the inhibitors of PKA, nor BFA are able to disturb the release of apoA-I induced cholesterol.
Localization (release) of apoA-I in BFA
1) Confidence 0.65 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2917427 Disease Relevance 0.39 Pain Relevance 0
ApoA-I induced cholesterol release is not linked to cholesterol synthesis
Localization (release) of ApoA-I
2) Confidence 0.65 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2917427 Disease Relevance 0.30 Pain Relevance 0
Consequently, BFA has no effect upon the apoA-I stimulated release of cholesterol.


Localization (release) of apoA-I in BFA
3) Confidence 0.60 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2917427 Disease Relevance 0.24 Pain Relevance 0
In addition, no data is currently available on the signalling pathways involved in the apoA-I induced secretion of apoE.
Localization (secretion) of apoA-I
4) Confidence 0.60 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2917427 Disease Relevance 0.33 Pain Relevance 0
Inhibition of HMG-CoA reductase by simvastatin has no effect on the apoA-I induced release of cholesterol (figure 4) suggesting that the increase in cholesterol in the cell medium derives from a cholesterol storage pool not related to a feed-back activation of HMG-CoA reductase.
Localization (release) of apoA-I
5) Confidence 0.60 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2917427 Disease Relevance 0.12 Pain Relevance 0
Moreover, treatment with PKA and adenylate cyclase inhibitors does not lead to a reduction in apoA-I induced cholesterol release (figure 2).
Localization (release) of apoA-I
6) Confidence 0.60 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2917427 Disease Relevance 0.38 Pain Relevance 0
Basal cholesterol release but not apoA-I stimulated cholesterol release is inhibited by brefeldin A (BFA)
Localization (cholesterol release) of apoA-I in BFA
7) Confidence 0.60 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2917427 Disease Relevance 0.18 Pain Relevance 0
Brefeldin A inhibits basal apoE secretion but not apoA-I induced apoE secretion
Localization (secretion) of apoA-I
8) Confidence 0.57 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2917427 Disease Relevance 0.30 Pain Relevance 0
Brefeldin A inhibits basal apoE secretion but not apoA-I induced apoE secretion
Localization (secretion) of apoA-I
9) Confidence 0.57 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2917427 Disease Relevance 0.29 Pain Relevance 0
Formation of nascent HDL is mediated by Abca1-dependent lipidation of newly-secreted Apoa1.
Localization (secr) of Apoa1 associated with disorder of lipid metabolism
10) Confidence 0.26 Published 2010 Journal PPAR Research Section Body Doc Link PMC2948931 Disease Relevance 0.25 Pain Relevance 0.15
kDa high-density lipoprotein complex composed of apolipoprotein A-I (apoA-I), haptoglobin-related protein (Hpr), apoliprotein L-I (APOL1), human cathelicidin antimicrobial peptide (hCAP18), GPI-specific phospholipase D (GPI-PLD), apolipoprotein A-II, and paraoxanase [106, 110], and (ii) TLF2, a 1000?
Localization (phospholipase D) of apoA-I associated with disorder of lipid metabolism
11) Confidence 0.20 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2826769 Disease Relevance 0.46 Pain Relevance 0
The concerted action of CETP and HL converts larger HDL2 into smaller HDL3 and releases lipid-free apoA-I and/or pre?
Localization (releases) of apoA-I
12) Confidence 0.06 Published 2010 Journal Lipids Health Dis Section Body Doc Link PMC2920871 Disease Relevance 1.35 Pain Relevance 0

General Comments

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