INT202683

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Context Info
Confidence 0.73
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 6
Disease Relevance 5.86
Pain Relevance 0.80

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

aging (FAS) protein complex assembly (FAS) cytoplasm (FAS)
signal transducer activity (FAS) cytosol (FAS) signal transduction (FAS)
Anatomy Link Frequency
hepatocytes 1
FAS (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 40 91.60 High High
Inflammatory marker 1 88.56 High High
rheumatoid arthritis 68 86.84 High High
cytokine 87 73.52 Quite High
ischemia 12 64.96 Quite High
abdominal pain 3 59.48 Quite High
Inflammatory mediators 3 59.28 Quite High
Bioavailability 9 55.68 Quite High
Inflammatory response 30 52.96 Quite High
Inflammation 168 50.00 Quite Low
Disease Link Frequency Relevance Heat
Death 95 99.56 Very High Very High Very High
Apoptosis 287 98.48 Very High Very High Very High
Cancer 153 98.40 Very High Very High Very High
Necrosis 38 98.16 Very High Very High Very High
Injury 82 95.32 Very High Very High Very High
INFLAMMATION 169 88.56 High High
Rheumatoid Arthritis 68 86.84 High High
Fatty Liver 27 84.40 Quite High
Stress 123 83.36 Quite High
Liver Disease 49 81.52 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
-mediated inhibition of TRAIL-signaling could not be accounted for by significant changes in TRAIL-R, procaspases-3,-8,-9, Fas-activated death domain protein (FADD), tumor necrosis factor receptor 1-associated death domain protein, silencer of death domain protein, FADD-like-interleukin-1?
Localization (changes) of Fas associated with necrosis, cancer and death
1) Confidence 0.73 Published 2009 Journal Mediators of Inflammation Section Body Doc Link PMC2842969 Disease Relevance 1.75 Pain Relevance 0.31
Activation of caspases-3 and -7 and an elevated release of soluble Fas and Fas ligand have also been detected at the end of extracorporeal circulation [6,8,10].
Localization (release) of Fas
2) Confidence 0.53 Published 2007 Journal J Cardiothorac Surg Section Body Doc Link PMC1783850 Disease Relevance 0.81 Pain Relevance 0.10
Activation of caspases-3 and -7 and an elevated release of soluble Fas and Fas ligand have also been detected at the end of extracorporeal circulation [6,8,10].
Localization (release) of Fas
3) Confidence 0.47 Published 2007 Journal J Cardiothorac Surg Section Body Doc Link PMC1783850 Disease Relevance 0.81 Pain Relevance 0.10
There are two sources of FAs for animal metabolism: Dietary FAs, and endogenously synthesized fatty acid synthase (FASN)-catalyzed FAs utilizing acetyl-CoA as primer, malonyl-CoA as two-carbon donor, and NADPH as reducing equivalent.
Localization (utilizing) of FAs
4) Confidence 0.27 Published 2008 Journal Mol Cancer Section Body Doc Link PMC2615789 Disease Relevance 0.60 Pain Relevance 0.09
Overall, the most relevant mechanisms leading to hepatocyte injury in these metabolically altered conditions involve an excess of FFAs: directly inducing hepatocyte apoptosis and stimulating production of TNF, which is considered in this context as an adipocytokine; increasing Fas ligand binding to Fas (CD-95) receptor in steatotic hepatocytes, leading to apoptosis; leading to impaired mitochondrial or peroxisomal ?
Localization (receptor) of Fas in hepatocytes associated with injury and apoptosis
5) Confidence 0.16 Published 2008 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2584013 Disease Relevance 1.63 Pain Relevance 0
Lee et al. [11,46] showed that an SFA (lauric acid), but not unsaturated FAs, could induce NF-?
Localization (unsaturated) of FAs
6) Confidence 0.08 Published 2010 Journal Fibrogenesis Tissue Repair Section Body Doc Link PMC2984459 Disease Relevance 0.26 Pain Relevance 0.20

General Comments

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