INT115889

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.36
First Reported 2003
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 27
Total Number 30
Disease Relevance 28.87
Pain Relevance 4.08

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

signal transduction (Fas) extracellular region (Fas) plasma membrane (Fas)
nucleus (Fas) cytoplasm (Fas)
Anatomy Link Frequency
T cells 3
brain 2
thymocytes 2
colon 1
epithelial cells 1
Fas (Mus musculus)
Pain Link Frequency Relevance Heat
opioid receptor 4 100.00 Very High Very High Very High
Chronic pancreatitis 6 99.74 Very High Very High Very High
antagonist 17 99.48 Very High Very High Very High
Opioid 8 99.24 Very High Very High Very High
rheumatoid arthritis 188 99.20 Very High Very High Very High
cytokine 123 99.00 Very High Very High Very High
chemokine 22 98.56 Very High Very High Very High
Inflammation 242 98.52 Very High Very High Very High
Arthritis 5 97.72 Very High Very High Very High
withdrawal 10 96.88 Very High Very High Very High
Disease Link Frequency Relevance Heat
Death 363 100.00 Very High Very High Very High
Cancer 124 100.00 Very High Very High Very High
Necrosis 30 100.00 Very High Very High Very High
Adenoma 12 100.00 Very High Very High Very High
Arthritis 12 99.84 Very High Very High Very High
Apoptosis 1252 99.82 Very High Very High Very High
Pancreatitis 8 99.74 Very High Very High Very High
Suicidal Behaviour 81 99.60 Very High Very High Very High
Disease 686 99.48 Very High Very High Very High
Disease Progression 2 99.44 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Toll-like receptor 3 signaling induces chronic pancreatitis through the Fas/Fas ligand-mediated cytotoxicity.
Fas Binding (ligand) of associated with chemokine and chronic pancreatitis
1) Confidence 0.36 Published 2009 Journal Tohoku J. Exp. Med. Section Title Doc Link 19282652 Disease Relevance 0.43 Pain Relevance 0.24
Toll-like receptor 3 signaling induces chronic pancreatitis through the Fas/Fas ligand-mediated cytotoxicity.
Fas Binding (ligand) of associated with chemokine and chronic pancreatitis
2) Confidence 0.36 Published 2009 Journal Tohoku J. Exp. Med. Section Title Doc Link 19282652 Disease Relevance 0.43 Pain Relevance 0.24
Effects of constitutive deletion of opioid receptors on the basal densities of Fas and Fas-associated protein with death domain (FADD) in the mouse brain: a delta-opioid tone inhibits FADD.
Fas Binding (deletion) of in brain associated with opioid receptor, opioid and death
3) Confidence 0.36 Published 2007 Journal Eur Neuropsychopharmacol Section Title Doc Link 17030115 Disease Relevance 0.34 Pain Relevance 0.61
Effects of constitutive deletion of opioid receptors on the basal densities of Fas and Fas-associated protein with death domain (FADD) in the mouse brain: a delta-opioid tone inhibits FADD.
Fas Binding (deletion) of in brain associated with opioid receptor, opioid and death
4) Confidence 0.36 Published 2007 Journal Eur Neuropsychopharmacol Section Title Doc Link 17030115 Disease Relevance 0.34 Pain Relevance 0.61
Other studies, however, have shown that Fas/Fas-L interaction is involved in bacterial Sag mediated apoptosis [36], [42]–[43].
Fas Binding (interaction) of associated with apoptosis
5) Confidence 0.35 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3008744 Disease Relevance 1.18 Pain Relevance 0
Apoptosis of lymphoma T cells induced by bacterial Sags involves Fas-Fas-L interaction
Fas Binding (interaction) of in T cells associated with lymphatic system cancer and apoptosis
6) Confidence 0.35 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3008744 Disease Relevance 1.82 Pain Relevance 0
MRL/lpr mice were generated by the insertion of the early transposable element ETn in the Fas gene, which causes a striking reduction in Fas mRNA expression and is associated clinically with marked acceleration of the lupus-like disease [39].
Fas gene Binding (associated) of associated with disease and systemic lupus erythematosus
7) Confidence 0.34 Published 2010 Journal Stem Cell Res Ther Section Body Doc Link PMC2873699 Disease Relevance 1.26 Pain Relevance 0
Surprisingly, administration of opioid antagonists or interference with the Fas-FasL interaction was able to block HU-induced reductions of splenocytes, but not thymocytes.
Fas-FasL Binding (interaction) of in thymocytes associated with antagonist and opioid
8) Confidence 0.27 Published 2003 Journal Cell Res. Section Abstract Doc Link 14728803 Disease Relevance 0.18 Pain Relevance 0.19
Mouse Fas-Fc- a competitive inhibitor of Fas-Fas-L interactions effectively inhibited apoptosis in the lymphomas studied confirming the involvement of the Fas-Fas-L pathway in apoptosis induced by bacterial Sags.
Fas-Fc Binding (interactions) of in Mouse associated with lymphatic system cancer and apoptosis
9) Confidence 0.27 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3008744 Disease Relevance 1.13 Pain Relevance 0
One involves the interaction of a death receptor such as the tumor necrosis factor receptor-1 (TNFR1) or the Fas receptor with its ligand and the second pathway depends on the participation of mitochondria.
Fas Binding (interaction) of associated with necrosis, cancer and death
10) Confidence 0.27 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3008744 Disease Relevance 1.85 Pain Relevance 0
Strategies to inhibit Fas–FasL interaction may be useful neuroprotective approaches for reducing apoptosis after SCI.
Fas Binding (interaction) of associated with spinal cord injury and apoptosis
11) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2935363 Disease Relevance 2.33 Pain Relevance 0.10
Surprisingly, administration of opioid antagonists or interference with the Fas-FasL interaction was able to block HU-induced reductions of splenocytes, but not thymocytes.
Fas-FasL Binding (interaction) of in thymocytes associated with antagonist and opioid
12) Confidence 0.21 Published 2003 Journal Cell Res. Section Abstract Doc Link 14728803 Disease Relevance 0.18 Pain Relevance 0.19
, nitrotyrosine, PAR, Fas ligand, Bax and Bcl-2
Fas Binding (ligand) of
13) Confidence 0.21 Published 2010 Journal Respir Res Section Body Doc Link PMC2836283 Disease Relevance 0.05 Pain Relevance 0.03
Approximately 3% of cortical cells expressed Fas on their cell surface at a high intensity (FasHi), while 20% of cultured neural cells expressed moderate levels of Fas on their cell surface (FasMod).
FasHi Binding (intensity) of in neural
14) Confidence 0.20 Published 2004 Journal BMC Neurosci Section Body Doc Link PMC395829 Disease Relevance 0.40 Pain Relevance 0
The best-investigated downstream signalling pathways of apoptosis have been described as being predominantly caspase-dependent, following either the extrinsic receptor-mediated activation of caspase-3/7 via binding to members of the tumor necrosis factor receptor (TNFR) superfamily (for example, Fas receptor [CD95] and TNFR-I [CD120?])
CD95 Binding (binding) of associated with necrosis, cancer and apoptosis
15) Confidence 0.19 Published 2008 Journal Crit Care Section Body Doc Link PMC2374615 Disease Relevance 1.44 Pain Relevance 0.11
FasHi = High intensity of cell surface Fas immuno-fluorescence
FasHi Binding (intensity) of
16) Confidence 0.18 Published 2004 Journal BMC Neurosci Section Body Doc Link PMC395829 Disease Relevance 0.44 Pain Relevance 0
FasMod = Moderate intensity of cell surface Fas immuno-fluorescence
FasMod Binding (intensity) of
17) Confidence 0.18 Published 2004 Journal BMC Neurosci Section Body Doc Link PMC395829 Disease Relevance 0.43 Pain Relevance 0
[77] and Fas/FasL interactions contribute to death of gastric epithelial cells [78].
Fas Binding (interactions) of in epithelial cells associated with death
18) Confidence 0.14 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2896618 Disease Relevance 0.75 Pain Relevance 0.12
Here the effect of continuous activation of Fas/FasL interaction through a repeated FasL gene transfer was explored to determine if this treatment could result in the death of inflammatory synoviocytes in RA synovium and elimination of RA tissue in vivo.
Fas Binding (interaction) of in synovium associated with inflammation, rheumatoid arthritis and death
19) Confidence 0.11 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1297566 Disease Relevance 1.83 Pain Relevance 0.55
Upregulation of Fas/FasL interaction in arthritic joints by virus vector mediated FasL gene transfer or anti-Fas antibody treatment intra-articularly can induce apoptosis in inflammatory synoviocytes, as has been identified by many groups [5,12-18].
Fas Binding (interaction) of in joints associated with inflammation, apoptosis and arthritis
20) Confidence 0.11 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1297566 Disease Relevance 1.82 Pain Relevance 0.53

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox