INT139176

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Context Info
Confidence 0.51
First Reported 2007
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 5
Total Number 7
Disease Relevance 5.26
Pain Relevance 0.92

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 (Fadd) protein complex (Fadd) cytoplasm (Fadd)
Anatomy Link Frequency
brain 1
Fadd (Mus musculus)
Fadd - A375M (2)
Pain Link Frequency Relevance Heat
Endogenous opioid 2 98.26 Very High Very High Very High
rheumatoid arthritis 54 94.64 High High
opioid receptor 2 92.12 High High
opiate 3 89.68 High High
agonist 10 89.12 High High
Arthritis 108 86.64 High High
Inflammatory response 3 86.08 High High
Opioid 3 83.60 Quite High
cerebral cortex 2 82.16 Quite High
Inflammation 47 63.20 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 258 99.44 Very High Very High Very High
Death 49 95.04 Very High Very High Very High
Rheumatoid Arthritis 54 94.64 High High
Hepatotoxicity 2 94.64 High High
Melanoma 189 88.80 High High
Arthritis 112 86.64 High High
INFLAMMATION 50 85.72 High High
Severe Combined Immunodeficiency 8 70.68 Quite High
Malignant Neoplastic Disease 13 69.40 Quite High
Cancer 114 50.00 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The results suggest that mu-receptors tonically stimulate (through endogenous opioid peptides) the activation of native Fas, whereas delta-receptors tonically inhibit the expression of Fas aggregates and that of FADD and phosphorylated FADD (Ser191) in the mouse brain.
Gene_expression (expression) of FADD in brain associated with endogenous opioid
1) Confidence 0.51 Published 2007 Journal Eur Neuropsychopharmacol Section Abstract Doc Link 17030115 Disease Relevance 0.16 Pain Relevance 0.60
This is in agreement with in vitro studies, and with previous reports indicating a major role for acid SMase and the FADD-caspase pathway in TNF?
Gene_expression (pathway) of FADD-caspase
2) Confidence 0.36 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2843740 Disease Relevance 0.60 Pain Relevance 0.04
To further confirm that TRAIL-signaling is involved, the mutant cell line A375M.FADD-DED that ectopically overexpresses a dominant negative mutant of the adaptor protein FADD, was produced.
Neg (negative) Gene_expression (overexpresses) of FADD
3) Confidence 0.22 Published 2010 Journal Mol Cancer Section Body Doc Link PMC3000402 Disease Relevance 0.85 Pain Relevance 0
Recently we showed that the FADD and caspase-8 deficient cells were completely resistant to Fas-induced apoptosis [17].
Gene_expression (resistant) of FADD associated with apoptosis
4) Confidence 0.18 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2671171 Disease Relevance 0.84 Pain Relevance 0
To further confirm that TRAIL-signaling is involved, the mutant cell line A375M.FADD-DED that ectopically overexpresses a dominant negative mutant of the adaptor protein FADD, was produced.
Neg (negative) Gene_expression (overexpresses) of FADD (A375M)
5) Confidence 0.17 Published 2010 Journal Mol Cancer Section Body Doc Link PMC3000402 Disease Relevance 0.80 Pain Relevance 0
To further confirm that TRAIL-signaling is involved, the mutant cell line A375M.FADD-DED that ectopically overexpresses a dominant negative mutant of the adaptor protein FADD, was produced.
Gene_expression (produced) of FADD (A375M)
6) Confidence 0.17 Published 2010 Journal Mol Cancer Section Body Doc Link PMC3000402 Disease Relevance 0.86 Pain Relevance 0
It was found that adenoviral vectors expressing FADD could induce apoptosis in synoviocytes both in vitro and in vivo, suggesting that this strategy may be effective in the treatment of RA [109].


Gene_expression (expressing) of FADD associated with rheumatoid arthritis and apoptosis
7) Confidence 0.17 Published 2008 Journal Mod Rheumatol Section Body Doc Link PMC2275302 Disease Relevance 1.15 Pain Relevance 0.27

General Comments

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