INT234919

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Context Info
Confidence 0.39
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 5
Disease Relevance 6.76
Pain Relevance 0.04

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

cell adhesion (Dsg2) plasma membrane (Dsg2)
Anatomy Link Frequency
epidermis 1
Dsg2 (Mus musculus)
Pain Link Frequency Relevance Heat
Kinase C 52 72.08 Quite High
metalloproteinase 24 5.00 Very Low Very Low Very Low
agonist 20 5.00 Very Low Very Low Very Low
corticosteroid 9 5.00 Very Low Very Low Very Low
addiction 8 5.00 Very Low Very Low Very Low
imagery 5 5.00 Very Low Very Low Very Low
Pain 4 5.00 Very Low Very Low Very Low
Inflammatory mediators 4 5.00 Very Low Very Low Very Low
antagonist 4 5.00 Very Low Very Low Very Low
cINOD 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Bullous Skin Disease 1276 99.74 Very High Very High Very High
Adhesions 217 99.60 Very High Very High Very High
Acantholysis 262 97.48 Very High Very High Very High
Blister 84 96.52 Very High Very High Very High
Disease 80 87.28 High High
Streptococcus Infection 9 86.00 High High
Skin Infection 21 83.20 Quite High
Skin Diseases 21 80.20 Quite High
Stress 16 79.20 Quite High
Monilethrix 1 76.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In pemphigus foliaceus (PF), patients develop pathogenic autoantibodies that target Dsg1 and promote cell-cell disadhesion in the superficial epidermis, where Dsg1 is highly expressed, but which lacks Dsg3 and Dsg2.
Negative_regulation (lacks) of Dsg2 in epidermis associated with bullous skin disease
1) Confidence 0.39 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.77 Pain Relevance 0
As outlined above, both direct and indirect mechanisms finally leading to a loss of desmoglein-mediated adhesion have been found to be involved in pemphigus acantholysis.
Negative_regulation (loss) of desmoglein associated with acantholysis, bullous skin disease and adhesions
2) Confidence 0.12 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.52 Pain Relevance 0
Second, antibody binding has been shown to trigger intracellular signalling pathways, which indirectly results in loss of desmoglein-mediated binding (b)
Negative_regulation (loss) of desmoglein
3) Confidence 0.09 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.10 Pain Relevance 0
The major goal for the future is to elucidate the primary signalling pathways responsible for the diverse effects of pemphigus IgG such as inhibition of desmoglein binding, depletion of desmosomal components, loss of desmosomes, reorganization of the cytoskeleton and finally the induction of acantholysis.
Negative_regulation (inhibition) of desmoglein associated with acantholysis and bullous skin disease
4) Confidence 0.09 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.36 Pain Relevance 0.04
Later on, with the identification of desmosomal cadherins as the target antigens of pemphigus autoantibodies and with more sophisticated cell biologic tools at hand, the ideas of direct antibody-mediated inhibition and of indirect signalling-mediated reduction of desmoglein binding were developed (Fig. 8).
Negative_regulation (reduction) of desmoglein associated with bullous skin disease
5) Confidence 0.09 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.01 Pain Relevance 0

General Comments

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