INT234888

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Context Info
Confidence 0.34
First Reported 2008
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 9
Total Number 12
Disease Relevance 11.73
Pain Relevance 0.11

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 2
other parts 1
Dsg2 (Mus musculus)
Pain Link Frequency Relevance Heat
metalloproteinase 54 74.84 Quite High
Kinase C 117 71.52 Quite High
Inflammatory mediators 9 36.76 Quite Low
agonist 45 5.00 Very Low Very Low Very Low
corticosteroid 21 5.00 Very Low Very Low Very Low
addiction 18 5.00 Very Low Very Low Very Low
imagery 12 5.00 Very Low Very Low Very Low
Pain 9 5.00 Very Low Very Low Very Low
antagonist 9 5.00 Very Low Very Low Very Low
cINOD 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Bullous Skin Disease 2916 99.46 Very High Very High Very High
Blister 216 99.40 Very High Very High Very High
Adhesions 498 98.30 Very High Very High Very High
Acantholysis 591 95.12 Very High Very High Very High
Disease 186 91.44 High High
Streptococcus Infection 21 90.92 High High
Targeted Disruption 129 90.52 High High
Skin Infection 51 83.20 Quite High
Skin Diseases 48 80.20 Quite High
Stress 36 78.64 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.
Dsg2 Binding (lacks) of in epidermis associated with bullous skin disease
1) Confidence 0.34 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.77 Pain Relevance 0
It is possible that Dsg2 counters the impact of PF Ig on these pathways, resulting in the retention of Dsg1 at the cell surface and maintenance of desmosome structure and function.
Dsg2 Binding (counters) of associated with bullous skin disease
2) Confidence 0.34 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.26 Pain Relevance 0
These experiments allowed us to compare the relative intensity of the ETA- and PF-induced blister formation in the presence or absence of Dsg2 in the superficial epidermis.
Dsg2 Neg (absence) Binding (absence) of in epidermis associated with blister and bullous skin disease
3) Confidence 0.33 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.76 Pain Relevance 0
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).
desmoglein Binding (binding) of associated with bullous skin disease
4) Confidence 0.10 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.96 Pain Relevance 0
An antibody directed against the putative transadhesive interface may directly induce steric hindrance, whereas antibodies directed against other parts of the desmoglein ectodomain could indirectly inhibit desmoglein binding by allosteric mechanisms.
desmoglein Binding (binding) of in other parts
5) Confidence 0.10 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.25 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.
desmoglein Binding (binding) of associated with acantholysis and bullous skin disease
6) Confidence 0.10 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.36 Pain Relevance 0.04
Therefore, “direct inhibition”, instead of “steric hindrance” of desmoglein binding should be used until discrimination between steric and allosteric effects is possible.


desmoglein Binding (binding) of
7) Confidence 0.10 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.31 Pain Relevance 0
First, antibodies could directly interfere with desmoglein transinteraction (a).
desmoglein Binding (transinteraction) of
8) Confidence 0.07 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.03 Pain Relevance 0
Finally, it has to be noted that, if direct inhibition occurs, it is not possible to discriminate at present whether interference with Dsg 3 binding in PV was mediated by steric hindrance, i.e. by blocking trans-interaction of desmoglein molecules by the bound autoantibody, or rather by allosteric effects, i.e. autoantibody-induced conformational changes of the Dsg 3 ectodomain, which in turn interfere with Dsg 3 transinteraction.
desmoglein Binding (interaction) of associated with bullous skin disease
9) Confidence 0.07 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.50 Pain Relevance 0
The desmosomal cadherins desmoglein and desmocollin undergo homophilic and heterophilic binding via interaction with the amino-terminal extracellular (EC) 1 domain of partner molecules on the same (cis) as well as on the neighbouring cell (trans).
desmoglein Binding (binding) of
10) Confidence 0.07 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.16 Pain Relevance 0
Since it was discovered that autoantibodies in pemphigus are directed to desmosomal adhesion molecules, it was believed that these autoantibodies might directly interfere with desmoglein binding (Fig. 8) (Amagai et al. 1991; Jones et al. 1986a; Koulu et al. 1984), a mechanism also refered to as “steric hindrance”(Sharma et al. 2007).
desmoglein Spec (might) Binding (binding) of associated with bullous skin disease and adhesions
11) Confidence 0.07 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.14 Pain Relevance 0.03
Direct inhibition of desmoglein binding
desmoglein Binding (binding) of
12) Confidence 0.07 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.24 Pain Relevance 0.04

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