INT234951

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Context Info
Confidence 0.29
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 11
Disease Relevance 11.20
Pain Relevance 0.03

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

cytosol (DSG1) plasma membrane (DSG1)
Anatomy Link Frequency
epidermis 2
keratinocyte 2
DSG1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Kinase C 143 58.16 Quite High
metalloproteinase 66 5.00 Very Low Very Low Very Low
agonist 55 5.00 Very Low Very Low Very Low
corticosteroid 22 5.00 Very Low Very Low Very Low
addiction 22 5.00 Very Low Very Low Very Low
Inflammatory mediators 11 5.00 Very Low Very Low Very Low
Pain 11 5.00 Very Low Very Low Very Low
imagery 11 5.00 Very Low Very Low Very Low
antagonist 11 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Bullous Skin Disease 3344 99.60 Very High Very High Very High
Acantholysis 715 99.12 Very High Very High Very High
Adhesions 561 91.92 High High
Mucocutaneous Lymph Node Syndrome 11 87.16 High High
Blister 132 87.00 High High
Repression 22 71.92 Quite High
Shock 22 68.52 Quite High
Stress 44 51.32 Quite High
Disease 198 50.56 Quite High
Apoptosis 209 26.56 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It is possible that antibody-mediated direct inhibition of Dsg binding may contribute to trigger cellular signalling events (Muller et al. 2008a; Sharma et al. 2007; Tsunoda et al. 2003).
Negative_regulation (inhibition) of Dsg Binding (binding) of
1) Confidence 0.29 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.20 Pain Relevance 0
According to this model, blistering in PF affects the superficial epidermis because Dsg 3 is present in the deep epidermis to compensate for the autoantibody-induced loss of Dsg 1 binding.
Negative_regulation (loss) of Dsg Binding (binding) of in epidermis associated with bullous skin disease
2) Confidence 0.29 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.12 Pain Relevance 0
If extracellular autoantibody-mediated direct inhibition of Dsg binding would be the primary cause of acantholysis, it is hard to imagine how this process should be blocked by modified intracellular signalling or low temperature.
Negative_regulation (inhibition) of Dsg Binding (binding) of associated with acantholysis
3) Confidence 0.29 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.04 Pain Relevance 0
Because of the latter, the desmoglein compensation hypothesis has been used to promote the idea that autoantibodies reduce Dsg binding by direct inhibition rather than by unspecific proteolysis (Mahoney et al. 1999).
Negative_regulation (reduce) of Dsg Binding (binding) of
4) Confidence 0.29 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.66 Pain Relevance 0
These autoantibodies induced keratinocyte dissociation and reduced binding of both Dsg 3- and Dsg 1-coated microbeads to the surface of cultured keratinocytes, as revealed by laser trapping (Heupel et al. 2007; Waschke et al. 2005).
Negative_regulation (reduced) of Dsg Binding (binding) of in keratinocyte
5) Confidence 0.21 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.82 Pain Relevance 0
In PV, when only Dsg 3 antibodies are present, no epidermal blistering would occur because Dsg 1 is considered to compensate for autoantibody-induced loss of Dsg 3 binding.
Negative_regulation (loss) of Dsg Binding (binding) of associated with bullous skin disease
6) Confidence 0.21 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.90 Pain Relevance 0
These studies provided first evidence that direct inhibition of Dsg binding alone cannot account for acantholysis in PV and raised the hypothesis that plakoglobin could be part of a receptor complex required to transfer the signal from autoantibody-bound Dsg 3 into the cell, a phenomenon referred to as “outside-in” signalling (Muller et al. 2008a).
Negative_regulation (inhibition) of Dsg Binding (binding) of associated with acantholysis and bullous skin disease
7) Confidence 0.21 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.79 Pain Relevance 0
In the latter study it was shown that activation was mediated, at least in part, by Dsg 1- and/or Dsg 3-specific antibodies because Dsg depletion by siRNA reduced p38MAPK activation by 50%.
Negative_regulation (reduced) of Dsg Binding (depletion) of
8) Confidence 0.21 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.03 Pain Relevance 0.03
However, because PF-IgG were shown to induce cellular signalling events but not to directly reduce Dsg 1 binding, it seems that direct inhibition of Dsg transinteraction is not essential to alter Dsg-mediated signalling (Heupel et al. 2007; Waschke et al. 2005).
Negative_regulation (inhibition) of Dsg Binding (transinteraction) of associated with bullous skin disease
9) Confidence 0.21 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.09 Pain Relevance 0
At present, compelling evidence indicates that acantholysis in PV and in PF is initiated by cellular signalling pathways rather than by direct inhibition of Dsg binding (Fig. 11).
Negative_regulation (inhibition) of Dsg Binding (binding) of associated with acantholysis and bullous skin disease
10) Confidence 0.21 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.43 Pain Relevance 0
However, because PF-IgG were shown to induce cellular signalling events but not to directly reduce Dsg 1 binding, it seems that direct inhibition of Dsg transinteraction is not essential to alter Dsg-mediated signalling (Heupel et al. 2007; Waschke et al. 2005).
Negative_regulation (reduce) of Dsg Binding (binding) of associated with bullous skin disease
11) Confidence 0.21 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.11 Pain Relevance 0

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