INT234908

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Context Info
Confidence 0.31
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 6
Disease Relevance 7.18
Pain Relevance 0.19

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 (Dsg3) plasma membrane (Dsg3)
Anatomy Link Frequency
epidermis 2
keratinocytes 2
Dsg3 (Mus musculus)
Pain Link Frequency Relevance Heat
Kinase C 78 77.92 Quite High
metalloproteinase 36 5.00 Very Low Very Low Very Low
agonist 30 5.00 Very Low Very Low Very Low
corticosteroid 12 5.00 Very Low Very Low Very Low
addiction 12 5.00 Very Low Very Low Very Low
Inflammatory mediators 6 5.00 Very Low Very Low Very Low
Pain 6 5.00 Very Low Very Low Very Low
imagery 6 5.00 Very Low Very Low Very Low
antagonist 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Bullous Skin Disease 1824 99.84 Very High Very High Very High
Acantholysis 390 99.12 Very High Very High Very High
Blister 72 90.08 High High
Disease 108 58.92 Quite High
Stress 24 47.68 Quite Low
Adhesions 306 47.04 Quite Low
Apoptosis 114 5.00 Very Low Very Low Very Low
Vohwinkel Syndrome 36 5.00 Very Low Very Low Very Low
Skin Diseases 30 5.00 Very Low Very Low Very Low
Heart Defects 24 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Therefore, it is possible that direct inhibition as a second pathway to reduce Dsg 3 binding in PV may explain the more severe phenotype of PV.
Negative_regulation (reduce) of Dsg 3 Binding (binding) of associated with bullous skin disease
1) Confidence 0.31 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 2.32 Pain Relevance 0.11
Recently, by using single-molecule atomic force microscopy (AFM), it was shown that PV-IgG as well as AK 23 directly interfered with homophilic Dsg 3 binding under cell free conditions (Heupel et al. 2007) which supports the hypothesis of direct inhibition of Dsg 3 binding in PV (Stanley and Amagai 2006).
Negative_regulation (inhibition) of Dsg 3 Binding (binding) of associated with bullous skin disease
2) Confidence 0.23 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.87 Pain Relevance 0
In addition, other mechanisms such as direct inhibition of Dsg 3 binding and Dsg 3 depletion from desmosomes as well as other signalling events seem to contribute to PV pathogenesis, whereas their role for acantholysis in PF is unclear.
Negative_regulation (inhibition) of Dsg 3 Binding (binding) of associated with acantholysis and bullous skin disease
3) Confidence 0.23 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.46 Pain Relevance 0.08
With respect to the second assumption the desmoglein compensation is based on, i.e. selective inactivation of Dsg 1 but not of Dsg 3 by Dsg 1-specific antibodies, it was shown recently that both PF-IgG (only containing Dsg 1-specific antibodies) and PV-IgG from patients with only Dsg 3-specific antibodies were equally effective to reduce binding of Dsg 1- and Dsg 3-coated beads to the surface of cultured keratinocytes (Heupel et al. 2007; Spindler et al. 2007).
Negative_regulation (reduce) of Dsg 3-coated Binding (binding) of in keratinocytes associated with bullous skin disease
4) Confidence 0.23 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.64 Pain Relevance 0
In PV, epidermal involvement would occur only when autoantibodies against both Dsg 1 and Dsg 3 are present because Dsg 1 is found in all epidermal layers and could compensate for loss of Dsg 3 binding when antibodies to Dsg 3 are solely presentFig. 10Immunostaining of Dsg 1 and Dsg 3 in PV lesional epidermis.
Negative_regulation (loss) of Dsg 3 Binding (binding) of in epidermis associated with bullous skin disease
5) Confidence 0.22 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.00 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 3 Binding (binding) of associated with bullous skin disease
6) Confidence 0.22 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.89 Pain Relevance 0

General Comments

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