INT234876

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Context Info
Confidence 0.59
First Reported 2008
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 29
Total Number 29
Disease Relevance 25.47
Pain Relevance 0.40

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
keratinocytes 4
epidermis 3
cleavage 1
Dsg3 (Mus musculus)
Pain Link Frequency Relevance Heat
Kinase C 234 79.52 Quite High
Pain 28 27.28 Quite Low
metalloproteinase 108 5.00 Very Low Very Low Very Low
agonist 90 5.00 Very Low Very Low Very Low
corticosteroid 37 5.00 Very Low Very Low Very Low
addiction 36 5.00 Very Low Very Low Very Low
imagery 19 5.00 Very Low Very Low Very Low
Inflammatory mediators 18 5.00 Very Low Very Low Very Low
antagonist 18 5.00 Very Low Very Low Very Low
cINOD 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 73 100.00 Very High Very High Very High
Bullous Skin Disease 5922 99.84 Very High Very High Very High
Acantholysis 1252 98.48 Very High Very High Very High
Adhesions 1071 98.40 Very High Very High Very High
Disease 502 98.16 Very High Very High Very High
Blister 292 94.16 High High
Autoimmune Disease 122 93.72 High High
Congenital Anomalies 11 91.80 High High
Streptococcus Infection 37 85.28 High High
Skin Infection 77 82.48 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Based on the assumption that autoantibodies neutralize adhesive functions, one would predict that loss of Dsg3 function in mice would mimic the phenotype of PV restricted to mucous membranes.
Negative_regulation (loss) of Dsg3 associated with bullous skin disease
1) Confidence 0.59 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2879910 Disease Relevance 1.14 Pain Relevance 0
Nevertheless, these mice enabled us for the first time to link the loss of DSG3 function to PV histopathology.
Negative_regulation (loss) of DSG3 associated with bullous skin disease
2) Confidence 0.59 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2879910 Disease Relevance 1.20 Pain Relevance 0
Nevertheless, the mechanism by which PV autoantibodies induce loss of DSG3 function and cause PV is still a controversial issue.
Negative_regulation (loss) of DSG3 associated with bullous skin disease
3) Confidence 0.59 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2879910 Disease Relevance 1.30 Pain Relevance 0
Loss of Dsc3 and Dsg3 Lead to Similar Histopathology but Target Different Tissues
Negative_regulation (Loss) of Dsg3
4) Confidence 0.59 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2879910 Disease Relevance 0.60 Pain Relevance 0
The hypotheses range from direct inhibition of desmoglein function to indirect loss of cell-cell adhesion.
Negative_regulation (inhibition) of desmoglein associated with adhesions
5) Confidence 0.59 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2879910 Disease Relevance 1.30 Pain Relevance 0
A likely explanation for the absence of lesions in these tissues lies in the expression of functionally redundant desmoglein isoforms which compensate for the loss of DSG3.
Negative_regulation (loss) of DSG3
6) Confidence 0.59 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2879910 Disease Relevance 0.55 Pain Relevance 0
This review focuses on mice that lack the desmosomal cadherins desmoglein 3 or desmocollin 3 in stratified epithelia.
Negative_regulation (lack) of desmoglein
7) Confidence 0.43 Published 2010 Journal Dermatology Research and Practice Section Abstract Doc Link PMC2879910 Disease Relevance 0.45 Pain Relevance 0
We thus hypothesized that ablating Dsc3 in mice might mimic the effects of loss of DSG3, leading to PV-like histopathology.
Negative_regulation (loss) of DSG3 associated with bullous skin disease
8) Confidence 0.43 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2879910 Disease Relevance 0.79 Pain Relevance 0
Mice with a targeted disruption of Dsg3 exhibited phenotypes very similar to those seen in PV patients and provided direct evidence for a role of DSG3 in maintaining cell-cell adhesion between keratinocytes.
Negative_regulation (disruption) of Dsg3 in keratinocytes associated with targeted disruption, bullous skin disease and adhesions
9) Confidence 0.43 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2879910 Disease Relevance 1.26 Pain Relevance 0
A likely explanation for the absence of lesions in these tissues lies in the expression of functionally redundant desmoglein isoforms which compensate for the loss of DSG3.
Negative_regulation (redundant) of desmoglein
10) Confidence 0.43 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2879910 Disease Relevance 0.60 Pain Relevance 0
Because depletion of Dsg 3 was first found in parallel with serine phosphorylation of Dsg 3, it was suggested that phosphorylation might be required for Dsg 3 degradation (Aoyama and Kitajima 1999; Aoyama et al. 1999; Bystryn and Rodriguez 1978; Rodriguez and Bystryn 1977).
Negative_regulation (depletion) of Dsg 3
11) Confidence 0.31 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.22 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 (depletion) of Dsg 3 associated with acantholysis and bullous skin disease
12) Confidence 0.31 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.46 Pain Relevance 0.08
Similarly, depletion of Dsg 3 has been convincingly shown in PV whereas depletion of Dsg 1 in both PV and PF is less clear (Yamamoto et al. 2007a).
Negative_regulation (depletion) of Dsg 3 associated with bullous skin disease
13) Confidence 0.31 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 2.37 Pain Relevance 0.11
Dsg 3 depletion was observed in DJM-1 cells at 40% confluence as well as in normal human keratinocytes.
Negative_regulation (depletion) of Dsg 3 in keratinocytes
14) Confidence 0.31 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.18 Pain Relevance 0
In contrast, in confluent HaCaT monolayers, a reduction of Dsg 3 half-life but no depletion of total cellular Dsg 3 was detected (Cirillo et al. 2006; Waschke et al. 2006).
Negative_regulation (reduction) of Dsg 3
15) Confidence 0.27 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.17 Pain Relevance 0
After 24 h, Dsg 3 but not Dsg 2, plakoglobin or desmoplakin was also depleted from the cytoskeletal fractions leading to reduced total cellular Dsg 3 levels (Calkins et al. 2006; Yamamoto et al. 2007a).
Negative_regulation (reduced) of Dsg 3
16) Confidence 0.27 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.24 Pain Relevance 0
In contrast, in confluent HaCaT monolayers, a reduction of Dsg 3 half-life but no depletion of total cellular Dsg 3 was detected (Cirillo et al. 2006; Waschke et al. 2006).
Neg (no) Negative_regulation (depletion) of Dsg 3
17) Confidence 0.27 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.17 Pain Relevance 0
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 Dsg3 in epidermis associated with bullous skin disease
18) Confidence 0.26 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.76 Pain Relevance 0
Interestingly, endocytosis and depletion of Dsg3 are increasingly recognized to contribute to pemphigus acantholysis (Calkins et al. 2006; Yamamoto et al. 2007a).
Negative_regulation (depletion) of Dsg3 associated with acantholysis and bullous skin disease
19) Confidence 0.23 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.68 Pain Relevance 0
The discrepancy between these conflicting findings may be explained in part by the notion that the desmoglein compensation hypothesis is based on the following two assumptions: (1) the expression pattern of Dsg 3 and Dsg 1 do not substantially overlap in epidermal and mucosal layers where the cleavage plane in PV and PF is located. (2) Dsg 1- and Dsg 3-specific autoantibodies only lead to inactivation of either Dsg 1 or Dsg 3, respectively.
Negative_regulation (inactivation) of Dsg 3 in cleavage associated with bullous skin disease
20) Confidence 0.23 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.74 Pain Relevance 0

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