INT234933

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Context Info
Confidence 0.71
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 31
Disease Relevance 38.52
Pain Relevance 0.20

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 17
basal cell 2
Dsg2 (Mus musculus)
Pain Link Frequency Relevance Heat
Kinase C 26 94.52 High High
corticosteroid 33 73.76 Quite High
cINOD 29 68.96 Quite High
imagery 31 5.00 Very Low Very Low Very Low
metalloproteinase 12 5.00 Very Low Very Low Very Low
agonist 10 5.00 Very Low Very Low Very Low
addiction 4 5.00 Very Low Very Low Very Low
Pain 2 5.00 Very Low Very Low Very Low
Inflammatory mediators 2 5.00 Very Low Very Low Very Low
antagonist 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 1247 100.00 Very High Very High Very High
Bullous Skin Disease 2348 99.82 Very High Very High Very High
Stress 8 99.48 Very High Very High Very High
Adhesions 479 99.34 Very High Very High Very High
Blister 1068 99.24 Very High Very High Very High
Disease 268 98.60 Very High Very High Very High
Acantholysis 188 98.40 Very High Very High Very High
Hyperplasia 29 96.88 Very High Very High Very High
Congenital Anomalies 29 93.08 High High
Skin Infection 153 88.72 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We assessed the expression of the Dsg2-Flag transgene in skin from newborn Tg mice by immunostaining; antibodies against Flag and Dsg2 (MP6) (Figure 1(b)) showed expression of Dsg2-Flag in the superficial cell layers.
Gene_expression (expression) of Dsg2 in skin associated with targeted disruption
1) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.54 Pain Relevance 0
Next, we wanted to assess whether ectopic expression of Dsg2 could protect against skin blister formation induced by PF pathogenic antibodies.
Gene_expression (expression) of Dsg2 in skin associated with blister and bullous skin disease
2) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.51 Pain Relevance 0
Also, suprabasal expression of Dsg2 in Tg mice offers greater protection against PF Ig, as compared to ETA (Figure 4).
Gene_expression (expression) of Dsg2 associated with targeted disruption and bullous skin disease
3) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.33 Pain Relevance 0
In keeping with the literature, we observed some negligible expression of endogenous Dsg2 in the basal cell layer.
Gene_expression (expression) of Dsg2 in basal cell
4) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.28 Pain Relevance 0
We also immunostained the same tissues for Dsg2-Flag to demonstrate that Tg, but not WT, mice expressed the Dsg2-Flag transgene (Figure 5(a), middle panels).
Gene_expression (expressed) of Dsg2 associated with targeted disruption
5) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 0.81 Pain Relevance 0
In this paper, we demonstrate that ectopic expression of Dsg2 in the superficial epidermis could limit both PF Ig- and ETA-induced skin blister formation, suggesting that steric hindrance plays a role in the mechanism of pemphigus.
Gene_expression (expression) of Dsg2 in epidermis associated with blister and bullous skin disease
6) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.43 Pain Relevance 0
Thus, our results demonstrate that, at the Western blot level, PF Ig depletes Dsg1 and that superficial expression of Dsg2 in Tg mice did not appear to modulate the level of Dsg1 in response to PF Ig.
Gene_expression (expression) of Dsg2 associated with targeted disruption and bullous skin disease
7) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.70 Pain Relevance 0
These results suggest that coexpression of Dsg2 with Dsg1 in the superficial epidermis may protect from the loss of Dsg1 by ETA although we cannot rule out the possibility that ectopic expression of Dsg2 may also impair the ETA-digestion of Dsg1 molecules.
Gene_expression (coexpression) of Dsg2 in epidermis
8) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.06 Pain Relevance 0
Collectively, our results demonstrate that ectopic expression of Dsg2 could partially compensate for the loss of Dsg1-mediated adhesion in response to ETA digestion.

2.3.

Gene_expression (expression) of Dsg2 associated with adhesions
9) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.20 Pain Relevance 0
We assessed the expression of the Dsg2-Flag transgene in skin from newborn Tg mice by immunostaining; antibodies against Flag and Dsg2 (MP6) (Figure 1(b)) showed expression of Dsg2-Flag in the superficial cell layers.
Gene_expression (expression) of Dsg2 in skin associated with targeted disruption
10) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.32 Pain Relevance 0
We observed that overexpression of Dsg2 provided enhanced protection against blister formation in response to ETA (Figure 2(c)).
Gene_expression (overexpression) of Dsg2 associated with blister
11) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 0.96 Pain Relevance 0
What remains to be addressed in future studies is (1) whether ectopic expression of Dsg2 alters the sensitivity of Dsg1 to degradation by ETA or loss of function upon antibody binding, and (2) whether the loss of Dsg1 function in pemphigus is caused by altered signaling and/or steric hindrance.
Gene_expression (expression) of Dsg2 associated with bullous skin disease
12) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 0.77 Pain Relevance 0.11
Next, we wanted to evaluate whether or not superficial expression of Dsg2 had an effect on Dsg1 fate and localization in response to PF Ig.
Gene_expression (expression) of Dsg2 associated with bullous skin disease
13) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.46 Pain Relevance 0
These results suggest that coexpression of Dsg2 with Dsg1 in the superficial epidermis may protect from the loss of Dsg1 by ETA although we cannot rule out the possibility that ectopic expression of Dsg2 may also impair the ETA-digestion of Dsg1 molecules.
Gene_expression (expression) of Dsg2 in epidermis
14) Confidence 0.71 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.04 Pain Relevance 0
In summary, we generated transgenic mice expressing Dsg2 in the superficial epidermis of newborn mice.

2.2.

Gene_expression (expressing) of Dsg2 in epidermis associated with targeted disruption
15) Confidence 0.62 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.13 Pain Relevance 0
In Tg mice treated with PF Ig, the presence of Dsg2 in the superficial epidermis helped retain Dsg1 at the cell-cell border (Figure 5(b), middle and right panels).
Gene_expression (presence) of Dsg2 in epidermis associated with targeted disruption and bullous skin disease
16) Confidence 0.62 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 0.80 Pain Relevance 0
Expression of Dsg2 in the Superficial Epidermis of Inv-Dsg2 Tg Mice
Gene_expression (Expression) of Dsg2 in Epidermis associated with targeted disruption
17) Confidence 0.55 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.66 Pain Relevance 0
In this paper, we showed that superficial expression of Dsg2 in Tg mice offers protection against skin blister formation in response to the bacterial toxin ETA and pathogenic PF antibodies.
Gene_expression (expression) of Dsg2 in skin associated with targeted disruption, blister and bullous skin disease
18) Confidence 0.55 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 0.97 Pain Relevance 0
In conclusion, superficial expression of Dsg2 appears to maintain the organization of Dsg1 in response to PF Ig treatment.


Gene_expression (expression) of Dsg2 associated with bullous skin disease
19) Confidence 0.55 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 0.91 Pain Relevance 0
To assess the ability of Dsg2 to enhance cell adhesion and to test the hypothesis that Dsg2 expression in the suprabasal epidermis can limit PF/ETA blister formation by increasing keratinocyte adhesion, we employed a transgenic mouse model expressing Dsg2 in the superficial epidermis under the involucrin promoter (Inv-Dsg2 Tg) [14].
Gene_expression (expressing) of Dsg2 in epidermis associated with targeted disruption, blister, bullous skin disease and adhesions
20) Confidence 0.55 Published 2010 Journal Dermatology Research and Practice Section Body Doc Link PMC2902105 Disease Relevance 1.92 Pain Relevance 0

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