INT234950

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Context Info
Confidence 0.36
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 29
Total Number 29
Disease Relevance 23.67
Pain Relevance 0.69

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 3
keratinocyte 3
plaque 2
teeth 2
myocardium 1
DSG1 (Homo sapiens)
Pain Link Frequency Relevance Heat
medulla 11 99.64 Very High Very High Very High
gABA 1 92.56 High High
Glutamate 1 91.36 High High
Neurotransmitter 1 90.52 High High
Chronic pancreatitis 30 89.68 High High
Kinase C 299 76.56 Quite High
vagus nerve 3 55.28 Quite High
Dopamine 1 17.24 Low Low
Nucleus accumbens 1 16.68 Low Low
amygdala 1 15.80 Low Low
Disease Link Frequency Relevance Heat
Dentinogenesis Imperfecta 258 100.00 Very High Very High Very High
Cleidocranial Dysplasia 171 99.92 Very High Very High Very High
Bullous Skin Disease 6992 99.84 Very High Very High Very High
Osteogenesis Imperfecta 45 99.76 Very High Very High Very High
Pancreatic Cancer 76 99.48 Very High Very High Very High
Acantholysis 1495 99.12 Very High Very High Very High
Pancreatitis 34 98.88 Very High Very High Very High
Heart Defects 92 98.08 Very High Very High Very High
Adenocarcinoma 28 97.08 Very High Very High Very High
Adhesions 1200 96.28 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
hK7 cleaves both recombinant Dsg1 and Dsg2 in vitro
Dsg1 Binding (recombinant) of
1) Confidence 0.36 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2628383 Disease Relevance 0.90 Pain Relevance 0.31
Immunoblotting for Dsg1 and Dsg2 in pancreatic cancer cell lines
Dsg1 Binding (Immunoblotting) of associated with pancreatic cancer
2) Confidence 0.36 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2628383 Disease Relevance 0.19 Pain Relevance 0
Individuals with DGI-I also have osteogenesis imperfecta.
DGI-I Binding (Individuals) of associated with osteogenesis imperfecta and dentinogenesis imperfecta
3) Confidence 0.33 Published 2008 Journal Orphanet J Rare Dis Section Body Doc Link PMC2600777 Disease Relevance 1.13 Pain Relevance 0
Like DD-I, DGI-III is associated with multiple periapical radiolucencies in noncarious teeth.
DGI Binding (associated) of in teeth associated with cleidocranial dysplasia and dentinogenesis imperfecta
4) Confidence 0.33 Published 2008 Journal Orphanet J Rare Dis Section Body Doc Link PMC2600777 Disease Relevance 1.53 Pain Relevance 0
DGI-III is also not associated with osteogenesis imperfecta and, unlike DGI-I and -II and DD-I and -II, it is associated with hypotrophy of dentine and resultant 'shell teeth' which are a distinguishing feature.
DGI Binding (associated) of in teeth associated with cleidocranial dysplasia, osteogenesis imperfecta and dentinogenesis imperfecta
5) Confidence 0.31 Published 2008 Journal Orphanet J Rare Dis Section Body Doc Link PMC2600777 Disease Relevance 1.60 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.
Dsg Binding (binding) of associated with acantholysis
6) Confidence 0.24 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.04 Pain Relevance 0
Therefore, if homophilic binding of Dsg 1 occurs in vivo, it has to be considered that it may contribute to effective intercellular adhesion only in the superficial epidermis.


Dsg Binding (binding) of in epidermis associated with adhesions
7) Confidence 0.24 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.21 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).
Dsg Binding (binding) of associated with acantholysis and bullous skin disease
8) Confidence 0.24 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.42 Pain Relevance 0
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).
Dsg Binding (binding) of in keratinocytes associated with bullous skin disease
9) Confidence 0.24 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.63 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).
Dsg Binding (binding) of in keratinocyte
10) Confidence 0.24 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.82 Pain Relevance 0
This indicates that Dsg 1 binding is strong only at extracellular Ca2+concentrations higher than 0.8 mM.
Dsg Binding (binding) of
11) Confidence 0.24 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.06 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).
Dsg Binding (binding) of associated with bullous skin disease
12) Confidence 0.24 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.06 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).
Dsg Binding (binding) of
13) Confidence 0.24 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.65 Pain Relevance 0
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).
Dsg Binding (binding) of
14) Confidence 0.24 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.
Dsg Binding (binding) of in epidermis associated with bullous skin disease
15) Confidence 0.24 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.11 Pain Relevance 0
These data indicate that PV-IgG and PF-IgG can reduce binding of Dsg 1 and Dsg 3, at least on the keratinocyte cell surface.
Dsg Binding (binding) of in keratinocyte associated with bullous skin disease
16) Confidence 0.24 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.79 Pain Relevance 0
However, no direct inhibition of Dsg 1 binding by PV-IgG and PF-IgG was detected by AFM.
Dsg Binding (binding) of associated with bullous skin disease
17) Confidence 0.18 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.85 Pain Relevance 0
These data suggest that autoantobodies interfere with Dsg 1 binding rather by indirect, cell-dependent mechanisms.
Dsg Binding (interfere) of
18) Confidence 0.18 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.67 Pain Relevance 0
It was found that the Ca2+ concentration for half-maximal binding activity of Dsg 1 is 0.8 mM Ca2+ and that binding is highly cooperative with the Hill coefficient being ?
Dsg Binding (binding) of
19) Confidence 0.18 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 0.05 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%.
Dsg Binding (depletion) of
20) Confidence 0.18 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.03 Pain Relevance 0.03

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