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1 urfaces was eliminated by preadsorption with desmoglein 3.
2 tibodies to the desmosomal adhesion protein, desmoglein 3.
3 those of controls by day 23, as does that of desmoglein 3.
4  with human desmoglein 2, and 50% with human desmoglein 3.
5 order like that observed for the full-length desmoglein 3.
6 proteins, including the desmosomal cadherin, desmoglein 3.
7 are directed against the desmosomal cadherin desmoglein 3.
8 erin, P-cadherin, and a desmosomal cadherin, desmoglein 3.
9 ion-dependent manner by desmoglein-1 but not desmoglein-3.
10 of cross-reacting with both desmoglein-1 and desmoglein-3.
11 ase caused by autoantibodies (IgG) targeting desmoglein 3, a desmosomal cadherin.
12 well established that autoantibodies against desmoglein 3 and desmoglein 1 (Dsg1) are relevant in the
13 mphigus vulgaris and pemphigus foliaceus are desmoglein 3 and desmoglein 1, respectively.
14 higus foliaceus (PF), autoantibodies against desmoglein-3 and desmoglein-1 induce epidermal cell deta
15 vulgaris the major pathogenic antibody binds desmoglein-3, and mediates mucosal disease.
16     We produced recombinant desmoglein-1 and desmoglein-3, and used them in highly sensitive and spec
17 1 antibodies in pemphigus foliaceus and anti-desmoglein 3 antibodies in pemphigus vulgaris are pathog
18 vels, but patients with ARAs had higher anti-desmoglein 3 antibody (DSG3 Abs) levels compared with th
19 the carboxy- terminal cytoplasmic domains of desmoglein 3 are important for targeting it to the desmo
20 affinity-purified anti-desmoglein 1 and anti-desmoglein 3 autoantibodies from pemphigus vulgaris sera
21 n, the pathogenic anti-desmoglein 1 and anti-desmoglein 3 autoantibodies in pemphigus vulgaris had pr
22 orbed in a concentration-dependent manner by desmoglein-3 but not by desmoglein-1.
23 a-catenin by 37%, gamma-catenin by 136%, and desmoglein 3 by 300%, whereas pretreatment with 0.25 mm
24 tinocyte cell surface desmocollin 3, but not desmoglein 3 by immunofluorescence, indicating distinct
25 racellular domain of the desmosomal cadherin desmoglein 3 cause potentially fatal blistering of the s
26 odies against the desmosomal cadherin, DSG3 (desmoglein-3), cause acantholysis.
27                                              Desmoglein 3 chimeric autoantibody receptor T cells (DSG
28                 These findings indicate that desmoglein 3 clustering and endocytosis are associated w
29 popolysaccharide, heat-shock cognate 70, and desmoglein-3 compared with DLE+SLE+ and DLE-SLE+ subject
30      We found that the expression pattern of desmoglein 3 correlated with different types of keratini
31           We showed that these antibodies to desmoglein-3 could be absorbed in a concentration-depend
32                                              Desmoglein 3 deficiency in mice leads to a phenotype cha
33  Many desmosomal components were identified (desmoglein 3, desmocolin A/B, desmoplakin I, plakoglobin
34  via impaired redistribution of desmoplakin, desmoglein 3, desmocollin 3, and E-cadherin to the plasm
35 pattern that may result from autoimmunity to desmoglein 3, desmocollin 3, or both desmosomal cadherin
36 rast, animals mutant for both P-cadherin and desmoglein 3 die before weaning.
37  in neonatal mice, it was proposed that anti-desmoglein 3 (Dsg 3) autoantibody causes PV.
38  presence of autoantibodies directed against desmoglein 3 (Dsg 3), a protein expressed on keratinocyt
39 lity of the purified full-length autoantigen desmoglein 3 (Dsg 3).Therefore, we expressed Dsg 3 using
40 ibodies (IgG) target the desmosomal cadherin desmoglein 3 (Dsg3) and compromise keratinocyte cell-cel
41 ies primarily targeting desmosomal cadherins desmoglein 3 (DSG3) and DSG1, leading to loss of keratin
42 toantibodies to desmosomal adhesion proteins desmoglein 3 (Dsg3) and Dsg1.
43 es caused by autoantibodies directed against desmoglein 3 (Dsg3) and/or desmoglein 1(Dsg1).
44 PK activation, whereas the signaling of anti-desmoglein 3 (Dsg3) antibody involved JNK and biphasic p
45 phigus vulgaris (PV), autoantibodies against desmoglein 3 (Dsg3) cause loss of cell-cell adhesion of
46                       Autoantibodies against desmoglein 3 (Dsg3) have also been detected in sera from
47 autoantibody-mediated disease, in which anti-desmoglein 3 (Dsg3) IgG autoantibodies cause life-threat
48 rder and disorder of the desmosomal cadherin desmoglein 3 (Dsg3) in living cells.
49 ge has been described in B cells reacting to desmoglein 3 (Dsg3) in the autoimmune disease pemphigus
50 or downregulation of the desmosomal cadherin desmoglein 3 (DSG3) in the pathogenesis of PV.
51  the skin mediated by autoantibodies against desmoglein 3 (Dsg3) on epidermal keratinocytes.
52 skin and is caused by autoantibodies against desmoglein 3 (Dsg3) on epidermal keratinocytes.
53                                 Detection of desmoglein 3 (DSG3), a metastatic biomarker for head and
54 ies directed against the desmosomal cadherin desmoglein 3 (Dsg3), the major autoantigen in PV, cause
55                                              Desmoglein 3 (Dsg3), the pemphigus vulgaris antigen, has
56 ibodies to the keratinocyte adhesion protein desmoglein 3 (Dsg3).
57 e caused by autoantibodies (autoAbs) against desmoglein 3 (Dsg3).
58 s and pemphigus foliaceus autoantibodies are desmoglein-3 (Dsg3) and desmoglein-1 (Dsg1), respectivel
59 abasilar layers of skin and mucosae and anti-desmoglein-3 (Dsg3) autoantibodies bound to the surface
60 se characterized by autoantibodies targeting desmoglein-3 (Dsg3), a critical adhesion molecule in epi
61 enic antibodies bind the desmosomal cadherin desmoglein-3 (dsg3), causing epidermal cell-cell detachm
62 ies directed against the desmosomal cadherin desmoglein-3 (Dsg3).
63 ies generated target the desmosomal cadherin desmoglein-3 (Dsg3).
64 e disease mediated by autoantibodies against desmoglein-3 (Dsg3).
65 le of rituximab, >90.7% reduction in average desmoglein 3 ELISA titers from baseline to months 3-9 wa
66 le of rituximab, >90.7% reduction in average desmoglein 3 ELISA titers from baseline to months 3-9 wa
67 onse to veltuzumab generally correlated with desmoglein 3 enzyme-linked immunosorbent assay index val
68 pontaneously to a physiological skin self-Ag desmoglein-3, epicutaneous applications of desmoglein-3
69                          Both P-cadherin and desmoglein 3 expression are restricted to the basal and
70 fundibulum and in epidermal inclusion cysts, desmoglein 3 expression was limited mainly to the basal
71 , these data showed that the perturbation of desmoglein 3 found in the Dsg3bal-Pas mice resulted in d
72 s lesions in neonatal mice, whereas the anti-desmoglein 3 fraction induced pemphigus vulgaris-like le
73 s shown that affinity-purified antibodies to desmoglein-3 from patients with pemphigus foliaceus and
74                         Antibody blockade of desmoglein 3 function in pemphigus vulgaris patients lea
75 t of plakoglobin/desmoglein 2 or plakoglobin/desmoglein 3; however, the stoichiometry of the plakoglo
76                        Genetic deficiency of desmoglein 3 in mice mimics autoimmunity to desmoglein 3
77  desmoglein 3 in mice mimics autoimmunity to desmoglein 3 in pemphigus vulgaris, with mucosal-dominan
78                    We detected antibodies to desmoglein-3 in 19 of 276 patients with pemphigus foliac
79 to determine the prevalence of antibodies to desmoglein-3 in patients with pemphigus foliaceus and fo
80 g desmoglein-3, epicutaneous applications of desmoglein-3 induced tolerance that is dependent on LCs.
81 e assembly and leads to the incorporation of desmoglein 3 into the desmosome.
82                                              Desmoglein 3 is a transmembrane component of desmosome c
83   We conclude that binding of plakoglobin to desmoglein 3 is an important step in desmosome assembly
84  localized to the adherens junction, whereas desmoglein 3 is found in desmosomes.
85                                        Thus, desmoglein 3 is identified as a target antigen in intrae
86 ta4 integrin, collagen XVII, E-cadherin, and desmoglein-3, is strongly reduced, whereas, surprisingly
87                                  Utilizing a desmoglein-3 mouse model (Dsg3(-/-)) or keratin 5-specif
88 at loss of P-cadherin leads to a more severe desmoglein 3 mutant phenotype in the double knockout mic
89 rent defect in epithelial cell adhesion, the desmoglein 3 mutant phenotype resembles that of patients
90 ies labeled a recombinant desmosomal protein desmoglein 3 on immunoblotting and the immunolabeling of
91 the deletion and causing a truncation of the desmoglein 3 polypeptide by 199 amino acids, eliminating
92 generated a myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein and expressed it in keratinocytes.
93 ecause hypomorphic expression of a truncated desmoglein 3 protein led to a spectrum of severe patholo
94 sion of the myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein resulted in a reduction in staining
95  expressing myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein underwent dramatic changes in cell
96         The myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein was found predominantly in the cyto
97 that resulted in expression of a hypomorphic desmoglein 3 protein with a truncation of an extracellul
98 t and persistent contacts with internalizing desmoglein 3 puncta in keratinocytes treated with IgG of
99 ion, the purified anti-desmoglein 1 and anti-desmoglein 3 showed no cross-reactivity.
100  pathology not observed in mice deficient in desmoglein 3, similar human genetic alterations may also
101 liaceus and fogo selvagem have antibodies to desmoglein-3 that may be involved in the pathogenesis of
102 lgaris (PV) is mediated by autoantibodies to desmoglein 3, the pemphigus vulgaris antigen (PVA).
103 nt extracellular domains of desmoglein 1 and desmoglein 3 to obtain affinity-purified anti-desmoglein
104  that this region is essential for targeting desmoglein 3 to the desmosome.
105 is issue, we engineered transgenic mice with desmoglein 3 under the control of the involucrin promote
106 3bal-Pas skin, the corresponding protein for desmoglein 3 was completely absent in the oral mucosal e
107 icle, and in cysts arising from these areas, desmoglein 3 was expressed throughout all layers of the
108 nsmembrane and intracellular region of human desmoglein 3, we could show that the cytoplasmic tail is
109         Additionally, steady-state levels of desmoglein 3 were decreased and desmosomes were reduced
110                         These mice expressed desmoglein 3 with the same distribution in epidermis as

 
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