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1 those of controls by day 23, as does that of desmoglein 3.
2 tibodies to the desmosomal adhesion protein, desmoglein 3.
3 with human desmoglein 2, and 50% with human desmoglein 3.
4 are directed against the desmosomal cadherin desmoglein 3.
5 order like that observed for the full-length desmoglein 3.
6 proteins, including the desmosomal cadherin, desmoglein 3.
7 erin, P-cadherin, and a desmosomal cadherin, desmoglein 3.
8 urfaces was eliminated by preadsorption with 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 well established that autoantibodies against desmoglein 3 and desmoglein 1 (Dsg1) are relevant in the
13 higus foliaceus (PF), autoantibodies against desmoglein-3 and desmoglein-1 induce epidermal cell deta
15 We produced recombinant desmoglein-1 and desmoglein-3, and used them in highly sensitive and spec
16 1 antibodies in pemphigus foliaceus and anti-desmoglein 3 antibodies in pemphigus vulgaris are pathog
17 the carboxy- terminal cytoplasmic domains of desmoglein 3 are important for targeting it to the desmo
18 affinity-purified anti-desmoglein 1 and anti-desmoglein 3 autoantibodies from pemphigus vulgaris sera
19 n, the pathogenic anti-desmoglein 1 and anti-desmoglein 3 autoantibodies in pemphigus vulgaris had pr
21 a-catenin by 37%, gamma-catenin by 136%, and desmoglein 3 by 300%, whereas pretreatment with 0.25 mm
22 tinocyte cell surface desmocollin 3, but not desmoglein 3 by immunofluorescence, indicating distinct
23 racellular domain of the desmosomal cadherin desmoglein 3 cause potentially fatal blistering of the s
26 popolysaccharide, heat-shock cognate 70, and desmoglein-3 compared with DLE+SLE+ and DLE-SLE+ subject
30 Many desmosomal components were identified (desmoglein 3, desmocolin A/B, desmoplakin I, plakoglobin
31 via impaired redistribution of desmoplakin, desmoglein 3, desmocollin 3, and E-cadherin to the plasm
32 pattern that may result from autoimmunity to desmoglein 3, desmocollin 3, or both desmosomal cadherin
35 presence of autoantibodies directed against desmoglein 3 (Dsg 3), a protein expressed on keratinocyt
36 lity of the purified full-length autoantigen desmoglein 3 (Dsg 3).Therefore, we expressed Dsg 3 using
37 ibodies (IgG) target the desmosomal cadherin desmoglein 3 (Dsg3) and compromise keratinocyte cell-cel
38 ies primarily targeting desmosomal cadherins desmoglein 3 (DSG3) and DSG1, leading to loss of keratin
41 PK activation, whereas the signaling of anti-desmoglein 3 (Dsg3) antibody involved JNK and biphasic p
42 phigus vulgaris (PV), autoantibodies against desmoglein 3 (Dsg3) cause loss of cell-cell adhesion of
44 autoantibody-mediated disease, in which anti-desmoglein 3 (Dsg3) IgG autoantibodies cause life-threat
46 ge has been described in B cells reacting to desmoglein 3 (Dsg3) in the autoimmune disease pemphigus
50 ies directed against the desmosomal cadherin desmoglein 3 (Dsg3), the major autoantigen in PV, cause
54 s and pemphigus foliaceus autoantibodies are desmoglein-3 (Dsg3) and desmoglein-1 (Dsg1), respectivel
55 abasilar layers of skin and mucosae and anti-desmoglein-3 (Dsg3) autoantibodies bound to the surface
56 enic antibodies bind the desmosomal cadherin desmoglein-3 (dsg3), causing epidermal cell-cell detachm
60 onse to veltuzumab generally correlated with desmoglein 3 enzyme-linked immunosorbent assay index val
61 pontaneously to a physiological skin self-Ag desmoglein-3, epicutaneous applications of desmoglein-3
63 fundibulum and in epidermal inclusion cysts, desmoglein 3 expression was limited mainly to the basal
64 , these data showed that the perturbation of desmoglein 3 found in the Dsg3bal-Pas mice resulted in d
65 s lesions in neonatal mice, whereas the anti-desmoglein 3 fraction induced pemphigus vulgaris-like le
66 s shown that affinity-purified antibodies to desmoglein-3 from patients with pemphigus foliaceus and
68 t of plakoglobin/desmoglein 2 or plakoglobin/desmoglein 3; however, the stoichiometry of the plakoglo
70 desmoglein 3 in mice mimics autoimmunity to desmoglein 3 in pemphigus vulgaris, with mucosal-dominan
72 to determine the prevalence of antibodies to desmoglein-3 in patients with pemphigus foliaceus and fo
73 g desmoglein-3, epicutaneous applications of desmoglein-3 induced tolerance that is dependent on LCs.
76 We conclude that binding of plakoglobin to desmoglein 3 is an important step in desmosome assembly
79 ta4 integrin, collagen XVII, E-cadherin, and desmoglein-3, is strongly reduced, whereas, surprisingly
81 at loss of P-cadherin leads to a more severe desmoglein 3 mutant phenotype in the double knockout mic
82 rent defect in epithelial cell adhesion, the desmoglein 3 mutant phenotype resembles that of patients
83 ies labeled a recombinant desmosomal protein desmoglein 3 on immunoblotting and the immunolabeling of
84 the deletion and causing a truncation of the desmoglein 3 polypeptide by 199 amino acids, eliminating
85 generated a myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein and expressed it in keratinocytes.
86 ecause hypomorphic expression of a truncated desmoglein 3 protein led to a spectrum of severe patholo
87 sion of the myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein resulted in a reduction in staining
88 expressing myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein underwent dramatic changes in cell
90 that resulted in expression of a hypomorphic desmoglein 3 protein with a truncation of an extracellul
92 pathology not observed in mice deficient in desmoglein 3, similar human genetic alterations may also
93 liaceus and fogo selvagem have antibodies to desmoglein-3 that may be involved in the pathogenesis of
95 nt extracellular domains of desmoglein 1 and desmoglein 3 to obtain affinity-purified anti-desmoglein
97 is issue, we engineered transgenic mice with desmoglein 3 under the control of the involucrin promote
98 3bal-Pas skin, the corresponding protein for desmoglein 3 was completely absent in the oral mucosal e
99 icle, and in cysts arising from these areas, desmoglein 3 was expressed throughout all layers of the
100 nsmembrane and intracellular region of human desmoglein 3, we could show that the cytoplasmic tail is
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