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1 CE constituents, including downregulation of desmoglein 1.
2 n disease mediated by autoantibodies against desmoglein 1.
3 g in an endemic area have antibodies against desmoglein 1.
4 of junctional integrity through cleavage of desmoglein 1.
5 lysis) and pathogenic autoantibodies against desmoglein 1.
6 ease characterized by autoantibodies against desmoglein 1.
7 mes (CD) as well as CD constituent proteins, desmoglein 1.
8 ssed no E-cadherin and significantly reduced Desmoglein 1.
9 s in the desmosomal proteins desmoplakin and desmoglein 1.
10 -dependent manner by desmoglein-3 but not by desmoglein-1.
11 how that repeats 1-4 are involved in binding desmoglein-1.
12 athogenic antibodies to the EC1-2 domains of desmoglein-1.
13 mao Verde differ in IgG subclass response to desmoglein-1.
14 oped world, is mediated by IgG antibodies to desmoglein-1.
15 associated with acquisition of antibodies to desmoglein-1.
16 ation of complexes formed by plakoglobin and desmoglein 1, 2, or 3 are further examined through immun
18 ression patterns of the desmoglein isotypes, desmogleins 1, 2, and 3 in the cutaneous epithelium, and
19 ein isoforms have been characterized, namely desmogleins 1, 2, and 3 that are expressed in a tissue-
21 desmoglein 4 shares 41% identity with human desmoglein 1, 37% with human desmoglein 2, and 50% with
22 circulating autoantibodies directed against desmoglein 1, a 160 kDa transmembrane desmosomal molecul
23 ion relied largely upon the up-regulation of desmoglein 1, a desmosomal cadherin that maintains the i
26 he cutaneous epithelium, and discovered that desmoglein 1 and 2 expression correlated with the state
29 esmoglein 3 to obtain affinity-purified anti-desmoglein 1 and anti-desmoglein 3 autoantibodies from p
31 By immunoprecipitation, the purified anti-desmoglein 1 and anti-desmoglein 3 showed no cross-react
35 soluble recombinant extracellular domains of desmoglein 1 and desmoglein 3 to obtain affinity-purifie
36 hs in understanding the interactions between desmoglein 1 and plakogloben in staphylococcal-mediated
37 et was coimmunoprecipitated with E-cadherin, Desmoglein 1 and Plakoglobin, suggesting that they form
38 eads to decreased cell surface expression of desmoglein 1 and re-localization of its C terminus diffu
40 us epithelia there are two major isoforms of desmoglein, 1 and 3, with different distributions in epi
43 to S. aureus showed enhanced degradation of desmoglein-1 and filaggrin, whereas small interfering RN
46 linked immunosorbent assay using recombinant desmoglein-1 and standardized the assay to enable compar
48 creased the protein levels of E-cadherin and desmogleins 1 and 3 by 300, 180, and 40%, respectively.
49 Specific staining of KC for E-cadherin and desmogleins 1 and 3 increased by 235, 228, and 148%, res
50 addition to AuAbs against adhesion molecules desmogleins 1 and 3, PV patients also produce an AuAb ag
56 uring keratinocyte apoptosis and also reveal desmoglein 1 as a previously unrecognized regulator of a
58 dies; however, the pathogenicity of the anti-desmoglein 1 autoantibodies in pemphigus vulgaris remain
59 of pemphigus vulgaris sera also contain anti-desmoglein 1 autoantibodies; however, the pathogenicity
66 ase in corneodesmosome density and increased desmoglein-1 content, with a decline in serine protease
68 hat UV-induced caspase cleavage of the human desmoglein 1 cytoplasmic tail results in distinct 17- an
69 the E-cadherin extracellular domain and the desmoglein-1 cytoplasmic domain, and these cells formed
71 eatment significantly increased abundance of desmoglein-1, desmocollin-1 and plakoglobin in the BPD g
72 ent in every sample, the desmosome proteins: desmoglein-1, desmocollin-1 and plakoglobin were signifi
75 D (SdrD) adhesin and the human skin protein desmoglein-1 (DSG-1), withstanding forces exceeding 2 na
77 egulation of KLK5 and abnormal expression of desmoglein 1 (DSG1) and filaggrin, but not PAR2 were ide
78 ase Area Index (PDAI) score of 45 or higher, desmoglein 1 (DSG1) antibodies greater than 20 IU/mL, an
79 that autoantibodies against desmoglein 3 and desmoglein 1 (Dsg1) are relevant in the pathogenesis of
81 ated by pathogenic, predominantly IgG4, anti-desmoglein 1 (Dsg1) autoantibodies and is endemic in Lim
84 G4 autoantibody response to the self-antigen desmoglein 1 (Dsg1) cross-reacts with the LJM11 sand fly
87 wasting (SAM) syndrome, caused by biallelic desmoglein 1 (DSG1) mutations, exhibit skin lesions remi
88 ecular specificity to cleave mouse and human desmoglein 1 (Dsg1) once after glutamic acid residue 381
89 istering disease caused by autoantibodies to desmoglein 1 (Dsg1) that cause loss of epidermal cell ad
90 loss of the keratinocyte-specific cadherin, Desmoglein 1 (Dsg1), controls paracrine signaling betwee
91 fferentiation-associated proteins, including desmoglein 1 (Dsg1), desmocollin 1 (Dsc1), and keratins
92 nds to DP and Dsc1a, and to a lesser extent, desmoglein 1 (Dsg1), while PG binds to Dsg1 and more wea
99 he desmosomal cadherins to mediate adhesion, desmoglein-1 (Dsg1), desmocollin-2 (Dsc2a) and plakoglob
106 multiple markers of differentiation (such as desmoglein-1 [Dsg1], keratin-1, and loricrin) and abroga
108 taxis (eotaxin 3, CCL26), barrier molecules (desmoglein 1, DSG1), tissue remodeling (periostin, POSTN
112 barrier function in association with loss of desmoglein-1 expression and has a regulatory role in rep
114 t the complex formed between plakoglobin and desmoglein 1 has an overall molecular weight greater tha
115 tion of the superficial desmosomal cadherin, desmoglein 1, impedes basal stratification in an in vitr
116 l, short hairpin RNA-mediated suppression of desmoglein 1 in differentiated keratinocytes protected c
117 nosorbent assay to detect antibodies against desmoglein 1 in serum samples from 60 patients with ende
118 We previously detected IgG antibodies to desmoglein-1 in 97% of patients, but also in 55% of norm
119 paired barrier function (mediated by loss of desmoglein-1), increased production and/or activity of t
120 PF), autoantibodies against desmoglein-3 and desmoglein-1 induce epidermal cell detachment (acantholy
123 pt that the production of antibodies against desmoglein 1 is initiated by exposure to an unknown envi
124 l that a 276-residue DSCR construct of human desmoglein 1 is intrinsically disordered and forms an in
126 d both by electron microscopy and by reduced desmoglein 1 levels in the stratum corneum (shown by imm
131 specificity of exfoliative toxin cleavage of desmoglein 1 resides not only in simple amino acid seque
137 ratinocytes by downregulating E-cadherin and Desmoglein 1, therefore frees melanoma cells from the co
140 th HGF-expressing adenovirus, E-cadherin and Desmoglein 1 were decreased in melanocytes, WM164 and WM
142 WM35, expressed normal level E-cadherin and Desmoglein 1, whereas most melanomas (18 out of 20) expr
143 spase-3 as the preferred enzyme that cleaves desmoglein 1 within its unique repeating unit domain at