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1 egulation of KLK5 and abnormal expression of desmoglein 1 (DSG1) and filaggrin, but not PAR2 were ide
2 that autoantibodies against desmoglein 3 and desmoglein 1 (Dsg1) are relevant in the pathogenesis of
3 ated by pathogenic, predominantly IgG4, anti-desmoglein 1 (Dsg1) autoantibodies and is endemic in Lim
6 G4 autoantibody response to the self-antigen desmoglein 1 (Dsg1) cross-reacts with the LJM11 sand fly
8 ecular specificity to cleave mouse and human desmoglein 1 (Dsg1) once after glutamic acid residue 381
9 istering disease caused by autoantibodies to desmoglein 1 (Dsg1) that cause loss of epidermal cell ad
10 fferentiation-associated proteins, including desmoglein 1 (Dsg1), desmocollin 1 (Dsc1), and keratins
14 he cutaneous epithelium, and discovered that desmoglein 1 and 2 expression correlated with the state
19 hs in understanding the interactions between desmoglein 1 and plakogloben in staphylococcal-mediated
20 et was coimmunoprecipitated with E-cadherin, Desmoglein 1 and Plakoglobin, suggesting that they form
21 eads to decreased cell surface expression of desmoglein 1 and re-localization of its C terminus diffu
25 uring keratinocyte apoptosis and also reveal desmoglein 1 as a previously unrecognized regulator of a
30 hat UV-induced caspase cleavage of the human desmoglein 1 cytoplasmic tail results in distinct 17- an
34 t the complex formed between plakoglobin and desmoglein 1 has an overall molecular weight greater tha
35 l, short hairpin RNA-mediated suppression of desmoglein 1 in differentiated keratinocytes protected c
37 l that a 276-residue DSCR construct of human desmoglein 1 is intrinsically disordered and forms an in
38 d both by electron microscopy and by reduced desmoglein 1 levels in the stratum corneum (shown by imm
41 specificity of exfoliative toxin cleavage of desmoglein 1 resides not only in simple amino acid seque
44 th HGF-expressing adenovirus, E-cadherin and Desmoglein 1 were decreased in melanocytes, WM164 and WM
46 spase-3 as the preferred enzyme that cleaves desmoglein 1 within its unique repeating unit domain at
49 ation of complexes formed by plakoglobin and desmoglein 1, 2, or 3 are further examined through immun
50 desmoglein 4 shares 41% identity with human desmoglein 1, 37% with human desmoglein 2, and 50% with
51 circulating autoantibodies directed against desmoglein 1, a 160 kDa transmembrane desmosomal molecul
52 ion relied largely upon the up-regulation of desmoglein 1, a desmosomal cadherin that maintains the i
55 taxis (eotaxin 3, CCL26), barrier molecules (desmoglein 1, DSG1), tissue remodeling (periostin, POSTN
57 ratinocytes by downregulating E-cadherin and Desmoglein 1, therefore frees melanoma cells from the co
58 WM35, expressed normal level E-cadherin and Desmoglein 1, whereas most melanomas (18 out of 20) expr
69 creased the protein levels of E-cadherin and desmogleins 1 and 3 by 300, 180, and 40%, respectively.
70 Specific staining of KC for E-cadherin and desmogleins 1 and 3 increased by 235, 228, and 148%, res
72 ression patterns of the desmoglein isotypes, desmogleins 1, 2, and 3 in the cutaneous epithelium, and
73 ein isoforms have been characterized, namely desmogleins 1, 2, and 3 that are expressed in a tissue-
74 us epithelia there are two major isoforms of desmoglein, 1 and 3, with different distributions in epi
81 multiple markers of differentiation (such as desmoglein-1 [Dsg1], keratin-1, and loricrin) and abroga
84 to S. aureus showed enhanced degradation of desmoglein-1 and filaggrin, whereas small interfering RN
86 linked immunosorbent assay using recombinant desmoglein-1 and standardized the assay to enable compar
89 ase in corneodesmosome density and increased desmoglein-1 content, with a decline in serine protease
92 barrier function in association with loss of desmoglein-1 expression and has a regulatory role in rep
93 We previously detected IgG antibodies to desmoglein-1 in 97% of patients, but also in 55% of norm
94 PF), autoantibodies against desmoglein-3 and desmoglein-1 induce epidermal cell detachment (acantholy
98 paired barrier function (mediated by loss of desmoglein-1), increased production and/or activity of t
106 Here we compared the assembly properties of desmoglein 2 (Dsg2) and desmocollin 2 (Dsc2), which are
113 ere enriched with the C-terminal fragment of desmoglein 2 (Dsg2), a desmosomal cadherin often overexp
114 moplakin, plakoglobin, plakophilin 2 (PKP2), desmoglein 2 (DSG2), and desmocollin 2 (DSC2), respectiv
115 in accumulation of the desmosomal cadherin, desmoglein 2 (Dsg2), at cell-cell interfaces accompanied
116 the entire ectodomain of desmosomal cadherin desmoglein 2 (Dsg2), using a combination of small-angle
119 sm underlying cAMP-mediated strengthening of desmoglein 2 binding was dependent on expression of the
122 ular weight greater than that of plakoglobin/desmoglein 2 or plakoglobin/desmoglein 3; however, the s
124 (JUP), Desmoplakin (DSP), Plakophilin 2, and Desmoglein 2), have been identified in patients with ARV
126 teractions along cell junctions and the mean desmoglein 2-mediated binding forces, whereas N-cadherin
127 e collected at different disease stages from desmoglein 2-mutant mice, a well characterized AC model.
130 nergic signaling enhances both the number of desmoglein 2-specific interactions along cell junctions
132 (CAR) (Ad2 and Ad5) and the CD46 (Ad35) and desmoglein-2 (Ad7) viral receptors all induce the cGAS/S
134 nd to IEC monolayers and induced cleavage of desmoglein-2 (DSG-2) but not E-cadherin, leading to disr
135 (42%), including desmoplakin (DSP) (n = 6), desmoglein-2 (DSG2) (n = 5), plakophilin-4 (PKP4) (n = 1
136 he palmitoylation of the desmosomal cadherin desmoglein-2 (Dsg2) and characterized the role that palm
137 of transmembrane desmosomal cadherins termed desmoglein-2 (Dsg2) and desmocollin-2 (Dsc2) that affili
140 of the other intestinal desmosomal cadherin, desmoglein-2 (Dsg2) that pairs with Dsc2, results in dec
141 akin (n=44; 39%), plakophilin-2 (n=38; 34%), desmoglein-2 (n=30; 26%), and desmocollin-2 (n=1; 1%), w
144 rent high-affinity receptors (CAR, CD46, and desmoglein-2), and the magnitude of the cGAS/STING DNA r
145 C caused by mutations in DSG2, which encodes desmoglein-2, a component of the cardiac desmosome.
147 ibodies (IgG) target the desmosomal cadherin desmoglein 3 (Dsg3) and compromise keratinocyte cell-cel
148 ies primarily targeting desmosomal cadherins desmoglein 3 (DSG3) and DSG1, leading to loss of keratin
151 PK activation, whereas the signaling of anti-desmoglein 3 (Dsg3) antibody involved JNK and biphasic p
153 autoantibody-mediated disease, in which anti-desmoglein 3 (Dsg3) IgG autoantibodies cause life-threat
155 ge has been described in B cells reacting to desmoglein 3 (Dsg3) in the autoimmune disease pemphigus
157 ies directed against the desmosomal cadherin desmoglein 3 (Dsg3), the major autoantigen in PV, cause
161 well established that autoantibodies against desmoglein 3 and desmoglein 1 (Dsg1) are relevant in the
162 the carboxy- terminal cytoplasmic domains of desmoglein 3 are important for targeting it to the desmo
163 a-catenin by 37%, gamma-catenin by 136%, and desmoglein 3 by 300%, whereas pretreatment with 0.25 mm
164 tinocyte cell surface desmocollin 3, but not desmoglein 3 by immunofluorescence, indicating distinct
165 racellular domain of the desmosomal cadherin desmoglein 3 cause potentially fatal blistering of the s
167 We found that the expression pattern of desmoglein 3 correlated with different types of keratini
169 onse to veltuzumab generally correlated with desmoglein 3 enzyme-linked immunosorbent assay index val
170 fundibulum and in epidermal inclusion cysts, desmoglein 3 expression was limited mainly to the basal
171 , these data showed that the perturbation of desmoglein 3 found in the Dsg3bal-Pas mice resulted in d
174 desmoglein 3 in mice mimics autoimmunity to desmoglein 3 in pemphigus vulgaris, with mucosal-dominan
177 We conclude that binding of plakoglobin to desmoglein 3 is an important step in desmosome assembly
179 the deletion and causing a truncation of the desmoglein 3 polypeptide by 199 amino acids, eliminating
180 generated a myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein and expressed it in keratinocytes.
181 ecause hypomorphic expression of a truncated desmoglein 3 protein led to a spectrum of severe patholo
182 sion of the myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein resulted in a reduction in staining
183 expressing myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein underwent dramatic changes in cell
185 that resulted in expression of a hypomorphic desmoglein 3 protein with a truncation of an extracellul
187 is issue, we engineered transgenic mice with desmoglein 3 under the control of the involucrin promote
188 3bal-Pas skin, the corresponding protein for desmoglein 3 was completely absent in the oral mucosal e
189 icle, and in cysts arising from these areas, desmoglein 3 was expressed throughout all layers of the
192 via impaired redistribution of desmoplakin, desmoglein 3, desmocollin 3, and E-cadherin to the plasm
193 pattern that may result from autoimmunity to desmoglein 3, desmocollin 3, or both desmosomal cadherin
194 pathology not observed in mice deficient in desmoglein 3, similar human genetic alterations may also
195 nsmembrane and intracellular region of human desmoglein 3, we could show that the cytoplasmic tail is
202 t of plakoglobin/desmoglein 2 or plakoglobin/desmoglein 3; however, the stoichiometry of the plakoglo
203 enic antibodies bind the desmosomal cadherin desmoglein-3 (dsg3), causing epidermal cell-cell detachm
207 higus foliaceus (PF), autoantibodies against desmoglein-3 and desmoglein-1 induce epidermal cell deta
209 popolysaccharide, heat-shock cognate 70, and desmoglein-3 compared with DLE+SLE+ and DLE-SLE+ subject
211 s shown that affinity-purified antibodies to desmoglein-3 from patients with pemphigus foliaceus and
213 to determine the prevalence of antibodies to desmoglein-3 in patients with pemphigus foliaceus and fo
214 g desmoglein-3, epicutaneous applications of desmoglein-3 induced tolerance that is dependent on LCs.
216 liaceus and fogo selvagem have antibodies to desmoglein-3 that may be involved in the pathogenesis of
219 We produced recombinant desmoglein-1 and desmoglein-3, and used them in highly sensitive and spec
220 pontaneously to a physiological skin self-Ag desmoglein-3, epicutaneous applications of desmoglein-3
221 ta4 integrin, collagen XVII, E-cadherin, and desmoglein-3, is strongly reduced, whereas, surprisingly
227 of the exon/intron organization of the human desmoglein 4 gene (DSG4) demonstrates that it is compose
228 RT-PCR on multiple tissue cDNA samples that desmoglein 4 has very specific tissue expression in sali
233 We identified a cadherin family member, desmoglein 4, which is expressed in the suprabasal epide
235 tissue cDNA we have demonstrated that mouse desmogleins 4, 5, and 6 are all expressed in the epiderm
237 ecursor of 1060 amino acid residues, and the desmoglein 6 transcript contains an open reading frame o
238 herin, N-cadherin, VE-cadherin (cadherin-5), desmoglein, alpha, beta and gamma catenin, p120(ctn) and
239 In contrast, the transmembrane proteins desmoglein and desmocollin are efficiently transported t
240 ar interactions of the desmosomal cadherins, desmoglein and desmocollin, are required for epidermal c
242 The desmosomal cadherins, comprising the desmogleins and desmocollins, are calcium-dependent tran
243 ansmembrane components of the desmosome, the desmogleins and desmocollins, are members of the cadheri
250 impairs the trafficking of the desmoplakins, desmoglein, and desmocollin to the cell surface; these p
253 d squamous epithelia, such as the epidermis, desmogleins are generally expressed in a differentiation
255 terized, at the genetic level, a novel human desmoglein cDNA sharing homology with desmogleins 1, 2,
256 ed and characterized; pemphigus antigens are desmogleins (cell adhesion molecules in desmosomes), and
262 It was assumed that PV is caused by anti-desmoglein (Dsg) 3 autoimmunity because absorption of PV
263 or (CAAR), consisting of the PV autoantigen, desmoglein (Dsg) 3, fused to CD137-CD3zeta signaling dom
266 us membranes caused by autoantibodies to the desmoglein (DSG) family proteins DSG3 and DSG1, leading
267 determined the feasibility of using an anti-desmoglein (Dsg) mAb, Px44, to deliver a biologically ac
268 ntrast to integrins and classical cadherins, desmoglein (Dsg) molecules are not known to elicit intra
270 ned for desmocollin (DSC)2, occludin (OCLN), desmoglein (DSG)1, tight junction protein 2, and gap jun
271 e levels of the desmosomal adhesion molecule desmoglein (Dsg)3 by reducing its membrane incorporation
272 epletion of the desmosomal adhesion molecule desmoglein (Dsg)3 induced by autoantibodies from patient
273 t is characterized by autoantibodies against desmoglein (Dsg)3, whereas mucosal and skin lesion-produ
276 ered intercellular attachments are formed by desmogleins (Dsgs) and desmocollins (Dscs), but the natu
279 une disease in which antibodies specific for desmogleins (Dsgs) cause loss of keratinocyte cell adhes
283 omolog as well as two additional novel mouse desmoglein genes situated within the mouse cluster.
284 pression of dominant negative E-cadherin and Desmoglein in melanocytes demonstrated that both molecul
286 demonstrate that differential expression of desmoglein isoforms affects the major function of epider
288 Until recently, three mouse and three human desmoglein isoforms had been characterized that are expr
290 t study has shown that altering the ratio of desmoglein isoforms influences epidermal barrier functio
291 Here, we examined expression patterns of the desmoglein isotypes, desmogleins 1, 2, and 3 in the cuta
292 e display technologies to isolate human anti-desmoglein monoclonal antibodies from a patient with pem
293 hogenic effects in anti-desmocollin and anti-desmoglein pemphigus, despite their identical clinical p
296 the disease and highlights the relevance of desmoglein-specific versus nondesmoglein autoantibodies,
298 decrease in the detergent-insoluble pool of desmoglein suggested a reduced association with the IF c
299 osphorylated Pg remained associated with the desmoglein tail after both short and long term EGFR acti
300 dulated by the molecular interactions of the desmoglein tail and suggests that these novel regulatory
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