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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 wasting (SAM) syndrome, caused by biallelic desmoglein 1 (DSG1) mutations, exhibit skin lesions remi
9 ecular specificity to cleave mouse and human desmoglein 1 (Dsg1) once after glutamic acid residue 381
10 istering disease caused by autoantibodies to desmoglein 1 (Dsg1) that cause loss of epidermal cell ad
11 fferentiation-associated proteins, including desmoglein 1 (Dsg1), desmocollin 1 (Dsc1), and keratins
16 he cutaneous epithelium, and discovered that desmoglein 1 and 2 expression correlated with the state
21 hs in understanding the interactions between desmoglein 1 and plakogloben in staphylococcal-mediated
22 et was coimmunoprecipitated with E-cadherin, Desmoglein 1 and Plakoglobin, suggesting that they form
23 eads to decreased cell surface expression of desmoglein 1 and re-localization of its C terminus diffu
27 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 l, short hairpin RNA-mediated suppression of desmoglein 1 in differentiated keratinocytes protected c
36 l that a 276-residue DSCR construct of human desmoglein 1 is intrinsically disordered and forms an in
39 specificity of exfoliative toxin cleavage of desmoglein 1 resides not only in simple amino acid seque
42 th HGF-expressing adenovirus, E-cadherin and Desmoglein 1 were decreased in melanocytes, WM164 and WM
43 spase-3 as the preferred enzyme that cleaves desmoglein 1 within its unique repeating unit domain at
46 desmoglein 4 shares 41% identity with human desmoglein 1, 37% with human desmoglein 2, and 50% with
47 circulating autoantibodies directed against desmoglein 1, a 160 kDa transmembrane desmosomal molecul
48 ion relied largely upon the up-regulation of desmoglein 1, a desmosomal cadherin that maintains the i
51 taxis (eotaxin 3, CCL26), barrier molecules (desmoglein 1, DSG1), tissue remodeling (periostin, POSTN
53 ratinocytes by downregulating E-cadherin and Desmoglein 1, therefore frees melanoma cells from the co
54 WM35, expressed normal level E-cadherin and Desmoglein 1, whereas most melanomas (18 out of 20) expr
65 creased the protein levels of E-cadherin and desmogleins 1 and 3 by 300, 180, and 40%, respectively.
66 Specific staining of KC for E-cadherin and desmogleins 1 and 3 increased by 235, 228, and 148%, res
68 ression patterns of the desmoglein isotypes, desmogleins 1, 2, and 3 in the cutaneous epithelium, and
69 ein isoforms have been characterized, namely desmogleins 1, 2, and 3 that are expressed in a tissue-
70 us epithelia there are two major isoforms of desmoglein, 1 and 3, with different distributions in epi
77 multiple markers of differentiation (such as desmoglein-1 [Dsg1], keratin-1, and loricrin) and abroga
80 to S. aureus showed enhanced degradation of desmoglein-1 and filaggrin, whereas small interfering RN
83 linked immunosorbent assay using recombinant desmoglein-1 and standardized the assay to enable compar
87 ase in corneodesmosome density and increased desmoglein-1 content, with a decline in serine protease
90 barrier function in association with loss of desmoglein-1 expression and has a regulatory role in rep
91 We previously detected IgG antibodies to desmoglein-1 in 97% of patients, but also in 55% of norm
92 PF), autoantibodies against desmoglein-3 and desmoglein-1 induce epidermal cell detachment (acantholy
96 paired barrier function (mediated by loss of desmoglein-1), increased production and/or activity of t
108 n with loss of desmosomal junctional protein desmoglein 2 (DSG2) is a hallmark in the pathogenesis of
111 ere enriched with the C-terminal fragment of desmoglein 2 (Dsg2), a desmosomal cadherin often overexp
112 moplakin, plakoglobin, plakophilin 2 (PKP2), desmoglein 2 (DSG2), and desmocollin 2 (DSC2), respectiv
113 in accumulation of the desmosomal cadherin, desmoglein 2 (Dsg2), at cell-cell interfaces accompanied
114 the entire ectodomain of desmosomal cadherin desmoglein 2 (Dsg2), using a combination of small-angle
118 sm underlying cAMP-mediated strengthening of desmoglein 2 binding was dependent on expression of the
122 (JUP), Desmoplakin (DSP), Plakophilin 2, and Desmoglein 2), have been identified in patients with ARV
124 eins which bind a critical junction protein, desmoglein 2, triggering the transient and specific open
125 teractions along cell junctions and the mean desmoglein 2-mediated binding forces, whereas N-cadherin
126 e collected at different disease stages from desmoglein 2-mutant mice, a well characterized AC model.
129 nergic signaling enhances both the number of desmoglein 2-specific interactions along cell junctions
131 (CAR) (Ad2 and Ad5) and the CD46 (Ad35) and desmoglein-2 (Ad7) viral receptors all induce the cGAS/S
133 nd to IEC monolayers and induced cleavage of desmoglein-2 (DSG-2) but not E-cadherin, leading to disr
134 (42%), including desmoplakin (DSP) (n = 6), desmoglein-2 (DSG2) (n = 5), plakophilin-4 (PKP4) (n = 1
135 he palmitoylation of the desmosomal cadherin desmoglein-2 (Dsg2) and characterized the role that palm
136 of transmembrane desmosomal cadherins termed desmoglein-2 (Dsg2) and desmocollin-2 (Dsc2) that affili
139 of the other intestinal desmosomal cadherin, desmoglein-2 (Dsg2) that pairs with Dsc2, results in dec
140 akin (n=44; 39%), plakophilin-2 (n=38; 34%), desmoglein-2 (n=30; 26%), and desmocollin-2 (n=1; 1%), w
141 model of ACM (homozygous knock-in of mutant desmoglein-2 [Dsg2(mut/mut)]) that recapitulates the car
142 xclusively express the desmosomal cadherins, Desmoglein-2 and Desmocollin-2 (Dsc2) that contribute to
147 ariants in desmosomal genes (desmoplakin and desmoglein-2) were identified in 12/25 of the cohort pre
148 rent high-affinity receptors (CAR, CD46, and desmoglein-2), and the magnitude of the cGAS/STING DNA r
149 C caused by mutations in DSG2, which encodes desmoglein-2, a component of the cardiac desmosome.
150 es in desmosomal proteins, plakophilin-2 and desmoglein-2, which have been reported to cause cardiac
152 ibodies (IgG) target the desmosomal cadherin desmoglein 3 (Dsg3) and compromise keratinocyte cell-cel
153 ies primarily targeting desmosomal cadherins desmoglein 3 (DSG3) and DSG1, leading to loss of keratin
156 PK activation, whereas the signaling of anti-desmoglein 3 (Dsg3) antibody involved JNK and biphasic p
158 autoantibody-mediated disease, in which anti-desmoglein 3 (Dsg3) IgG autoantibodies cause life-threat
160 ge has been described in B cells reacting to desmoglein 3 (Dsg3) in the autoimmune disease pemphigus
163 ies directed against the desmosomal cadherin desmoglein 3 (Dsg3), the major autoantigen in PV, cause
167 well established that autoantibodies against desmoglein 3 and desmoglein 1 (Dsg1) are relevant in the
168 the carboxy- terminal cytoplasmic domains of desmoglein 3 are important for targeting it to the desmo
169 a-catenin by 37%, gamma-catenin by 136%, and desmoglein 3 by 300%, whereas pretreatment with 0.25 mm
170 tinocyte cell surface desmocollin 3, but not desmoglein 3 by immunofluorescence, indicating distinct
171 racellular domain of the desmosomal cadherin desmoglein 3 cause potentially fatal blistering of the s
174 We found that the expression pattern of desmoglein 3 correlated with different types of keratini
176 onse to veltuzumab generally correlated with desmoglein 3 enzyme-linked immunosorbent assay index val
177 fundibulum and in epidermal inclusion cysts, desmoglein 3 expression was limited mainly to the basal
178 , these data showed that the perturbation of desmoglein 3 found in the Dsg3bal-Pas mice resulted in d
181 desmoglein 3 in mice mimics autoimmunity to desmoglein 3 in pemphigus vulgaris, with mucosal-dominan
183 the deletion and causing a truncation of the desmoglein 3 polypeptide by 199 amino acids, eliminating
184 generated a myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein and expressed it in keratinocytes.
185 ecause hypomorphic expression of a truncated desmoglein 3 protein led to a spectrum of severe patholo
186 sion of the myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein resulted in a reduction in staining
187 expressing myc-tagged truncated Dsg3bal-Pas desmoglein 3 protein underwent dramatic changes in cell
189 that resulted in expression of a hypomorphic desmoglein 3 protein with a truncation of an extracellul
191 is issue, we engineered transgenic mice with desmoglein 3 under the control of the involucrin promote
192 3bal-Pas skin, the corresponding protein for desmoglein 3 was completely absent in the oral mucosal e
193 icle, and in cysts arising from these areas, desmoglein 3 was expressed throughout all layers of the
195 via impaired redistribution of desmoplakin, desmoglein 3, desmocollin 3, and E-cadherin to the plasm
196 pattern that may result from autoimmunity to desmoglein 3, desmocollin 3, or both desmosomal cadherin
197 pathology not observed in mice deficient in desmoglein 3, similar human genetic alterations may also
204 enic antibodies bind the desmosomal cadherin desmoglein-3 (dsg3), causing epidermal cell-cell detachm
208 higus foliaceus (PF), autoantibodies against desmoglein-3 and desmoglein-1 induce epidermal cell deta
210 popolysaccharide, heat-shock cognate 70, and desmoglein-3 compared with DLE+SLE+ and DLE-SLE+ subject
212 s shown that affinity-purified antibodies to desmoglein-3 from patients with pemphigus foliaceus and
214 to determine the prevalence of antibodies to desmoglein-3 in patients with pemphigus foliaceus and fo
215 g desmoglein-3, epicutaneous applications of desmoglein-3 induced tolerance that is dependent on LCs.
217 liaceus and fogo selvagem have antibodies to desmoglein-3 that may be involved in the pathogenesis of
220 We produced recombinant desmoglein-1 and desmoglein-3, and used them in highly sensitive and spec
221 pontaneously to a physiological skin self-Ag desmoglein-3, epicutaneous applications of desmoglein-3
222 ta4 integrin, collagen XVII, E-cadherin, and desmoglein-3, is strongly reduced, whereas, surprisingly
228 of the exon/intron organization of the human desmoglein 4 gene (DSG4) demonstrates that it is compose
229 RT-PCR on multiple tissue cDNA samples that desmoglein 4 has very specific tissue expression in sali
234 We identified a cadherin family member, desmoglein 4, which is expressed in the suprabasal epide
236 tissue cDNA we have demonstrated that mouse desmogleins 4, 5, and 6 are all expressed in the epiderm
238 ecursor of 1060 amino acid residues, and the desmoglein 6 transcript contains an open reading frame o
239 herin, N-cadherin, VE-cadherin (cadherin-5), desmoglein, alpha, beta and gamma catenin, p120(ctn) and
240 In contrast, the transmembrane proteins desmoglein and desmocollin are efficiently transported t
241 ar interactions of the desmosomal cadherins, desmoglein and desmocollin, are required for epidermal c
243 ens junctions, desmosomal cadherins - called desmogleins and desmocollins - link intermediate filamen
244 The desmosomal cadherins, comprising the desmogleins and desmocollins, are calcium-dependent tran
245 ansmembrane components of the desmosome, the desmogleins and desmocollins, are members of the cadheri
249 impairs the trafficking of the desmoplakins, desmoglein, and desmocollin to the cell surface; these p
252 d squamous epithelia, such as the epidermis, desmogleins are generally expressed in a differentiation
254 terized, at the genetic level, a novel human desmoglein cDNA sharing homology with desmogleins 1, 2,
255 ed and characterized; pemphigus antigens are desmogleins (cell adhesion molecules in desmosomes), and
259 ssion profiles of the desmosomal PV antigens desmoglein (Dsg) 3 and 1 but not of the adherens junctio
264 or (CAAR), consisting of the PV autoantigen, desmoglein (Dsg) 3, fused to CD137-CD3zeta signaling dom
268 us membranes caused by autoantibodies to the desmoglein (DSG) family proteins DSG3 and DSG1, leading
269 determined the feasibility of using an anti-desmoglein (Dsg) mAb, Px44, to deliver a biologically ac
270 ntrast to integrins and classical cadherins, desmoglein (Dsg) molecules are not known to elicit intra
271 ity of T(H) and T(FH) cell subsets to induce desmoglein (Dsg)-specific autoantibodies by memory B cel
272 ed against two desmosomal adhesion proteins, desmoglein (Dsg)1 and Dsg3 (also known as DG1 and DG3),
274 ned for desmocollin (DSC)2, occludin (OCLN), desmoglein (DSG)1, tight junction protein 2, and gap jun
275 e levels of the desmosomal adhesion molecule desmoglein (Dsg)3 by reducing its membrane incorporation
276 epletion of the desmosomal adhesion molecule desmoglein (Dsg)3 induced by autoantibodies from patient
277 t is characterized by autoantibodies against desmoglein (Dsg)3, whereas mucosal and skin lesion-produ
280 ered intercellular attachments are formed by desmogleins (Dsgs) and desmocollins (Dscs), but the natu
283 une disease in which antibodies specific for desmogleins (Dsgs) cause loss of keratinocyte cell adhes
287 omolog as well as two additional novel mouse desmoglein genes situated within the mouse cluster.
288 pression of dominant negative E-cadherin and Desmoglein in melanocytes demonstrated that both molecul
289 Until recently, three mouse and three human desmoglein isoforms had been characterized that are expr
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