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1                                              Dsg1 (desmoglein 1) is a member of the cadherin family o
2                                              Dsg1 is specifically expressed in stratified epidermis a
3                                              Dsg1 lacking N-terminal ectodomain residues required for
4                                              Dsg1 loss-of-function mutations in humans result in skin
5                                              Dsg1.myc, but not Dsc1a, Dsc1b, disrupted desmosome asse
6 odies against desmoglein 3 and desmoglein 1 (Dsg1) are relevant in the pathogenesis of pemphigus vulg
7 enic, predominantly IgG4, anti-desmoglein 1 (Dsg1) autoantibodies and is endemic in Limao Verde, Braz
8 s (PF), autoantibodies against desmoglein 1 (Dsg1) cause blisters.
9 y response to the self-antigen desmoglein 1 (Dsg1) cross-reacts with the LJM11 sand fly salivary glan
10                                Desmoglein 1 (Dsg1) is a cadherin restricted to stratified tissues of
11                                Desmoglein 1 (Dsg1) is a desmosomal cadherin that is essential to epid
12 city to cleave mouse and human desmoglein 1 (Dsg1) once after glutamic acid residue 381 between extra
13 se caused by autoantibodies to desmoglein 1 (Dsg1) that cause loss of epidermal cell adhesion.
14 eratinocyte-specific cadherin, Desmoglein 1 (Dsg1), controls paracrine signaling between normal melan
15 associated proteins, including desmoglein 1 (Dsg1), desmocollin 1 (Dsc1), and keratins 1 and 10 (K1/K
16 Dsc1a, and to a lesser extent, desmoglein 1 (Dsg1), while PG binds to Dsg1 and more weakly to Dsc1a a
17 tracellular domains 3 and 4 of desmoglein 1 (Dsg1).
18 ic IgG4 autoantibodies against desmoglein 1 (Dsg1).
19  desmosomal cadherin component desmoglein 1 (Dsg1).
20 blistering and pathogenic anti-desmoglein-1 (Dsg1) autoantibodies.
21 cadherins to mediate adhesion, desmoglein-1 (Dsg1), desmocollin-2 (Dsc2a) and plakoglobin were expres
22 es are desmoglein-3 (Dsg3) and desmoglein-1 (Dsg1), respectively.
23 nst a desmosomal glycoprotein, desmoglein-1 (Dsg1).
24 against the desmosomal antigen desmoglein-1 (Dsg1).
25 , and the desmosomal cadherin, desmoglein-1 (Dsg1).
26 e desmosomal core glycoprotein desmoglein-1 (Dsg1).
27 rs of differentiation (such as desmoglein-1 [Dsg1], keratin-1, and loricrin) and abrogated MAL/SRF si
28 inst desmoglein 3 (Dsg3) and/or desmoglein 1(Dsg1).
29 F) possess pathogenic IgG anti-desmoglein 1-(Dsg1) autoantibodies.
30 importance of these findings, treatment of 2 Dsg1-deficient patients with an IL-12/IL-23 antagonist o
31 which signals Cx43 turnover, increased after Dsg1 depletion, while lysosomal inhibition restored Cx43
32 t and specific autoantibody response against Dsg1 and other keratinocyte cadherins in these individua
33 ace adhesion proteins desmoglein (Dsg) 3 and Dsg1.
34                                     Dsg3 and Dsg1 are members of the desmoglein subfamily of the cadh
35 aris patients after incubation with Dsg3 and Dsg1 fusion proteins.
36 ding to Dsg3 or Dsg1 alone, or both Dsg3 and Dsg1.
37 PV autoantibodies bind Dsg3 or both Dsg3 and Dsg1.
38  characterized by autoantibodies to Dsg3 and Dsg1.
39 al adhesion proteins desmoglein 3 (Dsg3) and Dsg1.
40   Coexpression of Dsc1a.myc or Dsc1b.myc and Dsg1.myc did not lead to their colocalization and failed
41       In contrast, Dsc1a.myc, Dsc1b.myc, and Dsg1.myc did not stably incorporate into desmosomes in a
42                                         Anti-Dsg1 monoclonal autoantibodies derived from FS patients
43 on of the heavy-chain gene usage of all anti-Dsg1 clones to only five genes, which determined their i
44 e correlation between these indexes and anti-Dsg1 and anti-Dsg3 enzyme-linked immunosorbent assay val
45  subset of PF patients who only express anti-Dsg1 of the IgG1 isotype throughout the course of their
46 ) where Dsg1 without Dsg3 is expressed, anti-Dsg1 antibodies alone can cause blisters.
47 1-/- mice resembles that resulting from anti-Dsg1 pemphigus foliaceus antibodies, pemphigus skin lesi
48      Mice immunized with LJM11 generate anti-Dsg1 Abs.
49 ensitivity, specificity, and PPV of IgG anti-Dsg1 were 87, 91, and 23%, respectively.
50  IgM anti-Dsg1 across ages, whereas IgG-anti-Dsg1 was detected in 2.9% (age 5-10 years), 7.3% (age 11
51 cterize the pathogenicity of their IgG1 anti-Dsg1.
52      Previously, we found that the IgG4 anti-Dsg1 autoantibodies only recognize a conformational epit
53 m LV (n=99, age 5-20 years) possess IgM anti-Dsg1 across ages, whereas IgG-anti-Dsg1 was detected in
54                     We propose that IgM anti-Dsg1 are common in FS patients in their native environme
55                                     IgM anti-Dsg1 epitopes are Ca2+ and carbohydrate-independent.
56                                     IgM anti-Dsg1 were detected in 58% FS LV patients (n=31), 19% of
57        High percentages of positive IgM anti-Dsg1 were found in healthy donors from four rural Amerin
58 ology, we used phage display to isolate anti-Dsg1 mAbs as single-chain variable fragments (scFvs) fro
59 rom pemphigus vulgaris patients with no anti-Dsg1 serum reactivity showed a proliferative response to
60                      The combination of anti-Dsg1 values of 20 or more IU/mL and/or anti-Dsg3 values
61 ent were predictors of higher titers of anti-Dsg1.
62                          The pathogenic anti-Dsg1 and anti-Dsg3 mAbs, which bind the transadhesive in
63                                   Serum anti-Dsg1 and anti-Dsg3 enzyme-linked immunosorbent assay val
64 py of a perilesional biopsy, with serum anti-Dsg1 or anti-Dsg3 antibodies (or both) detected by ELISA
65              These results suggest that anti-Dsg1 autoantibodies in FS are initially raised against t
66                              Therefore, anti-Dsg1/3 AuAb-free PV can be a model for elucidating the r
67 osomal antigen BP180 and desmosomal antigens Dsg1 and Dsg3, respectively.
68                                           As Dsg1 promotes epidermal differentiation in addition to p
69 increases, exposing a potential link between Dsg1 deficiency and epidermal metabolism.
70 igen (GalNAc-alpha1-O-Ser/Thr), did not bind Dsg1 and did not show a protective effect against the di
71 O-glycan-specific plant lectin jacalin binds Dsg1 and inhibits the interaction of Dsg1/PF IgG.
72               Over 90% are specific for both Dsg1 and Dsg3 indicating extensive cross-reactivity betw
73            The UVB-induced reduction in both Dsg1 transcript and protein was associated with reduced
74               Our findings suggest that both Dsg1 autoantigen and LJM11 environmental Ag could be the
75 us vulgaris sera have IgG reactivity to both Dsg1 and Dsg3, suggesting that Dsg1 may also participate
76  pemphigus vulgaris patients respond to both Dsg1 and Dsg3.
77 all identified IgG4 mAbs cross-react to both Dsg1 and LJM11 Ags.
78 hese PV patients showed reactivity with both Dsg1 and Dsg3, whereas the remaining four reacted only w
79 Galbeta1-3GalNAcalpha-O-Ser/Thr), also bound Dsg1 and blocked the skin blistering.
80                    Antibodies against BP180, Dsg1, and Dsg3, when injected into neonatal mice, induce
81 inocytes because of compensatory adhesion by Dsg1 do not activate p38.
82  214 FS patients and 261 healthy controls by Dsg1 ELISA.
83 and prevents the loss of adhesion induced by Dsg1 truncation.
84 ferentiation through the desmosomal cadherin Dsg1.
85 tive Gal4 depends on an F box protein called Dsg1/Mdm30.
86 uman, ETA binds, but does not cleave, canine Dsg1.
87 n human Dsg1 and either human Dsg3 or canine Dsg1, we show that for cleavage, human-specific amino ac
88 epidermis and mucous membrane that coexpress Dsg1 and Dsg3, antibodies against either desmoglein alon
89 m those patients that exhibited the combined Dsg1/Dsg3 autoantibody reactivity showed a proliferative
90 syndrome patients (n = 7) revealed decreased Dsg1 and Cx43 plasma membrane localization compared with
91        Here, we show that ectodomain-deleted Dsg1 (Delta381-Dsg1) mimics the toxin-cleaved cadherin,
92  show that ectodomain-deleted Dsg1 (Delta381-Dsg1) mimics the toxin-cleaved cadherin, disrupts desmos
93 tional adhesion in cells expressing Delta381-Dsg1 or treated with exfoliative toxin A.
94            Compared with controls, depleting Dsg1 via short hairpin RNA resulted in further reduction
95 n, in the DSG1 gene coding for a desmoglein (Dsg1), results in the deletion of the first and much of
96        In keratinocytes, several desmoglein (Dsg1-4) and desmocollin (Dsc1-3) isoforms are coexpresse
97  CSN and desmosomal components, Desmoglein1 (Dsg1) and Desmoplakin (Dp), to promote epidermal differe
98 odels, showing that a single mAb can disrupt Dsg1 function to cause disease.
99             We show that the retromer drives Dsg1 recycling from the endo-lysosomal system to the pla
100                                      Ectopic Dsg1 expression increased cell-cell dye transfer, which
101 herin and the extracellular domain of either Dsg1 or Dsc2a were expressed in L cells.
102 oglein proteins, and demonstrate that either Dsg1 or Dsg3 alone is sufficient to maintain keratinocyt
103 liferative response after exposure to either Dsg1 or Dsg3 fusion proteins.
104    Whole transcriptome analysis of embryonic Dsg1-/- skin showed a delay in expression of adhesion/di
105 quamous epithelial cells that do not express Dsg1 or Dsc1.
106 xtensive aggregation, but L cells expressing Dsg1 or Dsc2a did not aggregate.
107           In addition, L cells co-expressing Dsg1, Dsc2a, and plakoglobin failed to aggregate.
108  desmoglein (Dsg) 3 and, to a lesser extent, Dsg1.
109           In concordance, immunostaining for Dsg1 but not for Dsg3 was reduced after 24 h of Ca(2+) c
110                 These data reveal a role for Dsg1 in regulating epidermal Cx43 turnover.
111    Consistent with this hypothesis, we found Dsg1 and Dsg3 expression overlapping in the companion la
112 or cleavage, human-specific amino acids from Dsg1 are necessary in extracellular domain 3 upstream of
113       However, presentation of peptides from Dsg1 by preDsg1-specific B cells may be one step in deve
114      Comparing epidermal transcriptomes from Dsg1-deficient mice and humans revealed a shared IL-17-s
115 an Dsg1 and chimeric molecules between human Dsg1 and either human Dsg3 or canine Dsg1, we show that
116             Using truncated mutants of human Dsg1 and chimeric molecules between human Dsg1 and eithe
117          As positive controls, we identified Dsg1 and Dsg3 ES targeted by PV sera.
118 he plakoglobin:E-cadherin ratio decreased in Dsg1-expressing cells with disrupted desmosomes, but a d
119  impaired intercellular adhesion observed in Dsg1-/- mice resembles that resulting from anti-Dsg1 pem
120 me mAbs plus exfoliative toxin to inactivate Dsg1 but not exfoliative toxin alone activate p38, sugge
121 used exfoliative toxin A (ETA) to inactivate Dsg1 in Dsg3-/- mice.
122                                     Instead, Dsg1 was required for suppression of epidermal growth fa
123 communication by secreting factors that keep Dsg1 expression low in the surrounding keratinocytes, wh
124 atinocytes resulting in chronic keratinocyte Dsg1 reduction contributes to melanoma cell movement ass
125 possessed natural antibodies targeting M3AR, Dsg1 and Dsg3 epitopes that were different from those ta
126 evious patient, were directed against mature Dsg1 (matDsg1) on the cell surface of keratinocytes and
127 l cohesion is prevalent in tumor metastasis, Dsg1 integrity was evaluated.
128 n re-introduction of wild-type Dsg1, but not Dsg1 constructs modeling SAM syndrome-causing mutations.
129 gs revealed increased Dsg3 molecules but not Dsg1 molecules binding strength in murine keratinocytes.
130 DP-NTP binds directly to plakoglobin but not Dsg1.
131                            In the absence of Dsg1, Gal4 is stable, nonubiquitylated, and unable to pr
132 ne RNA and protein levels; in the absence of Dsg1, Gal4 target genes are transcribed, but the resulti
133                            In the absence of Dsg1, retromer association with and expression of the gl
134 e restricted to the first 161 amino acids of Dsg1, whereas the linear epitopes are spread throughout
135 ith active disease inhibited the adhesion of Dsg1/Dsc1 and Dsg3/Dsc3 beads, respectively.
136 hesive interface, blocked the aggregation of Dsg1/Dsc1 and Dsg3/Dsc3 beads, respectively, whereas non
137 yndrome, pathogenesis depends on cleavage of Dsg1 by a bacterial protease, exfoliative toxin A, which
138   Kinetic studies monitoring the cleavage of Dsg1 by ETA, ETB, and ETD demonstrated kcat/Km values of
139 ts show that SCC25 cells exhibit cleavage of Dsg1, which is blocked by proteinase inhibitor treatment
140  we test the hypothesis that coexpression of Dsg1 and Dsg3 in keratinocytes protects against patholog
141 the mechanism by which genetic deficiency of Dsg1 causes chronic inflammation is unknown.
142 and organotypic skin equivalents depleted of Dsg1 exhibited reduced Cx43 expression, rescued upon re-
143  sera and the normal tissue distributions of Dsg1 and Dsg3 determine the sites of blister formation.
144 ised against the COOH-terminal EC5 domain of Dsg1 in individuals without skin disease; in genetically
145  epitopes on the COOH-terminal EC5 domain of Dsg1, (b) disease onset was associated with the emergenc
146 e in response to the extracellular domain of Dsg1.
147 s on the NH2-terminal EC1 and EC2 domains of Dsg1 leading to disease onset.
148 interfering RNAs that silenced expression of Dsg1 and/or Dsg3 proteins, blocked approximately 50% of
149                        Ectopic expression of Dsg1 in keratinocyte monolayers rescued the UVB-induced
150  in keratinocytes, and ectopic expression of Dsg1 rescued defects in differentiation seen upon loss o
151 lation is not involved in the interaction of Dsg1/jacalin or Dsg1/PF IgG.
152 n binds Dsg1 and inhibits the interaction of Dsg1/PF IgG.
153 ed that loss of Bcr or MAL reduced levels of Dsg1 mRNA in keratinocytes, and ectopic expression of Ds
154 , R55, promotes the membrane localization of Dsg1 and a trafficking-deficient mutant associated with
155    A reciprocal relationship between loss of Dsg1 and neddylated EGFR was observed in a carcinoma mod
156 yond impairing the physical barrier, loss of Dsg1 function through gene mutation results in a psoriat
157 isruption correlated with the recruitment of Dsg1.myc, but not Dsc1a or Dsc1b, into a Triton-insolubl
158 icipating in cell-cell adhesion, the role of Dsg1 in aiding differentiation after UVB damage was test
159 ndent on the calcium-stabilized structure of Dsg1.
160 conformational epitopes in the N terminus of Dsg1.
161 acalin to O-linked TF carbohydrate motifs on Dsg1 impairs the Dsg1/PF autoantibody interactions and a
162 se proteins interacted with Dsg1 and rely on Dsg1 and desmoplakin for robust cortical localization.
163    ScFv mAbs demonstrated binding to Dsg3 or Dsg1 alone, or both Dsg3 and Dsg1.
164 volved in the interaction of Dsg1/jacalin or Dsg1/PF IgG.
165 tely 1:1 stoichiometry; however, plakoglobin:Dsg1 complexes exhibited a 6:1 stoichiometry.
166 aining of A431DE cells (E-cadherin positive, Dsg1 negative) with pemphigus sera showed negative resul
167  cell surface of keratinocytes and precursor Dsg1 (preDsg1) in the cytoplasm.
168 ibodies, bead assays coated with recombinant Dsg1, Dsc1, Dsg3, or Dsc3 ectodomains were developed.
169 y FS patients in response to endogenous self-Dsg1 and exogenous LJM11 sand fly Ag.
170       These mAbs will be useful for studying Dsg1 function and mechanisms of blister formation in PF
171 sponse to Dsg1 loss, we deleted the 3 tandem Dsg1 genes in mice.
172                         We hypothesized that Dsg1 compensates for the loss of Dsg3 in the anagen hair
173                  In this study, we show that Dsg1 is not only required for maintaining epidermal tiss
174 ivity to both Dsg1 and Dsg3, suggesting that Dsg1 may also participate in the autoimmune response of
175 ch Cx43 silencing inhibited, suggesting that Dsg1 promotes GJ function through Cx43.
176                                          The Dsg1 fusion protein used in this study has minimal seque
177                These autoantibodies bind the Dsg1 ectodomain and trigger keratinocyte cell detachment
178 d TF carbohydrate motifs on Dsg1 impairs the Dsg1/PF autoantibody interactions and abrogates its path
179 in A, which removes residues 1 to 381 of the Dsg1 ectodomain.
180 nreported enhancer regulatory regions of the Dsg1 gene.
181 e molecule for cadherin function, and of the Dsg1 protein and hence desmosomes in epidermal function.
182 and consequently decreases expression of the Dsg1 transcriptional activator Grhl1.
183 of the companion layer, and particularly the Dsg1 and Dsg3 in this layer, in anchoring the anagen hai
184                                        These Dsg1-reactive FS T cells exhibited a CD4-positive memory
185                                         This Dsg1-SFK-ErbB2 axis also helps maintain tight junctions
186 tent, desmoglein 1 (Dsg1), while PG binds to Dsg1 and more weakly to Dsc1a and DP.
187 a proliferative response to Dsg3, but not to Dsg1.
188 eloped from these patients also responded to Dsg1, and this antigen-specific response was shown to be
189        To determine the systemic response to Dsg1 loss, we deleted the 3 tandem Dsg1 genes in mice.
190           However, the cellular responses to Dsg1 cleavage that precipitate keratinocyte separation t
191         The mutated ETs bind specifically to Dsg1 by immunofluorescence colocalization and by coimmun
192 s without pemphigus have B cell tolerance to Dsg1, we cloned mAbs from two patients with thrombotic t
193  that plakoglobin sequestration by truncated Dsg1 destabilizes other cadherins.
194 ial to the pathogenic potential of truncated Dsg1.
195   In addition, we demonstrate that truncated Dsg1 remains associated with its catenin partner, plakog
196 n, rescued upon re-introduction of wild-type Dsg1, but not Dsg1 constructs modeling SAM syndrome-caus
197  GJA1 gene expression was not decreased upon Dsg1 loss, we hypothesized that Cx43 reduction was due t
198  superficial epidermis of normal mice) where Dsg1 without Dsg3 is expressed, anti-Dsg1 antibodies alo
199 n 2 (Dsc2), which are widely expressed, with Dsg1 and Dsc1, which are expressed in the differentiated
200               These proteins interacted with Dsg1 and rely on Dsg1 and desmoplakin for robust cortica
201 ein (Dsg) AuAbs in the sera of patients with Dsg1/3 AuAb-negative acute PV are pathogenic, because Ig
202  anti-E-cadherin antibodies cross-react with Dsg1, whereas others may represent independent antibodie
203 dent antibodies that do not cross-react with Dsg1.

 
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