ライフサイエンスコーパス: claudin

1 expression of MMP2, MMP9, VEGF, Occludin and Claudin.

2 arrier composed of reactive astrocyte TJs of claudin 1 (CLDN1), CLDN4, and junctional adhesion molecu

3 f patients with AD (loricrin, filaggrin, and claudin 1) but showed characteristic alterations in lipi

4 Claudin-1 (Cld-1), a tight-junction integral protein der

5 Claudin-1 (CLDN-1), CLDN8, CLDN11, CXADR-like membrane p

6 Other cell surface molecules, such as CD81, Claudin-1 (CLDN1), Occludin (OCLN), SR-BI, and low-densi

7 intestinal epithelial tight junction protein claudin-1 (CLDN1).

8 our findings provide evidence for a role of claudin-1 and occludin in epidermal regeneration with po

9 Here, we investigated the TJ proteins claudin-1 and occludin in ex vivo skin wound healing mod

10 ADAM15 co-localised with Claudin-1 and ZO1 at cell-cell junctions.

11 TJ complex proteins claudin-1 and zonula occludens-1 were upregulated follow

12 f MDA-MB-231 ADAM15A expressing cells showed Claudin-1 at cell-cell junctions, in the cytoplasm and n

13 taining barrier and highlight the HIF-1alpha/claudin-1 axis as a potential therapeutic target for EoE

14 y analysis identified a repressed HIF-1alpha/claudin-1 axis, which was restored via pharmacologic HIF

15 gen metabolism, tissue hypoxia, and impaired claudin-1 barrier via repression of HIF-1alpha/claudin-1

16 thelial cells indicates that aquaporin 1 and claudin-1 both remain normally polarized in all genotype

17 However, for claudin-1 effects on scratch wound healing were more pro

18 1A knockdown suppressed HIF-1alpha-dependent claudin-1 expression and epithelial barrier function, as

19 on in T47D cells by shRNA reduced endogenous Claudin-1 expression confirming a role for ADAM15 in reg

20 /Akt/mTOR pathway was involved in regulating Claudin-1 expression downstream of ADAM15.

21 ee of C and E isoforms led to an increase in Claudin-1 expression in MDA-MB-231 cells, while ADAM15B

22 ry human keratinocytes showed that decreased claudin-1 expression resulted in significantly impaired

23 n confirming a role for ADAM15 in regulating Claudin-1 expression.

24 , ADAM15E was the principal variant inducing Claudin-1 expression.

25 We found that induction of claudin-1 gene expression in mature podocytes caused pro

26 The appearance of claudin-1 in the TJ complex reduced claudin-5 strands (h

27 n endothelial cells and cells overexpressing claudin-1 indicated that newly synthesized claudin-1 was

28 unolabeling of kidney proteins revealed that claudin-1 induction destabilized the SD protein complex

29 Moreover, claudin-1 induction was associated with an endothelial p

30 Mechanistically, claudin-1 interacted with both nephrin and podocin throu

31 sed at the normal blood-brain barrier (BBB), claudin-1 is expressed in pathological conditions.

32 e blood microvessels we have identified that claudin-1 is highly expressed in leaky brain microvessel

33 Our results reveal that claudin-1 is incorporated in BBB tight junction complex,

34 T pathway was significantly attenuated after claudin-1 knockdown, and protein levels of extracellular

35 AM15 in ADAM15 over-expressing cells reduced Claudin-1 levels.

36 , exhibited upregulated expression levels of claudin-1 mRNA and protein in podocytes.

37 We found significant upregulation of claudin-1 mRNA and protein, a nonspecific claudin for bl

38 Targeting claudin-1 with a claudin-1 peptide improves brain endothelial barrier per

39 In VZV-infected HPNCs, claudin-1 redistributed to the nucleus; E-cadherin was l

40 audin-1 barrier via repression of HIF-1alpha/claudin-1 signaling, which was restored by transgenic ex

41 g claudin-1 indicated that newly synthesized claudin-1 was present on the cell membrane (~45%), was i

42 Targeting claudin-1 with a claudin-1 peptide improves brain endoth

43 Targeting claudin-1 with a specific C1C2 peptide improved brain en

44 proteins (ie, zonula occludens-1, Occludin, Claudin-1) that critically regulate epithelial paracellu

45 electively controlling tight junction CLDN1 (claudin-1).

46 he tight junction proteins zona occludens-1, claudin-1, and claudin-5, which were significantly reduc

47 r function, such as filaggrin, occludin, and claudin-1, and mRNA levels of filaggrin, loricrin, and i

48 lls (HPNCs) were examined for alterations in claudin-1, E-cadherin, and N-cadherin.

49 e gene expression of claudins, in particular claudin-1, is markedly upregulated in the podocyte, acco

50 thelial integrity with reduced expression of claudin-1, occludin, and E-cadherin and decreased number

51 or measurement of CD11c, CD3, CD4, tryptase, claudin-1, occludin, E-cadherin, and vascular endothelia

52 nexin A3 colocalized with cathepsin B and C, claudin-1, phosphorylated ERK1/2, and CD44, but not with

53 e resolved the ultrastructural change in the claudin-1-induced SD-TJ transition.

54 catalytic function dependent upregulation of Claudin-1.

55 ediated mechanism, independent of effects on claudin-1.

56 cyclin D1, c-Myc, COX-2, MMP-7, MMP-14, and Claudin-1.

57 However, the function of renal Claudin-10 in humans remains undetermined.

58 e mutation caused significant differences in Claudin-10 membrane localization and tight junction stra

59 the gene encoding the tight junction protein Claudin-10, show enhanced paracellular magnesium and cal

60 In mice claudin-11 was not detected, but intracameral injection

61 iRNA-mediated suppression of TJ transcripts, claudin-11, zonula-occludens-1 (ZO-1) and tricellulin in

62 testinal barrier marker genes (claudin 3 and claudin 15) expression, and rescued increased serum cyto

63 lar channelopathy caused by mutations in the claudin-16 and claudin-19 genes.

64 Phosphorylated claudin-16 and Trpv5 are colocalized in the luminal memb

65 rane of the mouse DCT tubule; phosphomimetic claudin-16 and Trpv5 interact in the yeast and mammalian

66 Knockdown of claudin-16 gene expression in transgenic mouse kidney de

67 nse FHHNC mutation c.908C>G (p.T303R) in the claudin-16 gene interferes with the phosphorylation in t

68 Unlike wildtype claudin-16, phosphomimetic claudin-16 is delocalized from the tight junction but re

69 ying the T303E mutation but not the wildtype claudin-16 or the T303R mutant protein increases the Trp

70 , PTH1R, from the mouse kidney abrogates the claudin-16 phosphorylation at T303.

71 h-Ca(2+) diet reduces the phosphorylation of claudin-16 protein at T303 in the DCT of mouse kidney vi

72 The claudin-16 protein carrying phosphorylation at residue T

73 The phosphomimetic claudin-16 protein carrying the T303E mutation but not t

74 e interferes with the phosphorylation in the claudin-16 protein.

75 Unlike wildtype claudin-16, phosphomimetic claudin-16 is delocalized fro

76 tion that is downregulated by IL-13 and that claudin-18 deficiency results in increased aeroantigen s

77 IL-13 decreased claudin-18 expression in primary human cells and in mice

78 Furthermore, TH2 inflammation suppresses claudin-18 expression, potentially promoting sensitizati

79 We sought to test the hypotheses that claudin-18 is a determinant of airway epithelial barrier

80 These data support the hypothesis that claudin-18 is an essential contributor to the airway epi

81 In patients with asthma, claudin-18 levels were compared with a three-gene-mean m

82 Claudin-18 levels were lowest among TH2-high patients wi

83 with asthma (n = 67) had significantly lower claudin-18 mRNA levels than did those from healthy contr

84 veness and serum IgE levels were compared in claudin-18 null and wild-type mice following aspergillus

85 Claudin-18 null mice had significantly higher serum IgE

86 Loss of claudin-18 was sufficient to impair epithelial barrier f

87 Claudin-18.1 is the only known lung-specific tight junct

88 Claudin-18.1 mRNA levels were measured in airway epithel

89 hy caused by mutations in the claudin-16 and claudin-19 genes.

90 b-cellular fractionation localized increased claudin 2 protein to the cytoskeleton.

91 act as a shuttle for the internalization of claudin 2 seen in experimental NEC.

92 Co-immunoprecipitation of caveolin-1 with claudin 2 suggests that caveolin-1 may act as a shuttle

93 and claudin 2, and increased trafficking of claudin 2 to the cytoskeleton.

94 Gene and protein expression of claudin 2 was increased in experimental NEC.

95 audin 2, increased binding of caveolin-1 and claudin 2, and increased trafficking of claudin 2 to the

96 nal permeability and increased expression of claudin 2, increased binding of caveolin-1 and claudin 2

97 The tight junctional pore-forming protein claudin-2 (CLDN-2) mediates paracellular Na(+) and water

98 caused by adenoviral-mediated expression of claudin-2 (Cldn2), a tight junction protein that forms p

99 Moreover, combining Claudin-2 and Afadin as prognostic markers better predic

100 cer tumors revealed that high levels of both Claudin-2 and Afadin in primary tumors were associated w

101 association was found between expression of Claudin-2 and age, gender, grade, stage, or patients' su

102 CLE had immediate increases in expression of claudin-2 and decreases in occludin.

103 Moreover, IL-22-mediated upregulation of Claudin-2 and loss of TEER can be suppressed with the tr

104 Immunohistochemical analysis of Claudin-2 and/or Afadin expression in 206 metastatic bre

105 Further, inhibition of claudin-2 by targeting casein kinase 2 (CK2) also amelio

106 rs used transgenic mouse models to show that claudin-2 deficiency attenuated colitis progression as w

107 A significant association was found between Claudin-2 expression and VDR and TGR5 expression.

108 found that vitamin D receptor (VDR) enhanced Claudin-2 expression in colon and that bile salt recepto

109 We conclude that Claudin-2 expression is significantly associated with bi

110 inal epithelial permeability by upregulating Claudin-2 expression through the JAK/STAT pathway.

111 Claudin-2 expression was examined by immunohistochemistr

112 Knocking down Claudin-2 expression with small interfering RNA reverses

113 tinal IL-10 expression and downregulated the claudin-2 expression.

114 Claudin-2 forms gated paracellular channels and allows s

115 of the tight junction proteins occludin and claudin-2 from intercellular junctions.

116 Here, we examined the expression of Claudin-2 in EAC and precancerous lesions and its associ

117 that interact with the PDZ-binding motif of Claudin-2 in liver metastatic breast cancer cells, inclu

118 Expression of claudin-2 increased from crypt to villus tip (P < .001)

119 ow demonstrate that the PDZ-binding motif of Claudin-2 is necessary for anchorage-independent growth

120 The tight junction protein claudin-2 is upregulated in inflammatory bowel disease,

121 Conversely, transgenic claudin-2 overexpression reduced disease severity.

122 Claudin-2 promotes breast cancer liver metastasis by ena

123 more, treatment of IL-22 in mice upregulates Claudin-2 protein in colonic epithelial cells.

124 Cebpd-deficient mice showed upregulation of Claudin-2 that correlated with increased intestinal perm

125 nd butyrate represses permeability-promoting claudin-2 tight-junction protein expression through an I

126 shikanth et al. examined the contribution of claudin-2 to immune-mediated colitis.

127 Thus, IL-22-induced claudin-2 upregulation drives diarrhea and pathogen clea

128 pithelium markedly induces the expression of Claudin-2, a cation-channel-forming tight junction prote

129 Afadin associates with Claudin-2, an interaction that requires the PDZ-binding

130 dant expression of Na(+)/Pi cotransporter 2, claudin-2, and aquaporin 1.

131 Relative to wild-type, claudin-2-deficient mice experienced severe disease, inc

132 colitis severity and C. rodentium burden in claudin-2-deficient, but not transgenic, mice, demonstra

133 y examined the role of Afadin as a potential Claudin-2-interacting partner that promotes breast cance

134 but not transgenic, mice, demonstrating that claudin-2-mediated protection is the result of enhanced

135 ction that requires the PDZ-binding motif of Claudin-2.

136 rier through IL-10RA-dependent repression of claudin-2.

137 ion of the epithelial tight junction protein claudin-2.

138 racellular water and Na(+) channel formed by claudin-2.

139 gs indicate that signaling downstream from a Claudin-2/Afadin complex enables the efficient formation

140 d decreased intestinal barrier marker genes (claudin 3 and claudin 15) expression, and rescued increa

141 Loss of claudin-3 also predicted poor patient survival.

142 Overall, these novel findings identify claudin-3 as a therapeutic target for inhibiting overact

143 e present the crystal structure of mammalian claudin-3 at 3.6 angstrom resolution.

144 e findings however contrasted an upregulated claudin-3 expression in other cancer types and implicate

145 The third transmembrane helix of claudin-3 is clearly bent compared with that of other su

146 Claudin-3 loss also upregulated the gp130/IL6/Stat3 sign

147 c and pharmacological studies confirmed that claudin-3 loss induces Wnt/beta-catenin activation, whic

148 icated by loss of the tight junction protein claudin-3 was not observed during acute infection despit

149 Claudin-3 was reduced in LSI animals with severe intesti

150 regimen, a novel and tissue-specific role of claudin-3, a tight junction integral protein, in inhibit

151 Claudin-3-/- mice revealed dedifferentiated and leaky co

152 ndent manner, differentiated colon cancer in claudin-3-/- mice versus WT-mice.

153 of non-junctional claudin molecules such as claudin-4 at apical membranes.

154 regulatory network in gastric cancer whereby claudin-4 expression is reduced by specific miRNAs, whic

155 genous RNAs (ceRNAs), resulting in increased claudin-4 expression.

156 this study, we discover a network regulating Claudin-4 in gastric cancer.

157 We observe that Claudin-4 is up-regulated in gastric cancer and is assoc

158 Claudin-4 reinforce proliferation, invasion, and EMT in

159 es some claudin tight junction proteins (eg, claudin-4) as receptors to form Ca2+-permeable pores in

160 Decreased claudin-4, caudin-7, and E-cadherin expression in Lpa1(-

161 important roles in the regulatory network of Claudin-4.

162 ng endogenous RNAs to affect the function of Claudin-4.

163 s, such as zonula occludens-1, occludin, and claudin-4.

164 HLEC(DeltaGATA2)) have altered expression of claudin 5 and VE-cadherin, and blocking miR-126 activity

165 the cell junction molecules VE-cadherin and claudin 5 in lymphatic vessels.

166 (elevated levels of tight-junction protein, Claudin 5, and reduced S100B levels in periphery).

167 the endothelial cell tight junction protein claudin-5 (Cldn5) and abnormal blood vessel morphology i

168 grity through loss of tight junction protein claudin-5 (cldn5) in male mice, promoting passage of cir

169 are tightly coupled, express high levels of Claudin-5 (CLDN5), a junctional protein that stabilizes

170 can-1 (OR = 1.004; 95% CI = 1.000-1.008) and claudin-5 (OR = 1.038; 95% CI = 1.004-1.074) had an adju

171 Stroke decreases claudin-5 abundance, and we found that EC-selective miR-

172 he amounts of major tight junction proteins, claudin-5 and occludin, in 12 brain regions dissected fr

173 ated BBB degradation by decrease of the TJPs claudin-5 and occludin.

174 ral endothelial cell tight-junction proteins claudin-5 and occludin.

175 levels of the tight junction proteins (TJPs) claudin-5 and occludin; increased expression of matrix-m

176 mportantly, the positive correlation between claudin-5 and synaptic markers, in particular synaptophy

177 EC expression paralleled decreased levels of claudin-5 and VE-PTP.

178 akage, and elevated levels of syndecan-1 and claudin-5 are strongly associated with severe plasma lea

179 chizophrenia in 22q11DS, leading to 75% less claudin-5 being expressed in endothelial cells.

180 omplex reduced claudin-5 strands (homophilic claudin-5 cis- and trans-interactions) and claudin-5/ZO-

181 cription factor to trigger the expression of claudin-5 downstream of JAM-A, to thus enhance vascular

182 , gain-of-function for C/EBP-alpha increased claudin-5 expression and decreased endothelial permeabil

183 chotic medications dose-dependently increase claudin-5 expression in vitro and in vivo while aberrant

184 din for blood vessels, and downregulation in claudin-5 expression.

185 Here, we show that a variant in the claudin-5 gene is weakly associated with schizophrenia i

186 population who are haploinsufficient for the claudin-5 gene.

187 suppression, reinforcing the crucial role of claudin-5 in normal neurological function.

188 while aberrant, discontinuous expression of claudin-5 in the brains of schizophrenic patients post m

189 d with significantly decreased expression of claudin-5 in the vasculature of various tissues, includi

190 ns) and claudin-5/ZO-1 interaction affecting claudin-5 incorporation into the TJ complex.

191 Claudin-5 is expressed in endothelial cells forming part

192 ion showed the opposite effects of decreased claudin-5 levels and increased endothelial permeability.

193 h norrin and VEGF were required for enriched claudin-5 localization at the tight junction.

194 deprivation (OGD)-induced down-regulation of claudin-5 mRNA and protein abundance and endothelial bar

195 EC-selective miR-15a/16-1 deletion enhanced claudin-5 mRNA and protein abundance in ischemic mouse b

196 rance of claudin-1 in the TJ complex reduced claudin-5 strands (homophilic claudin-5 cis- and trans-i

197 ble 'knockdown' mouse model, we further link claudin-5 suppression with psychosis through a distinct

198 develop seizures and die after 3-4 weeks of claudin-5 suppression, reinforcing the crucial role of c

199 BP-alpha then directly binds the promoter of claudin-5 to thereby promote its transcription.

200 ly, JAM-A-C/EBP-alpha-mediated regulation of claudin-5 was lost in blood vessels from tissue biopsies

201 reover, levels of the tight junction protein claudin-5 were increased with norrin and VEGF or with VE

202 such as DLL4 (Delta-like protein 4), CLDN5 (claudin-5), VWF (von Willebrand factor), and CDH5 (VE-ca

203 ; AII spectrin fragments, 1.9-fold increase; claudin-5, 2.7-fold increase; sodium-potassium-chloride

204 und to the 3' untranslated region (3'UTR) of Claudin-5, and lentivirus-mediated ablation of miR-15a/1

205 association with the tight junction protein, claudin-5, has previously been identified.

206 hanced presence of TJ proteins, occludin and claudin-5, on EVs.

207 hrough EPAC to up-regulate the expression of claudin-5, to thus decrease endothelial permeability.

208 ey roles in vascular stabilization including claudin-5, vascular endothelial-protein tyrosine phospha

209 EC association increases Ezh2 recruitment to claudin-5, VE-PTP, and vWf promoters, causing gene downr

210 ve complex-2) binding to promoter regions of claudin-5, VE-PTP, and vWf.

211 on proteins zona occludens-1, claudin-1, and claudin-5, which were significantly reduced after heme e

212 c claudin-5 cis- and trans-interactions) and claudin-5/ZO-1 interaction affecting claudin-5 incorpora

213 he establishment of the blood-brain barrier (claudin 5a, zona occludens 1a and b).

214 Finally, we validated Claudin 7 and CD81 determination in EVs from 60 BC patie

215 electrochemical paper-based immunosensor for Claudin 7 and CD81 determination, as well as its validat

216 timum conditions, the limit of detection for Claudin 7 was 0.4 pg mL(-1), with a wide linear range of

217 ss of the cell junctional proteins EpCAM and claudin 7 was also prevented.

218 roarray analysis revealed down-regulation of Claudin-7 and E-cadherin in HCT116-MT vs. HCT116-WT.

219 Alteration of Claudin-7, as well as both Claudin-7 and E-cadherin respectively caused tight junct

220 pCAM decreased its ability to associate with claudin-7 and targeted it for internalization and lysoso

221 ptase and link HAI-2, matriptase, EpCAM, and claudin-7 in a functionally important pathway that cause

222 beta-catenin-mediated loss of E-cadherin and Claudin-7 in HCT116-P and HCT116-MT cells.

223 Claudin-7 was also down-regulated in HCT116-P vs. HCT116

224 sphorylated Na(+)/Cl(-) cotransporter (NCC), claudin-7, and cleaved forms of epithelial Na(+) channel

225 Alteration of Claudin-7, as well as both Claudin-7 and E-cadherin resp

226 xpress the tight junction-associated protein claudin-7.

227 nd lysosomal degradation in conjunction with claudin-7.

228 Increased claudin-8 abundance was associated with a reduction in p

229 ar permeability to sodium, whereas decreased claudin-8 abundance was associated with the opposite eff

230 aC or alpha-ENaC knockout mice did not alter claudin-8 abundance.

231 ciated with parallel and specific changes in claudin-8 abundance.

232 pithelial sodium channel (ENaC) subunits and claudin-8 affect paracellular permeability.

233 ma-subunit knockout mice displayed decreased claudin-8 expression, confirming the cell culture experi

234 ENaC subunits to assess the ENaC's effect on claudin-8 expression.

235 ific coupling between ENaC gamma-subunit and claudin-8 expression.

236 Claudin-8 overexpression and silencing reproduced these

237 ting expression of the transmembrane protein claudin-8, we used cultured mouse cortical collecting du

238 Here, we present crystal structures of human claudin-9 (hCLDN-9) in complex with cCpE at 3.2 and 3.3

239 unction, eg, during inflammation facilitates claudin accessibility.

240 ight junctions composed of barrier-enforcing claudins and exhibits a higher transepithelial resistanc

241 ent ligands to label SNAP/CLIP-tags fused to claudins and occludin to identify their spatial traffick

242 r, our data attest to the novel concept that claudins and the TJ have essential roles in podocyte pat

243 ecific binding by CpE causes dissociation of claudins and tight junctions (TJs), resulting in cytotox

244 CpE disrupts gut homeostasis by dissociating claudins and TJs to affect epithelial adhesion and inter

245 However, although binding between claudins and ZO-1/2/3 and between ZO-1/2/3 and numerous

246 and adherens junction proteins such as ZO-1, claudin, and JAM-A; however, exposure of SCs to inflamma

247 roteins (e.g., zonula occludens, E-cadherin, claudins, and occludin).

248 Claudins are a family of integral membrane proteins and

249 t model, we speculate that newly synthesized claudins are added at strand breaks and free ends; these

250 h are characterized by apical dislocation of claudins are CPE-susceptible.

251 We find that claudins are first delivered to the lateral membrane and

252 helial tight junction (TJ) proteins, such as claudins, are essential for regulation and function of t

253 Claudin association with actin is also dependent on ZO-1

254 r, which involves removal and replacement of claudins both in the steady state and during junction re

255 changes the positions of residues related to claudin-claudin interactions and affects the morphology

256 arboxy-terminal sequences and that different claudins compete for tight junction localization.

257 use TAL segments with subsequent analysis of claudin expression by immunostaining and confocal micros

258 The effect of IL-13 on claudin expression was determined in primary human airwa

259 The claudin family of proteins is integral to the tight junc

260 of claudin-1 mRNA and protein, a nonspecific claudin for blood vessels, and downregulation in claudin

261 Silencing of other claudins had no such effects, and re-expression of an si

262 his is followed by slow replacement of older claudins in the strands.

263 ion of tight junction proteins (occludin and claudin) in 13% CP group were higher than the other two

264 diabetic nephropathy, the gene expression of claudins, in particular claudin-1, is markedly upregulat

265 Claudins interact within the same (cis) and opposing (tr

266 Claudin interaction properties were examined using heter

267 l roles in podocyte pathophysiology and that claudin interactions with SD components may facilitate S

268 Claudin is the major component of tight junction and pol

269 ctively, our experiments suggest that HPO-30/Claudin localizes the DMA-1/LRR-TM receptor on PVD dendr

270 Our data also suggest that claudin-low breast cancer can develop from luminal cells

271 Claudin-low breast cancer is an aggressive subtype that

272 pression signature and most closely resemble claudin-low breast cancer.

273 immune cell gene signatures distinguish the claudin-low subtype clinically as well as in mouse model

274 s), are thought to serve as the TICs for the claudin-low subtype of breast cancer.

275 nc finger E-box binding homeobox 1 (ZEB1) in claudin-low tumor cells or forced expression of ZEB1 in

276 Despite adaptive immune cell infiltration in claudin-low tumors, treatment with immune checkpoint inh

277 We find that GFP claudins make easily visualized dynamic strand patches b

278 junction (SJ) integrity by transporting the claudin Megatrachea (Mega) to the SJ.

279 highlighted potential association of select claudins, modulated by the obesity, with signaling and m

280 estricted by accessibility of non-junctional claudin molecules such as claudin-4 at apical membranes.

281 ed inhibitor (LEKTI), filaggrin, E-cadherin, claudin, occludin, desmoglein-1 was found, independent o

282 ants of interaction properties, a set of TAL claudin protein chimeras was created and analyzed.

283 protective against NEC by regulation of key claudin proteins.

284 ially redundant pathway, dependent on HPO-30/Claudin, regulates formation of 2 degrees and 3 degrees

285 dn19 to form joint strands; and (iv) further claudin segments in addition to ECS2 are crucial for tra

286 ed alterations to 2 epitopes known to enable claudin self-assembly and expose high-affinity interacti

287 previous documentation of the mechanism for claudin strand assembly in a fibroblast model, we specul

288 Although claudin strand behavior in fibroblasts may not fully rec

289 A network of claudin strands creates continuous cell-cell contacts to

290 stration of the ability of ZO-1 to stabilize claudin strands.

291 J-restructuring by organ and tissue-specific claudin switching characterize obese organs.

292 s secretes an enterotoxin (CpE) that targets claudins through its C-terminal receptor-binding domain

293 It uses some claudin tight junction proteins (eg, claudin-4) as recep

294 We speculate that intermittent tethering of claudins to actin may allow for accommodation of the par

295 We further demonstrate that claudin trafficking and half-life depend on carboxy-term

296 The expression of claudins was measured by gene and protein analysis.

297 ii) cldn10b does not interact with other TAL claudins, whereas cldn3 and cldn16 can interact with cld

298 t rather than continuous association between claudin, ZO-1, and actin.

299 ght junctions depend on interactions between claudins, ZO scaffolding proteins, and the cytoskeleton.

300 last system to examine relationships between claudins, ZO-1, occludin, and actin.