ライフサイエンスコーパス: claudin

1 ution of selected tight junctions-associated claudins.

2 keratins and tight-junction proteins such as claudins.

3 The tight junction protein claudin 1 (Cldn-1) has been reported to be down-regulate

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

5 ched controls, we assessed the filaggrin and claudin 1 genotypes, the phenotypes by dermatoscopy, and

6 ns appeared normal, immunohistochemistry for claudin 1 showed no reduction in protein amounts, and mo

7 n protein amounts, and molecular analysis of claudin 1 was unremarkable.

8 evels of MIR29A and B, but reduced levels of Claudin-1 (CLDN1) and nuclear factor-kappaB-repressing f

9 d that E-cadherin is closely associated with claudin-1 (CLDN1) and occludin (OCLN) on the cell membra

10 munoprecipitation (ChIP) analysis identified claudin-1 (CLDN1) as a prominent HIF target gene.

11 immunosorbant assay using a recombinant CD81-claudin-1 (CLDN1) fusion protein to detect and quantify

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

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

14 actors, including the tight junction protein claudin-1 (CLDN1).

15 tion of the specific tight junction proteins claudin-1 and -3 in adult brain endothelial cells.

16 y the observation of decreased expression of claudin-1 and nuclear beta-catenin in brain endothelial

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

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

19 uently found in perineurial cells expressing claudin-1 around nerve bundles.

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

21 oclonal antibody specific for the TJ protein claudin-1 eliminates chronic HCV infection without detec

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

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

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

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

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

27 Although LC claudin-1 levels were dramatically reduced in the absenc

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

29 in vivo Here, we report the generation of a claudin-1 transgenic mouse model with doxycycline-induci

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

31 We found that claudin-1, a tight junction protein, and small proline-r

32 n Transwell permeable supports and expressed claudin-1, claudin-4, and claudin-8-key proteins for tig

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

34 and localization of tight junction proteins (claudin-1, ZO-1) were visualized by immunofluorescence.

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

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

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

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

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

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

41 erum follicle-stimulating hormone and higher claudin-11 expression along the blood-testis barrier.

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

43 nt ERK activation also altered expression of claudin-11, p27, cyclin D1, and cyclin D2 in TM4 cells,

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

45 with antagomiRs against these miRs relieved claudin-14 gene silencing and caused an ADH-like phenoty

46 Genetic ablation of claudin-14 or the use of a loop diuretic in mice abrogat

47 three tight junction genes from the kidney--claudin-14, -16, and -19--as critical for calcium imbala

48 have been shown to repress the expression of claudin-14, the negative regulator of the paracellular p

49 n of the PDZ domain of nNOS to claudin-3 and claudin-14, two tight junction tetraspan membrane protei

50 te the compelling biologic evidence that the claudin-14/16/19 proteins form a regulated paracellular

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

52 irway epithelial permeability changes due to claudin-18 deficiency were measured in 16HBE cells and c

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

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

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

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

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

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

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

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

61 Claudin-18 null mice had significantly higher serum IgE

62 deficiency were measured in 16HBE cells and claudin-18 null mice.

63 barrier function by impairing the ability of claudin-18 to interact with a scaffold protein, zonula o

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

65 ated with increased, transient disruption of claudin-18, zonula occludens 1, and zonula occludens 2 l

66 tion of the structural transmembrane protein claudin-18.

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

68 Claudin-18.1 mRNA levels were measured in airway epithel

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

70 Starvation reduced the membrane presence of claudin-2 and increased its cytoplasmic, lysosomal local

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

72 It is a VDRE required for the regulation of Claudin-2 by vitamin D.

73 In both cells, claudin-2 channels display conductances of ~90 pS.

74 echnique that detects flux across individual claudin-2 channels within the tight junction of cultured

75 increased gut permeability through increased claudin-2 expression and related to local and systemic r

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

77 Absence of VDR decreased Claudin-2 expression by abolishing VDR/promoter binding.

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

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

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

81 Claudin-2 expression was examined by immunohistochemistr

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

83 Claudin-2 forms gated paracellular channels and allows s

84 We conclude that claudin-2 forms gated paracellular channels and speculat

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

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

87 sed murine models to investigate the role of claudin-2 in maintaining energy efficiency in the kidney

88 pithelial cells led to significant decreased Claudin-2 in VDR(-/-) and VDR(DeltaIEC) mice.

89 Claudin-2 is a tight junction protein that mediates para

90 In the proximal tubule (PT) of the kidney, claudin-2 mediates paracellular sodium reabsorption.

91 and aPKC interact to regulate trafficking of claudin-2 out of the lysosome-directed pathway.

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

93 tagenesis and chemical derivatization of the claudin-2 pore.

94 Our data showed that VDR-enhances Claudin-2 promoter activity in a Cdx1 binding site-depen

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

96 tight junction components demonstrates that claudin-2 protein levels are decreased.

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

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

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

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

101 adherin, zonula occluden 1 (ZO-1), occludin, claudin-2, tumor necrosis factor alpha (TNF-alpha), and

102 Notably, the contribution of claudin-2, which has been linked to IL-13, does not medi

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

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

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

106 We found that claudin-2-null mice conserve sodium to the same extent a

107 nimals, oxygen consumption in the kidneys of claudin-2-null mice was markedly increased, resulting in

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

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

110 ion injury was more severe in the absence of claudin-2.

111 Rab14 results in increased TER and decreased claudin-2.

112 luding increased TER and decreased levels of claudin-2.

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

114 s by lysosomal degradation of the TJ protein claudin-2.

115 Claudin-21 also allows the paracellular passage of large

116 Here we show for the first time that claudin-21, which is more highly expressed in the embryo

117 Our findings suggest that claudin-21-based TJs allow the passage of small and larg

118 to genes expressed in epithelial cells like Claudin 23, and to EMT inducer genes like Zeb2, Notch2 a

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

120 ity association of the PDZ domain of nNOS to claudin-3 and claudin-14, two tight junction tetraspan m

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

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

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

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

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

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

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

128 Although glucose transporter 1, claudin-3, and plasmalemma vesicular-associated protein

129 ion in the ileum, VE-cadherin, occludin, and claudin-3, Western blot analyses were conducted.

130 caused a loss of the tight junction protein claudin-3, which was ameliorated by genetic ablation of

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

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

133 involving increased inflammation and loss of claudin-3.

134 transcription factor, as well as E-cadherin, claudin 4 (Cldn4), and the small GTPase Rab25.

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

136 Taken together, (111)In-cCPE.GST targets claudin-4 expression in frank tumors and preneoplastic t

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

138 for known targets, including ROCK and ezrin, claudin-4 expression, and barrier permeability.

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

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

141 Claudin-4 is overexpressed in several premalignant precu

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

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

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

145 The expression of claudin-4, a protein involved in tight junction complexe

146 permeable supports and expressed claudin-1, claudin-4, and claudin-8-key proteins for tight junction

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

148 BALB/neuT mice, which spontaneously develop claudin-4-expressing breast cancer lesions.

149 significantly higher than in (111)In-GST or claudin-4-negative HT1080 tumors (6.72 +/- 0.18 vs. 3.88

150 The uptake of (111)In-cCPE.GST in claudin-4-positive MDA-MB-468 xenograft tumors in athymi

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

152 s enterotoxin (cCPE) is a natural ligand for claudin-4.

153 situ along with a delay in up-regulation of claudin-4.

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

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

156 Tight junction components ZO-1, claudin 5, and occludin were decreased at both the trans

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

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

159 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

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

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

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

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

164 Claudin-5 depletion only mimicked ZO-1 effects on barrie

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

166 gs, Efavirenz, but not other NNRTIs, altered claudin-5 expression, increased endothelial permeability

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

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

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

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

171 eno-associated virus-mediated suppression of claudin-5 in the mouse brain results in localized BBB di

172 Claudin-5 is expressed in endothelial cells forming part

173 Claudin-5 is necessary and sufficient to diminish alveol

174 trate that in response to alcohol, increased claudin-5 paradoxically accompanies an increase in parac

175 Critically, a claudin-5 peptide mimetic reverses the deleterious effec

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

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

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

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

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

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

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

183 ion and caused re-expression of occludin and claudin-7 (CLDN7).

184 nes encoding tight junction proteins such as claudin-7 and occludin and other cell-to-cell and cell-t

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

186 correlation between the expression level of claudin-7 and those of SPRY2 and ZEB1 in human colon tum

187 demonstrate a previously undescribed role of claudin-7 as a colon cancer suppressor and suggest that

188 Rab25 expression counteracted the effects of claudin-7 expression and not only increased proliferatio

189 atocyte nuclear factor 4alpha in controlling claudin-7 expression during IEC differentiation.

190 Most notably, forced claudin-7 expression in poorly differentiated and highly

191 Claudin-7 expression is increased as epithelial cells di

192 t, CRC cell lines, which exhibited decreased claudin-7 expression, also exhibited promoter DNA hyperm

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

194 By contrast, knockdown of claudin-7 in HT-29 or DLD-1 cells induced epithelial-to-

195 EpCAM stabilizes claudin-7 in IECs, and HAI-2 regulates the cell surface

196 ase and also failed to efficiently stabilize claudin-7 in IECs.

197 However, the role of claudin-7 in the regulation of colon tumorigenesis remai

198 In normal colon, claudin-7 is one of the highly expressed claudin protein

199 gulated kinase 1/2 that were suppressed upon claudin-7 overexpression.

200 n cancer suppressor and suggest that loss of claudin-7 potentiates EMT to promote colon cancer, in a

201 Importantly, a claudin-7 signature gene profile generated by overlappin

202 sing claudin-7-manipulated cells) with human claudin-7 signature genes identified high-risk CRC patie

203 othesized that HAI-2, matriptase, EpCAM, and claudin-7 were functionally linked.

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

205 high-throughput transcriptome analysis using claudin-7-manipulated cells) with human claudin-7 signat

206 nd lysosomal degradation in conjunction with claudin-7.

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

208 Claudin-8 (CLDN8), a multigene family protein that const

209 KO approach, we have found that deletion of claudin-8 in the collecting duct of mouse kidney caused

210 orts and expressed claudin-1, claudin-4, and claudin-8-key proteins for tight junction formation.

211 unction, eg, during inflammation facilitates claudin accessibility.

212 a occludens 1 (ZO-1), demonstrating that one claudin affects the ability of another claudin to intera

213 Here we show that the claudin affinity for PDZ1 is dependent on the presence o

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

215 are required for the correct localization of claudins and hence formation of the TJ.

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

217 ng structural components of tight junctions (Claudins and ZO proteins), adherens junctions (VE-cadher

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

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

220 generate profiles of transporters, channels, claudins, and selected regulators in both sexes and asse

221 Claudins are a family of integral membrane proteins and

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

223 Claudins are expressed differentially during intestinal

224 In the thick ascending limb, claudins are important for the reabsorption of calcium a

225 Claudins are tetraspan transmembrane tight-junction prot

226 Claudins are tight-junction membrane proteins that funct

227 Claudins are tight-junction transmembrane proteins that

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

229 show a lack of expression of E-CADHERIN and CLAUDIN, being this profile characteristic of the epithe

230 The intracellular C terminus of claudins binds to the N-terminal PDZ domain of zonula oc

231 s Na(+), similar to the typical channel-type claudins claudin-2 and -15.

232 The claudins Cldn10b, -16, and -19 facilitate cation reabsor

233 Thus, claudin controlled claudin-scaffold protein interactions

234 luminal-regulatory genes Elf5 and Hey1, and claudin down-regulation.

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

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

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

238 turn, depend on the regulated expression of claudin family proteins.

239 In addition, certain claudins function as paracellular channels for small ion

240 Claudins have a paracellular barrier function.

241 In the proximal tubule, claudins have a role in the bulk reabsorption of salt an

242 To determine if EpCAM regulates claudins in LC and immune responses to externally applie

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

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

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

246 Claudin interaction properties were examined using heter

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

248 ferential incorporation of newly synthesized claudins into break sites.

249 tive pores at the TJs, although the specific claudins involved and their functional mechanisms are st

250 y screens identify as an invasion factor the claudin-like apicomplexan microneme protein (CLAMP), whi

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

252 Claudin-low breast cancer is an aggressive subtype that

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

254 CSF1R signaling in MDA-MB-231 xenografts (a claudin-low cell line) leads to increased tumor size by

255 lting in low levels of this protein in basal/claudin-low cell lines and primary tumors.

256 ted and regulated by TGFbeta specifically in claudin-low cell lines.

257 lated by CSF1R downstream of TGFbeta only in claudin-low cell lines.

258 o, CSF1R inhibition results in a reversal of claudin-low marker expression by significant upregulatio

259 ression profile mimicked that found in basal/claudin-low molecular subtype within the triple negative

260 ive breast cancers (including basal-like and claudin-low molecular subtypes) represent 20% to 25% of

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

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

263 breast cancer cells and is biased toward the claudin-low subtype.

264 breast cancer (TNBC) includes basal-like and claudin-low subtypes for which no specific treatment is

265 Taken together, these findings indicate that claudin-low tumor cells rely on SIK2 to restrain maladap

266 e in an in vivo primary, syngeneic p53(null) claudin-low tumor model that is normally deficient in mi

267 d the metastatic potential of this p53(null) claudin-low tumor model.

268 hed in cancer stem cells (CSCs), which makes claudin-low tumor models particularly attractive for stu

269 Claudin-low tumors are a highly aggressive breast cancer

270 our data suggest that miR-200c expression in claudin-low tumors offers a potential therapeutic applic

271 the tumor-infiltrating lymphocytes (TILs) in claudin-low tumors, and Tregs isolated from tumor-bearin

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

273 in diverse mammary epithelial cells induced claudin-low-like TNBC with Met, Birc2/3-Mmp13-Yap1, and

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

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

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

277 In the distal nephron, claudins need to form cation barriers and chloride pores

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

279 occludin and reduced phosphorylated tyrosine claudin, phosphorylated tyrosine occludin, and phosphory

280 is built by several membrane proteins, with claudins playing the most prominent role.

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

282 Claudin protein family members, of which there are at le

283 on, claudin-7 is one of the highly expressed claudin proteins and its knockdown in mice results in al

284 Of the 23 identified human claudin proteins, nine possess a tyrosine at the -6 posi

285 Thus, claudin controlled claudin-scaffold protein interactions are a novel target

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

287 pulse-chase-pulse analysis using SNAP-tagged claudins showed preferential incorporation of newly synt

288 Although claudin strand behavior in fibroblasts may not fully rec

289 dependent of interaction with ZO-1 or actin, claudin strands break and reanneal; pulse-chase-pulse an

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 The TJ is composed of claudins that consist of four transmembrane segments, tw

293 function by coordinating interactions among claudins, the tight junction scaffold, and the cytoskele

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

295 t one claudin affects the ability of another claudin to interact with the tight-junction scaffold.

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

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.