ライフサイエンスコーパス: ZO-1

1 ZO-1 binds numerous transmembrane and cytoplasmic protei

2 ZO-1 depletion led to tight junction disruption, redistr

3 ZO-1 domains that mediate interactions with occludin and

4 ZO-1 is thus a central regulator of VE-cadherin-dependen

5 ZO-1 reactivity was patchy in Col12a1(-/-), Col14a1(-/-)

6 ZO-1 small interfering RNA and cDNA transfection experim

7 ZO-1 small interfering RNA and overexpression experiment

8 ZO-1 was required for junctional recruitment of JACOP, w

9 ZO-1-associated nucleic acid binding protein (ZONAB)/Dbp

10 ceptor (VDR), E-cadherin, zonula occluden 1 (ZO-1), occludin, claudin-2, tumor necrosis factor alpha

11 omponent of the occludin/zonula occludens 1 (ZO-1) adhesion complex at the BTB, structurally interact

12 barrier (BBB) occludin and zona occludens 1 (ZO-1) expression were significantly decreased; and micro

13 sly found that depleting zonula occludens 1 (ZO-1) family proteins in MDCK cells induces a highly org

14 (CLDN23), occludin, and Zonulae occludens 1 (ZO-1) in primary human keratinocytes.

15 with a scaffold protein, zonula occludens 1 (ZO-1), demonstrating that one claudin affects the abilit

16 unction-associated protein zona occludens 1 (ZO-1), translocation of ZO-1 to cell-cell borders, and t

17 ), and redistribution of zonula occludens-1 (ZO-1) and cadherins.

18 the tight junction marker zona occludens-1 (ZO-1) and end-binding protein-1 (EB-1), which is specifi

19 e tight junction markers zonula occludens-1 (ZO-1) and occludin.

20 transcripts, claudin-11, zonula-occludens-1 (ZO-1) and tricellulin in human SC endothelial monolayers

21 IL-1beta-induced loss of zonula occludens-1 (ZO-1) at the tight junctions and alterations in F-actin

22 Zonula occludens-1 (ZO-1) binds the carboxy terminus of Cx43, and we have pr

23 Zonula occludens-1 (ZO-1) is a submembrane scaffolding protein that may disp

24 ht junction (TJ) protein Zonula Occludens-1 (ZO-1).

25 (PSD-95)/Discs large (Dlg)/zona occludens-1 (ZO-1)] interactions with members of the PSD-95 family, a

26 tion proteins occludin and zona occludin- 1 (ZO-1).

27 ce (R(T)), dissociation of zona occludins 1 (ZO-1) from the tight junction complex, and bacterial tra

28 al barrier [anti-zonula occludens protein 1 (ZO-1) and anti-occludin], and hypoxia [anti-pimonidazole

29 ation of tight junction proteins (claudin-1, ZO-1) were visualized by immunofluorescence.

30 tight junction proteins, such as claudin-1, ZO-1, and occludin, are unchanged.

31 ludin or monomeric red fluorescent protein 1-ZO-1.

32 l cells expressed the TJ proteins claudin-5, ZO-1, and ZO-2; HIV-1 decreased TJ proteins expression a

33 ype CMs, ephrin-B1 interacted with claudin-5/ZO-1 complex at the lateral membrane, whereas the comple

34 Here we show that the alpha5beta1/ZO-1 complex decreases the resistance to force of alpha5

35 8, and 373 exhibited a significantly altered ZO-1 interaction profile, while mutants with S residues

36 tion via the H19-encoded miR-675 by altering ZO-1 and E-cadherin expression posttranscriptionally.

37 Although ZO-1 is retained at the tight junction, occludin is lost

38 requires occludin, claudin-1, claudin-2, and ZO-1.

39 ke N-cadherin, desmoplakin, connexin-43, and ZO-1 was significantly perturbed upon pressure overload,

40 Cx43 (connexin 43), Cx45 (connexin 45), and ZO-1 (zonula occludens-1) were identified as novel mRNA

41 this issue, Choi et al. show that afadin and ZO-1 regulate tension and maintain zonula adherens archi

42 might be involved to suppress E-cadherin and ZO-1 expression and ectopic expression of a constitutive

43 ads to delayed recruitment of E-cadherin and ZO-1 to junctions, as well as a delay in tight junction

44 GB1 induced downregulation of E-cadherin and ZO-1, and upregulation of vimentin mRNA transcription an

45 redistribution of TJ proteins (e.g., CAR and ZO-1) from the cell-cell interface to cell cytosol cause

46 concept, its ability to enhance Neph1-CD and ZO-1 binding was tested.

47 nfirmed by increased occludin, cingulin, and ZO-1 protein.

48 ein levels of JAM-A, occludin, cingulin, and ZO-1 several-fold in glomeruli and loosened their attach

49 wever, although binding between claudins and ZO-1/2/3 and between ZO-1/2/3 and numerous cytoskeletal

50 nteracting with F-actin, the Par complex and ZO-1, Alix ensures the formation and maintenance of the

51 ionarily conserved class II PSD-95, Dlg, and ZO-1 (PDZ)-binding motif within cyclin D1.

52 Thus both a PDZ-binding motif and ZO-1 are necessary for Cx50 intercellular channel format

53 Junctional proteins Neph1 and ZO-1 and their interaction is an important determinant o

54 analysis showed that ISD enhanced Neph1 and ZO-1 interaction under in vitro and in vivo conditions.

55 reased TER, and the decrease in occludin and ZO-1 caused by IFNgamma treatment of T(84) cells.

56 and was followed by decreasing occludin and ZO-1 expression at 4 and 8 hours, respectively.

57 e expressing fluorescent-tagged occludin and ZO-1 fusion proteins to link occludin endocytosis to TNF

58 ith the tight junction proteins occludin and ZO-1 in a tyrosine phosphorylation-dependent manner.

59 t the interaction of DEP-1 with occludin and ZO-1 is specific.

60 in, and tight junction proteins occludin and ZO-1 was unchanged, the formation of these junctions aft

61 ion and altered localization of occludin and ZO-1, as seen in animals undergoing burn alone.

62 y a loss of association between occludin and ZO-1, likely the result of reduced occludin phosphorylat

63 d expression of the TJ proteins occludin and ZO-1, reduced cell proliferation, and increased sequestr

64 x disease, expression levels of Occludin and ZO-1,-2 were not significantly affected.

65 n assays, AT1002 decreased ZO-1-occludin and ZO-1-claudin 1 interactions coincident with PKCalpha-dep

66 estinal tight junction proteins occludin and ZO-1.

67 Claudins, occludin, and ZO-1 were examined using PCR, immunoblotting, and confoc

68 audin-3, claudin-4, claudin-5, occludin, and ZO-1) and adherent junctional proteins (E-cadherin and b

69 udin-2, claudin-3, claudin-19, occludin, and ZO-1, but changes in the morphology of the junctions and

70 t junction proteins claudin-2, occludin, and ZO-1.

71 the expression of E-cadherin, vimentin, and ZO-1 (genes known to play a role in cellular proliferati

72 basal polarization (i.e., presence of apical ZO-1 and basolateral E-cadherin) and columnar shape.

73 tight and adherens junction proteins such as ZO-1, claudin, and JAM-A; however, exposure of SCs to in

74 Markers of apical-basal polarity, such as ZO-1, were mislocalized along the lateral and basal memb

75 data suggests that tight junction-associated ZO-1 exists in three pools, two of which exchange with c

76 and specific disruption of the TJ-associated ZO-1 and cytoskeletal-F-actin proteins, correlated with

77 loss of intercellular hepatic TJ-associated ZO-1 protein expression was evident with progressive cli

78 ng between claudins and ZO-1/2/3 and between ZO-1/2/3 and numerous cytoskeletal proteins has been dem

79 plaques, while the S373E mutant did not bind ZO-1 at all.

80 TOCA-1 adds a PDZ-binding motif, which binds ZO-1, targeting TOCA-1 to barrier contacts.

81 by canine kidney cell lines depleted of both ZO-1 and -2.

82 S365E, S368A, S368E, and S373A mutants bound ZO-1 throughout the GJ plaques, while the S373E mutant d

83 broblasts; strand dynamics is constrained by ZO-1 binding.

84 y tight junction formation, as determined by ZO-1 localization.

85 The distribution of N-cadherin, ZO-1, and F-actin was visualized by fluorescence microsc

86 protein complexes (e.g., occludin-ZO-1, CAR-ZO-1, and N-cadherin-ss-catenin), through a down-regulat

87 and cytoskeleton: VE-cadherin, p120-catenin, ZO-1, cortactin, and VASP.

88 lon-mediated MEK1-ERK1/2 activation, causing ZO-1 dissociation from occludin, disrupting endothelial

89 construct a structural model of the Neph1-CD.ZO-1-PDZ1 complex.

90 than continuous association between claudin, ZO-1, and actin.

91 m to examine relationships between claudins, ZO-1, occludin, and actin.

92 expression of the tight junction components ZO-1 and E-cadherin and the formation of ZO-1 containing

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

94 s of junctional proteins such as connexin43, ZO-1, occludin, and claudin11 were up-regulated in the a

95 Conversely, ZO-1 exchange was accelerated in transgenic mice express

96 Relative to controls, Cx43/ZO-1 colocalization in the IBZ was reduced by alphaCT1 b

97 y decreases in connexons, inhibition of Cx43/ZO-1 reduced the extent of perinexal interaction, increa

98 Cx43 half-life) following disruption of Cx43/ZO-1.

99 arge/ZO-1 (PDZ)-binding domain, reduces Cx43/ZO-1 interaction and GJ size remodeling in vitro.

100 previously shown that inhibition of the Cx43/ZO-1 interaction increases GJ size by 48 h.

101 lung carcinoma that presented a cytonuclear ZO-1 pattern was significantly more angiogenic that that

102 nic that that without detectable cytonuclear ZO-1 expression.

103 pools, two of which exchange with cytosolic ZO-1.

104 ncreased VEGF, CD105, and GFAP and decreased ZO-1/occludin levels in the Cbs(+/-) retinas.

105 immunoprecipitation assays, AT1002 decreased ZO-1-occludin and ZO-1-claudin 1 interactions coincident

106 igher intestinal permeability with decreased ZO-1 and occludin protein expression in the intestinal t

107 ier function and suggest that MLCK-dependent ZO-1 exchange is essential to this mechanism of barrier

108 f, FCIGRL, that increases PKCalpha-dependent ZO-1 and myosin 1C serine/threonine phosphorylation.

109 eractions coincident with PKCalpha-dependent ZO-1 serine/threonine phosphorylation.

110 CPEB has been depleted, randomly distributed ZO-1 mRNA leads to the loss of cell polarity.

111 the wild-type protein but not of PSD95, Dlg, ZO-1 (PDZ), or leucine rich repeat domain mutants restor

112 the Cdc42/Rac interaction binding PSD-95/Dlg/ZO-1 (CRIB-PDZ) module that alters PDZ ligand binding.

113 se libraries we screened the nine PSD-95/Dlg/ZO-1 (PDZ) domains of human Densin-180, Erbin, Scribble,

114 PDZ (PSD-95/Dlg/ZO-1) binding domains often serve as cellular traffic en

115 ble counterparts, displays a PDZ (PSD-95/Dlg/ZO-1) domain located at its N terminus involved in subce

116 ole for the Cdh23 C-terminal PDZ (PSD-95/Dlg/ZO-1)-binding motif and observed that Cdh23 bound simila

117 rt that N-cadherin binds to PSD-95/SAP90/DLG/ZO-1 (PDZ) domain 2 of the glutamate receptor interactin

118 PSD-95/SAP90/DLG/ZO-1 (PDZ) domain-mediated protein-protein interactions

119 lass of ligand specificity in a PSD95, DLG1, ZO-1 (PDZ) domain preferentially occurs through class-br

120 her in the presence or absence of endogenous ZO-1.

121 ibition in a manner that required endogenous ZO-1 expression.

122 We found that 15(S)-HETE enhances ZO-1 phosphorylation at Thr-770/772 residues via PKCepsi

123 Mammary epithelial (Eph4) cells KO for ZO-1 showed junctional DbpA, demonstrating that ZO-1 is

124 helial cells and mouse tissues knock-out for ZO-1 do not show increased proliferation, as predicted b

125 Inability to disengage from ZO-1 correlated with increased GJ plaque size and increa

126 gesting that the inability to disengage from ZO-1 prevented maturation of functional into nonfunction

127 es channel accrual, while disengagement from ZO-1 is critical for GJ channel closure and transitionin

128 , CK-19), and tight junction proteins (e.g., ZO-1), and impaired their migration/invasion capacity in

129 Levels of VEGF, GFAP, ZO-1, and occludin were determined by immunoblotting.

130 f TOCA-1 does not alter FRAP kinetics of GFP ZO-1 or occludin, but longer term (12 h) time-lapse micr

131 The His-ZO-1-PDZ1 (first PDZ domain of zonula occludens) domain

132 rmeability are neither due to the changes in ZO-1 expression nor cell viability.

133 etinas concomitant with a marked decrease in ZO-1 and occludin.

134 localization of TJ proteins are disrupted in ZO-1/-2-depleted cells.

135 l membrane and fluid were initially found in ZO-1-positive vesicles, which were distinct from DFV, cl

136 both IkappaBalpha and p65 phosphorylation in ZO-1-overexpressing cells, and subsequent p65 silencing

137 show that an effector loop, the U6 region in ZO-1, forms a novel intramolecular interaction with the

138 These effects, including ZO-1 downregulation, were rescued by overexpression of c

139 unction (TJ) protein localization, including ZO-1, occludin, and claudin-1.

140 of other tight junction proteins (including ZO-1) was not associated with alveolar fluid clearance o

141 of WT mice ex vivo, 15(S)-HETE also induced ZO-1 phosphorylation and endothelial TJ disruption in a

142 that the conserved PDZ (PSD95, Discs large, ZO-1) domain-containing protein PATJ (Pals1-associated t

143 embrane-associated PDZ (PSD-95, Discs-large, ZO-1) domain-containing protein isoforms, in the modulat

144 binds to all three PDZ (PSD-95, Discs-large, ZO-1) domains of PSD-95, the principal PSD scaffold, and

145 etermined that the class I PSD-95/Disc Large/ZO-1 (PDZ)-binding domain of NleH was important for its

146 1) contains an N-terminal PSD-95/Discs large/ZO-1 (PDZ) domain and a central lipid-binding Bin/amphip

147 een one of its PSD-95/drosophila discs large/ZO-1 (PDZ) domains and the C-terminus of a subset of Fzd

148 nd postsynaptic density (PSD)-95/Discs Large/ZO-1 (PDZ) domains, which are present in many synaptic s

149 erminal ligand motifs for PSD-95/discs large/ZO-1 (PDZ) domains; via interaction with PDZ domain-cont

150 which are defined by the PSD-95/Discs large/ZO-1 (PDZ)-Src homology 3 (SH3)-guanylate kinase domain

151 PDZ (PSD95/Discs large/ZO-1) domains are ubiquitous protein interaction motifs

152 ulatory factor) family of PSD-95/Discs-large/ZO-1 (PDZ) scaffolding proteins.

153 a) binding domain and the PSD-95/Discs-large/ZO-1 (PDZ)-binding sequence of DAT, was made membrane-pe

154 actions of its N-terminal PSD-95/Discs-large/ZO-1 (PDZ)-like domain.

155 proteins are a family of PSD-95/Discs-large/ZO-1 (PDZ)-scaffolding proteins, three of which (NHERFs

156 independent of the DHHC5 PSD-95/Discs-large/ZO-1 homology (PDZ) binding motif, but requires a approx

157 rating a postsynaptic density-95/disks-large/ZO-1 (PDZ)-binding domain, reduces Cx43/ZO-1 interaction

158 vitro binding assays showed that full-length ZO-1 does not interact with DbpA.

159 er, the free ABR interfered with full-length ZO-1 exchange and reduced basal barrier function.

160 he claudin family; scaffolding proteins like ZO-1; and some cytoskeletal, signaling, and cell polarit

161 atenin, laminin V, and tight junction marker ZO-1.

162 asured by altered localization of TJ markers ZO-1 and Occludin, decreased transepithelial electrical

163 Claudin-5 depletion only mimicked ZO-1 effects on barrier formation, whereas the effects o

164 higher intestinal expressions of Ki67, MUC2, ZO-1, IgA, mucin and lower barrier permeability than tho

165 In this study, Neph1-ZO-1 structural complex was screened for the presence of

166 Loss of JAM-A, Afadin, or PDZ-GEF2, but not ZO-1 or PDZ-GEF1, similarly decreased cellular levels of

167 on of cell junction proteins (e.g., occluden-ZO-1, N-cadherin-ss-catenin).

168 ts [Occludin, Claudin-1, -2, Zona occludens (ZO-1, -2)].

169 ntermolecular interactions between occludin, ZO-1, and select claudins, and may have therapeutic pote

170 upting protein distribution (e.g., occludin, ZO-1) at the BTB, illustrating that rictor is a crucial

171 d adhesion protein complexes (e.g., occludin-ZO-1, CAR-ZO-1, and N-cadherin-ss-catenin), through a do

172 localized with F-actin, TJ proteins occludin/ZO-1 and basal ES (ectoplasmic specialization) proteins

173 adhesion kinase (FAK), creating the occludin/ZO-1/FAK/P-glycoprotein regulatory complex.

174 ylation-dependent regulation of the occludin:ZO-1 complex.

175 first direct demonstration of the ability of ZO-1 to stabilize claudin strands.

176 is next showed the proangiogenic activity of ZO-1 in both ex vivo and in vivo angiogenesis assays.

177 role of CREB in Tat-mediated alterations of ZO-1 was confirmed in brain microvessels in mice with CR

178 calization at endothelial cell boundaries of ZO-1 and VE-Cadherin, two components of tight and adhere

179 alization and activity, whereas depletion of ZO-1 and ZO-2, which is associated with reduced ZO-3 exp

180 eins that are within molecular dimensions of ZO-1 by fusing biotin ligase to either its N or C termin

181 fications provoke selective disengagement of ZO-1 from its binding partners, occludin, claudin 1, and

182 l actomyosin ring (PAMR), and dislocation of ZO-1 and cadherins.

183 testinal IEC6 cells revealed displacement of ZO-1 and occludin from intercellular boundaries.

184 ion integrity, promoting the displacement of ZO-1, and disorganization of cytoskeletal assembly.

185 -related phenotypes including: disruption of ZO-1-positive cell-cell junctions in tumour blood vessel

186 I:C) on R(T), as well as the dissociation of ZO-1 and occludin from the tight junction complex.

187 results show that double knockdown (dKD) of ZO-1/ZO-2 elevates the apical epithelial tension and eff

188 interactions between the first PDZ domain of ZO-1 (fused to eDHFR) and the C-terminal YV motif of cla

189 The COOH-terminal domain of ZO-1 was required for its association with myosin 1C.

190 lar clutch model of adhesion, this effect of ZO-1 leads to a decrease in the density and intensity of

191 Darby canine kidney cells depleted either of ZO-1, or one of the related proteins ZO-2 and ZO-3 (ZO p

192 The ends of ZO-1 are embedded in different functional subcompartment

193 rks were identified near the N and C ends of ZO-1.

194 occludin exchange, but increases exchange of ZO-1, claudin-1, and claudin-2, thereby causing the mobi

195 Expression of ZO-1 in WT endothelia at P14 was diffuse and localized t

196 n as well as decreased protein expression of ZO-1, whereas TNF-alpha and IL-8 mucosal transcript expr

197 ttenuated HIV-mediated altered expression of ZO-1.

198 nts ZO-1 and E-cadherin and the formation of ZO-1 containing tight junctions.

199 present in leader positions at the front of ZO-1-rich invading cords of cells, where they extend vim

200 n experiments verified that loss and gain of ZO-1 function govern the transition of connexons into GJ

201 Immunolocalization of ZO-1 and VE-cadherin demonstrated organization of the ju

202 ticle examines the functional involvement of ZO-1 in CXCL8/IL-8 chemokine expression in lung and brea

203 thermore, small interfering RNA knockdown of ZO-1 completely inhibited the formation of gap junctions

204 at resulted in a decrease in total levels of ZO-1 but significantly upregulated ZO-1 protein expressi

205 REB in modulation of nuclear localization of ZO-1 and maintaining the integrity of endothelial monola

206 ermore, Wnt4 causes membrane localization of ZO-1 and occludin in tight junctions.

207 (CPEB1) mediates the apical localization of ZO-1 mRNA, which encodes a critical tight junction compo

208 cance of Tat-induced nuclear localization of ZO-1.

209 tinal barrier function and prevented loss of ZO-1 at the TJs in vivo.

210 and severe disruption and mislocalization of ZO-1 and claudin-1 proteins.

211 llized the entire PDZ3-SH3-GUK core motif of ZO-1.

212 also stimulates threonine phosphorylation of ZO-1 in the mediation of endothelial TJ disruption and i

213 L8/IL-8 expression via a cytonuclear pool of ZO-1.

214 ty is a key factor in NEC, Epo regulation of ZO-1 in the human fetal immature H4 intestinal epithelia

215 el of Neph1-CD, and the crystal structure of ZO-1-PDZ1 to construct a structural model of the Neph1-C

216 duced Rho signaling and nuclear targeting of ZO-1.

217 in zona occludens 1 (ZO-1), translocation of ZO-1 to cell-cell borders, and the formation of typical

218 rotected against Tat-induced upregulation of ZO-1 in the nuclei and activation of CREB.

219 association with actin is also dependent on ZO-1, but colocalization demonstrates intermittent rathe

220 IL-1beta treatment had no effect on ZO-1 gene (tjp1) or protein expression.

221 teraction between actin and alpha-catenin or ZO-1.

222 ion of miR-675 processing from H19, promoted ZO-1 and E-cadherin expression, and restored the epithel

223 OCEL mutated within a recently proposed ZO-1-binding domain (K433) could not inhibit TNF effects

224 iption activity of the TJ-associated protein ZO-1-associated nucleic acid binding protein (ZONAB) wer

225 ncytokeratin, the junctional complex protein ZO-1, collagen type IV, as well as UB and collecting duc

226 on between Cx43 and the cytoskeletal protein ZO-1 is exclusively decreased at the late stage of PoH.

227 ion of mRNAs encoding tight junction protein ZO-1 and adherens junction E-cadherin, resulting in the

228 ogy and expression of tight junction protein ZO-1 and pump protein Na+/K+ ATPase alpha1 after culture

229 e localization of the tight junction protein ZO-1 consistent with a defect in the epithelial tight ju

230 but knockdown of the tight-junction protein ZO-1 enhanced permeability to oxalate and mannitol in pa

231 Moreover, the tight junction protein ZO-1 is mislocalized in the tal1-deficient endocardium,

232 demonstrate that the tight junction protein ZO-1 regulates tension acting on VE-cadherin-based adher

233 tosis and loss of the tight-junction protein ZO-1.

234 through targeting the tight junction protein ZO-1.

235 ith the expression of tight junction protein ZO-1.

236 ccludin to the structural organizing protein ZO-1 contributes to the regulation of barrier properties

237 complex of the junction scaffolding protein ZO-1 and the F-BAR-domain protein TOCA-1.

238 cal association with the scaffolding protein ZO-1, but the significance of the interaction is unknown

239 ociated with stabilization of the TJ protein ZO-1 and mediated by the miR-155 target protein Rheb.

240 n by supporting expression of the TJ protein ZO-1.

241 xpression of the tight junction (TJ) protein ZO-1, leading to a model whereby ZO-1 acts by sequesteri

242 he known role of zonula occludens-1 protein (ZO-1) in gap junction (GJ) function, we generated and an

243 edistribution of the tight junction proteins ZO-1 and occludin to lateral membranes of shedding cells

244 ed expression of the tight junction proteins ZO-1 and occludin.

245 y disorganized lymphatic junctional proteins ZO-1 and VE-cadherin.

246 associated guanylate kinase (MAGUK) proteins ZO-1, -2, and -3.

247 ssion of tight junction-associated proteins (ZO-1 and VE-cadherin) and PVM/M stabilizing neural cell

248 d a preservation of tight junction proteins (ZO-1 and occludin) composing the BBB.

249 antibodies against tight junction proteins, ZO-1, and claudin-1 and by measuring apical-basolateral

250 r that was modulated by, but did not require ZO-1 PDZ2.

251 In the retina, ZO-1 disruption began by 4 hours and was followed by dec

252 on increased barrier function and stabilized ZO-1 at the tight junction but did not affect claudin-1,

253 was examined and demonstrated Epo-stimulated ZO-1 expression in a dose-dependent manner through the P

254 and other cytoskeletal proteins, suggesting ZO-1 and -2 might regulate cytoskeletal activity at cell

255 t intracameral injection of siRNAs targeting ZO-1 and tricellulin increased outflow facility signific

256 ion assays indicated that inhibition targets ZO-1 binding with Cx43 in GJs as well as connexons in an

257 onfunctional/endocytic channels, rather than ZO-1 interfering with GJ endocytosis directly.

258 nd actin fibers at cell peripheries and that ZO-1 knockdown attenuated Cx43 assembly.

259 It is concluded that ZO-1 regulates the rate of undocked connexon aggregation

260 Taken together, our results demonstrate that ZO-1 regulates CXCL8/IL-8 expression via the NF-kappaB s

261 1 showed junctional DbpA, demonstrating that ZO-1 is not required to sequester DbpA at junctions.

262 e studies are the first direct evidence that ZO-1 limits solute permeability in established tight jun

263 Collectively, our results indicate that ZO-1 binding regulates channel accrual, while disengagem

264 seen in the ZO-1 knockdown, suggesting that ZO-1 and -2 are not functionally redundant for these fun

265 we define the interface between the ZO-1 PDZ3-SH3-U5-GuK (PSG) and occludin coiled-coil (CC)

266 ese data demonstrate a critical role for the ZO-1 ABR in barrier function and suggest that MLCK-depen

267 lity or morphological phenotypes seen in the ZO-1 knockdown, suggesting that ZO-1 and -2 are not func

268 ylation sites located in the vicinity of the ZO-1 binding site.

269 in complex with the cytoplasmic tail of the ZO-1 PDZ3 ligand, junctional adhesion molecule A (JAM-A)

270 een identified in the proximal region of the ZO-1 promoter.

271 ed macrophages led to the degradation of the ZO-1 protein, which correlated with increased SCB permea

272 The structure of the ZO-1 SH3-GUK domain confirms that the interdependent fol

273 Identification of the ZO-1/TOCA-1 complex provides novel insights into the und

274 us, our results support the concept that the ZO-1 shuttle from the cell junction to the cytonuclear c

275 and a predominantly basic helix V within the ZO-1 GuK domain.

276 bit TNF effects, but OCEL mutated within the ZO-1 SH3-GuK-binding region (K485/K488) remained functio

277 the downregulated genes included OCLN, TJP1 (ZO-1), FZD7, CDH1 (E-cadherin), and LAMA5.

278 experiments demonstrated loss of binding to ZO-1 when these residues were individually mutated to al

279 00 proteins tagged by biotin ligase fused to ZO-1, with both identical and distinct proteins near the

280 ion of CXCL8/IL-8 promoter that responded to ZO-1.

281 Intriguingly, these transitional ZO-1 binding/release and channel-aging steps are mediate

282 l-cell borders, and the formation of typical ZO-1 honeycomb patterns that are indicative of tight-jun

283 levels of ZO-1 but significantly upregulated ZO-1 protein expression in the nuclei.

284 Endothelial junctions were analyzed using ZO-1.

285 oxyl tails of Cxs and actin cytoskeleton via ZO-1 may regulate GJ assembly and growth.

286 In vitro, ZO-1 lacking the actin binding region (ABR) was not stab

287 cologic MLCK inhibition also blocked in vivo ZO-1 exchange in wild-type, but not long MLCK(-/-), mice

288 TJ) protein ZO-1, leading to a model whereby ZO-1 acts by sequestering DbpA at the TJ.

289 Unlike wild-type Cx43, in which ZO-1 binding is restricted to the periphery of GJ plaque

290 s in the blood and tumor are associated with ZO-1 expression and metastatic progression in early-stag

291 transiently diminished its association with ZO-1.

292 nd integrin alpha5beta1 forms a complex with ZO-1 in cells at the edge of migrating monolayers, regul

293 The transport results were consistent with ZO-1 and VE-cadherin immunocytochemistry and expression

294 ng MI includes an interaction of p-cSrc with ZO-1 and subsequent loss of scaffolding of Cx43 leaving

295 mposed of Cx43 co-localized extensively with ZO-1 and actin fibers at cell peripheries and that ZO-1

296 is associated with loss of interaction with ZO-1 and severe conduction delays.

297 Independent of interaction with ZO-1 or actin, claudin strands break and reanneal; pulse

298 localization of three of these proteins with ZO-1 as examples.

299 Biotin tagging with ZO-1 expands the tight junction proteome and defines sub

300 Biotin ligase tagging with ZO-1 was applied to identify a more complete tight junct