ライフサイエンスコーパス: ZO-1

1 ZO-1 (Zona occludens 1), encoded by the tight junction p

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

3 ZO-1 domains that mediate interactions with occludin and

4 ZO-1 interacts with the actin cytoskeleton, gap, and adh

5 ZO-1 is a key protein responsible for maintaining approp

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

7 ZO-1 protein has a unique physiological role in cardiac

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

9 ZO-1 small interfering RNA and cDNA transfection experim

10 ZO-1 small interfering RNA and overexpression experiment

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

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

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

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

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

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

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

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

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

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

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

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

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

24 that the accumulation of Zonula Occludens-1 (ZO-1) at TJs closely scales with tension of the adjacent

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

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

27 acaques exhibited loss of zonal occludens-1 (ZO-1) staining, indicative of a compromised blood-brain

28 blished interaction with zonula occludens-1 (ZO-1), and was building homophilic cis- and trans-intera

29 tight junction protein, Zonula occludens-1 (ZO-1).

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

31 tight junction protein, Zonula occludens-1 (ZO-1).

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

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

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

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

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

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

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

39 B tight junction protein (zonula ocludens-1; ZO-1) localization and expression, cytoskeletal organiza

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

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

42 5 cis- and trans-interactions) and claudin-5/ZO-1 interaction affecting claudin-5 incorporation into

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

44 8, and 373 exhibited a significantly altered ZO-1 interaction profile, while mutants with S residues

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

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

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

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

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

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

51 with IL-1beta, TNFalpha and hypoxia, ALP and ZO-1 were decreased, MUC2 increased, and MUC5AC remained

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

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

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

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

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

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

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

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

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

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

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

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

64 estinal tight junction proteins occludin and ZO-1.

65 of the tight junction proteins, occludin and ZO-1.

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

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

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

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

70 Arhgap21, Pdlim2, Pdlim7, Rims2, Scrib, and ZO-1.

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

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

73 ions via the known binding domain as well as ZO-1's MAGUK domain and YAP's N-terminal proline-rich do

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

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

76 junction, we find that the affinity between ZO-1 and actin is surprisingly weak, and we propose a mo

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 quite penetrant (lipophilic molecules, Cx30, ZO-1, Occludin).

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

96 We find loss of Cx43/ZO-1 complexing during Ad5 infection by co-immunoprecipi

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

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

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

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

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

108 Here, we used the Tiam2 PSD-95/Dlg/ZO-1 (PDZ) domain and a quadruple mutant (QM), engineere

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

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

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

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

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

114 MPDZ is a multi-PDZ (PSD95/DLG1/ZO-1) domain scaffold present at apical cell junctions w

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

116 cilium loss, less tight junction expression (ZO-1), and more detachment of epithelial cells than is s

117 stable incorporation of retrogradely flowing ZO-1 clusters into TJs.

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

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

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

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

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

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

124 We generated ZO-1 CM-specific knockout (KO) mice using alpha-Myosin H

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

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

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

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

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

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

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

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

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

134 nction/adherens junction proteins, including ZO-1, occludin, and E-cadherin.

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

136 crib in PDZ formation, potentially involving ZO-1 and Hippo signaling.

137 dothelial expression of Na/K ATPase, Cox IV, ZO-1, N-CAM, and CD166 was observed.

138 Non-junctional ZO-1 clusters form by phase separation, and direct actin

139 hin the YSL, which transports non-junctional ZO-1 clusters toward the TJ.

140 phase separation and flow of non-junctional ZO-1 confer mechanosensitivity to TJs.

141 icantly decreased TER and reduced junctional ZO-1 localization, while increasing FD4 permeability in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 Finally, by tuning the affinity of ZO-1 to actin, we demonstrate that epithelial monolayers

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

174 hase separation, and direct actin binding of ZO-1 is required for stable incorporation of retrogradel

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

176 However, the contribution of ZO-1 to cardiac physiology remains poorly defined.

177 There was a decrease of ZO-1 tight junction localization with 100 mum H(2)O(2),

178 Global deletion of ZO-1 in the mouse is lethal by embryonic day 11.5.

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

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

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

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

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

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

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

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

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

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

191 by a decrease in the protein expressions of ZO-1 and occludin and elevated mRNA expression of interl

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

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

194 The function of ZO-1 in cardiac myocytes (CM) is largely unknown.

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

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

197 formation and/or junctional incorporation of ZO-1 clusters is impaired, then TJs lose their mechanose

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

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

200 ot altered despite decreased localization of ZO-1 and Cx43 at the ventricular intercalated disc and m

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

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

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

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

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

206 used greater CE cell loss, including loss of ZO-1 junctional contacts and corneal edema, in female th

207 Tamoxifen-induced loss of ZO-1 led to atrioventricular (AV) block without changes

208 howed no significant change with the loss of ZO-1, Connexin-45 and Coxsackie-adenovirus (CAR) protein

209 Further, with loss of ZO-1, ZO-2 protein was increased significantly in ventri

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 We aim to determine the role of ZO-1 in cardiac function.

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

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

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

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

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

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

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

223 (YAP2) and tight junction protein 1 (TJP1 or ZO-1), uncovering interactions via the known binding dom

224 show that a specific isoform of Polychaetoid/ZO-1, Pyd-P, is essential for Drosophila SDs, since, in

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

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

227 mino-acid sequence in the TJ adaptor protein ZO-1, which is responsible for actin binding, and show t

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

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

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

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

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

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

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

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

236 through targeting the tight junction protein ZO-1.

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

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

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

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

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

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

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

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

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

246 n of the endothelial tight junction proteins ZO-1 and occludin, key mechanisms underlying vascular in

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

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

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

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

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

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

253 veal Cx43 gap junction remodeling by reduced ZO-1 complexing.

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

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

256 ft ventricular ejection fraction, suggesting ZO-1 is differentially required for AV node and ventricu

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

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

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

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

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

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

263 1 showed junctional DbpA, demonstrating that ZO-1 is not required to sequester DbpA at junctions.

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

265 dy, immunohistochemical staining showed that ZO-1 is abundantly expressed in the human AV node and co

266 unostaining analyses of AV nodes showed that ZO-1 loss decreased Cx (connexin) 40 expression and inte

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

268 s explained by a parallel role played by the ZO-1 homologue Polychaetoid.

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

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

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

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

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 zebrafish suggest a conserved role for Tjp1a/ZO-1 in promoting junctional remodeling in podocytes.

279 ls because of diminished binding affinity to ZO-1.

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

281 00 proteins tagged by biotin ligase fused to ZO-1, with both identical and distinct proteins near the

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

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

284 Actomyosin tension triggers ZO-1 junctional accumulation by driving retrograde actom

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

286 Uniquely, ZO-1 is dispensable for function of the working myocardi

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

288 Endothelial junctions were analyzed using ZO-1.

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

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

291 While ZO-1-associated proteins such as vinculin, connexin 43,

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

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

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

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

296 Direct Cx43 interaction with ZO-1 plays a critical role in gap junction regulation.

297 in cultured cells, working in parallel with ZO-1 proteins, particularly at multicellular junctions.

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