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1 electively controlling tight junction CLDN1 (claudin-1).
2 on interactions between HCV and CD81 but not claudin 1.
3 ial cell markers paired box protein PAX2 and claudin-1.
4 function and plasma membrane localisation of Claudin-1.
5 localization, including ZO-1, occludin, and claudin-1.
6 f the barrier-forming tight junction protein claudin-1.
7 In contrast to NRC, Can 10 does not express claudin-1.
8 ger E-box binding homeobox-box1 (ZEB-1) with claudin-1.
9 tion of the tight junction proteins ZO-1 and claudin-1.
10 junction (TJ) proteins occludin, JAM-A, and claudin-1.
11 catalytic function dependent upregulation of Claudin-1.
12 ediated mechanism, independent of effects on claudin-1.
13 cyclin D1, c-Myc, COX-2, MMP-7, MMP-14, and Claudin-1.
14 etween mutant BRAF and the loss of Cdx-2 and claudin-1.
15 en reported in four tight junction proteins (claudin 1, 14, 16, and zona occludens 2), nine gap junct
16 lls possess mRNAs encoding ZO-1, -2, and -3, claudin-1, -2, -4, and -8, occludin, and connexin-32.
20 the TJ-associated proteins actin, occludin, claudin-1, -3, and -5, and ZO-1 and -2 were analyzed by
24 junction adhesion molecule 1, occludin, and claudin-1/4 with minimal effects on the cytoplasmic plaq
25 ne phosphorylation and its dissociation from claudins 1/5, induces endothelial TJ disruption and its
27 ematical modeling shows that the majority of claudin-1 (76 +/- 5%) is stably localized at the tight j
28 ferentiation and effector functions, such as claudin-1, a Cdx-2 target gene encoding a critical tight
30 product has 91% identity to a mouse protein, claudin-1, a tight junction (TJ)-associated protein.
31 ubset tested expressed significant levels of Claudin-1, a tight junction protein needed for HCV infec
32 e selectively required for the expression of claudin-1, a tight junction protein that was recently id
37 is speculated that cholestasis is caused by Claudin-1 absence, leading to increased paracellular per
41 ression studies, certain claudins, including claudin-1 and -4, are postulated to increase, whereas ot
45 s against tight junction proteins, ZO-1, and claudin-1 and by measuring apical-basolateral movements
47 ccludin and enhanced membrane association of claudin-1 and claudin-2 by IL-15 required the presence o
52 nts, showed a similar pattern of increase in claudin-1 and HDAC-2 mRNA expression throughout all stag
54 y the observation of decreased expression of claudin-1 and nuclear beta-catenin in brain endothelial
55 B member I, and the tight-junction proteins claudin-1 and occludin have been identified as essential
56 our findings provide evidence for a role of claudin-1 and occludin in epidermal regeneration with po
58 meability selectively in ileum (up-regulated claudin-1 and occludin) and a significant reduction in B
59 height/crypt depth ratio, and mRNA levels of claudin-1 and occludin, no significant differences were
64 croscopic analyses confirmed the presence of claudin-1 and ZO-1 in Z310 cells at cell-cell contact si
66 rmed that tight junction proteins (occludin, claudin-1 and zona occludens-1) are internalized through
69 in, p120 and beta-catenins, occludin, JAM-1, claudins 1 and 4, and ZO-1) in T84 epithelial cells.
70 of ZO-1 from its binding partners, occludin, claudin 1, and myosin 1C, coincident with opening of tjs
71 ter 6 hours of treatment with HGF, occludin, claudin-1, and beta-catenin were redistributed from the
72 in exchange, but increases exchange of ZO-1, claudin-1, and claudin-2, thereby causing the mobile fra
73 unction proteins zona occludens-1, occludin, claudin-1, and claudin-4, as well as that of desmosomal
74 icrin, and tight junction proteins occludin, claudin-1, and claudin-4, at mRNA and protein levels.
75 he tight junction proteins zona occludens-1, claudin-1, and claudin-5, which were significantly reduc
77 tion of the TJ proteins, ZO-1, occludin, and claudin-1, and is associated with increased paracellular
78 l intercellular TJ proteins (occludin, ZO-1, claudin-1, and JAM) and subjacent AJ (beta-catenin and E
79 r function, such as filaggrin, occludin, and claudin-1, and mRNA levels of filaggrin, loricrin, and i
80 creases in expression of zonula occludens 1, claudin-1, and occludin in rectosigmoid mucosa; the effe
81 lls were transfected with a plasmid encoding Claudin-1, and stable Claudin-1-expressing clones were i
82 d Madin-Darby canine kidney cells, occludin, claudin-1, and ZO-1 were absent from cell-cell contacts
83 n-activated protein kinase (MAPK), occludin, claudin-1, and ZO-1 were recruited to the cell membrane,
84 ounts of the TJ proteins ZO-1, occludin, and claudin-1; and marked disorganization of the actin cytos
88 f MDA-MB-231 ADAM15A expressing cells showed Claudin-1 at cell-cell junctions, in the cytoplasm and n
89 taining barrier and highlight the HIF-1alpha/claudin-1 axis as a potential therapeutic target for EoE
90 y analysis identified a repressed HIF-1alpha/claudin-1 axis, which was restored via pharmacologic HIF
91 gen metabolism, tissue hypoxia, and impaired claudin-1 barrier via repression of HIF-1alpha/claudin-1
92 thelial cells indicates that aquaporin 1 and claudin-1 both remain normally polarized in all genotype
93 ly suppressed the mRNA and protein levels of claudin-1 but had only minor effects on the expression o
95 f patients with AD (loricrin, filaggrin, and claudin 1) but showed characteristic alterations in lipi
96 cell complex molecules such as annexin-2 and claudin-1, but also focal adhesion components such as DO
97 Because antibodies directed against CD81 and claudin-1, but not antibodies directed against scavenger
98 try factors CD81, scavenger receptor BI, and claudin-1; by interferon; and by reagents that inhibit N
101 bstitutions of these residues did not impair claudin-1 cell surface expression or lateral protein int
102 testinal permeability in vivo and changes in claudin-1, claudin-2, and myosin IXB genes expression, w
103 molecular weight complex containing at least claudin-1, claudin-2, and occludin; the difference in th
104 docytes used as a negative control expressed claudin-1, claudin-2, and protein gene product 9.5, whic
106 onstrate that EMT is associated with loss of claudin-1, claudin-2, occludin, and E-cadherin expressio
108 n Transwell permeable supports and expressed claudin-1, claudin-4, and claudin-8-key proteins for tig
109 hilic solutes, and the TJ proteins occludin, claudin-1, claudin-4, junctional adhesion molecule, and
110 significantly, whereas no obvious change of claudin-1, claudin-4, zonula occludens protein 1, and zo
111 s in ZO-2 expression, but not with occludin, claudin-1, claudin-5 or ZO-1 expression in ovine cerebra
113 measure the protein expression of occludin, claudin-1, claudin-5, zonula occludens (ZO)-1, and ZO-2,
115 ctions within the plasma membrane, including claudin-1-claudin-1 and claudin-1-CD81 interactions.
120 arrier composed of reactive astrocyte TJs of claudin 1 (CLDN1), CLDN4, and junctional adhesion molecu
122 evels of MIR29A and B, but reduced levels of Claudin-1 (CLDN1) and nuclear factor-kappaB-repressing f
123 d that E-cadherin is closely associated with claudin-1 (CLDN1) and occludin (OCLN) on the cell membra
125 immunosorbant assay using a recombinant CD81-claudin-1 (CLDN1) fusion protein to detect and quantify
129 ve expression cloning approach we identified claudin-1 (CLDN1), a tight junction component that is hi
131 ier and increased expression of TJ proteins, claudin-1 (CLDN1), claudin-23 (CLDN23), occludin, and Zo
132 Other cell surface molecules, such as CD81, Claudin-1 (CLDN1), Occludin (OCLN), SR-BI, and low-densi
145 e structural and functional roles of various claudin-1 domains in HCV entry, we applied a mutagenesis
149 audin-1 and a synthetic peptide based on the claudin-1 ECL-2 offered no protection to Caco-2 cells.
152 80), because peptides corresponding to other claudin-1 EL domains failed to influence TJ function.
155 oclonal antibody specific for the TJ protein claudin-1 eliminates chronic HCV infection without detec
156 tibodies and HCV particles increase CD81 and claudin-1 endocytosis, supporting a model wherein HCV st
159 hibitors restore cell-cell junctions, rescue claudin 1 expression, and abrogate growth and disseminat
161 1A knockdown suppressed HIF-1alpha-dependent claudin-1 expression and epithelial barrier function, as
162 ckdown of Rab3Gap1 prevented plasma membrane Claudin-1 expression and the formation of a barrier comp
163 urther show a functional correlation between claudin-1 expression and TSA-mediated regulation of inva
164 cells showed a positive correlation between claudin-1 expression and tumor growth and metastasis.
166 on in T47D cells by shRNA reduced endogenous Claudin-1 expression confirming a role for ADAM15 in reg
169 Furthermore, we demonstrate that changes in claudin-1 expression have significant effects on growth
171 t a novel post-transcriptional regulation of claudin-1 expression in colon cancer cells and further s
172 lecular mechanism(s) underlying dysregulated claudin-1 expression in colon cancer remains poorly unde
173 ver, the mechanisms underlying the increased claudin-1 expression in colorectal cancer remains unknow
174 is issue of Oncogene, Suh et al. reported on claudin-1 expression in hepatocellular carcinoma (HCC),
175 rt an inverse relationship between Smad4 and claudin-1 expression in human colorectal carcinoma tumor
176 ee of C and E isoforms led to an increase in Claudin-1 expression in MDA-MB-231 cells, while ADAM15B
177 t and widely used HDAC inhibitors, inhibited claudin-1 expression in multiple colon cancer cell lines
180 thermore, this Smad4-dependent inhibition of claudin-1 expression is independent of TGF-beta signalin
181 hibition of PKC signaling in cells with high claudin-1 expression resulted in decreased claudin-1 exp
182 ry human keratinocytes showed that decreased claudin-1 expression resulted in significantly impaired
184 HT29 colon cancer cell lines down-regulates claudin-1 expression through transcriptional repression
186 expressed claudin-1, or SW620 cells in which claudin-1 expression was repressed, to determine the eff
194 sed to eDHFR) and the C-terminal YV motif of claudin-1 (fused to GFP) in single microscope images at
196 ched controls, we assessed the filaggrin and claudin 1 genotypes, the phenotypes by dermatoscopy, and
201 Here, we report an increased expression of claudin-1 in human primary colon carcinoma and metastasi
203 tein kinase C (PKC) can affect expression of claudin-1 in rat choroid plexus cells, and we observed a
206 ata establish the function and regulation of claudin-1 in the perineurium as the major sealing compon
213 n endothelial cells and cells overexpressing claudin-1 indicated that newly synthesized claudin-1 was
215 unolabeling of kidney proteins revealed that claudin-1 induction destabilized the SD protein complex
218 ays, AT1002 decreased ZO-1-occludin and ZO-1-claudin 1 interactions coincident with PKCalpha-dependen
220 data suggest Rab3Gap1 mediated exocytosis of Claudin-1 is an important component of epidermal barrier
221 Expression of the tight junction protein claudin-1 is dysregulated in colon tumors and associates
223 e blood microvessels we have identified that claudin-1 is highly expressed in leaky brain microvessel
227 the expression of a tight junction protein, claudin-1, is increased during colon carcinogenesis and
228 e gene expression of claudins, in particular claudin-1, is markedly upregulated in the podocyte, acco
229 on of other TJ and AJ proteins such as ZO-1, claudin-1, JAM, beta-catenin, and E-cadherin were down-r
230 rearrangement of key TJ proteins: occludin, claudin-1, junctional adhesion molecule-A, and zonula oc
232 T pathway was significantly attenuated after claudin-1 knockdown, and protein levels of extracellular
239 key HCV receptor/coreceptor molecules CD81, claudin-1, low-density lipoprotein receptor (LDLr), occl
240 we propose that cell-cell contacts formed by claudin-1 may generate specialized membrane domains that
244 ond to CPE, while transfectants expressing a Claudin-1 mutant with the corresponding ECL-2 residue ch
245 thelial integrity with reduced expression of claudin-1, occludin, and E-cadherin and decreased number
246 dition, expression of cell adhesion proteins claudin-1, occludin, and e-cadherin are also increased.
247 or measurement of CD11c, CD3, CD4, tryptase, claudin-1, occludin, E-cadherin, and vascular endothelia
250 SW480 colon cancer cells that overexpressed claudin-1, or SW620 cells in which claudin-1 expression
251 Ninety-five renal biopsies were stained for claudin-1 (PEC marker), CD44 (activated PECs), and LKIV6
253 nexin A3 colocalized with cathepsin B and C, claudin-1, phosphorylated ERK1/2, and CD44, but not with
254 During normal mouse epidermal development, Claudin-1 plasma membrane localisation and Rab3Gap1 cell
255 e expression of Smad4 in Smad4-deficient but claudin-1-positive SW480 or HT29 colon cancer cell lines
256 een HCV E2 and its two co-receptors CD81 and claudin-1 probably triggered the activation of AKT.
258 947 did not prevent the Smad4 suppression of claudin-1 protein expression in either SW480 or HT29 cel
259 genous occludin protein led to a recovery in claudin-1 protein level, relocation of the zonula occlud
260 kdown resulted in decreases in claudin-7 and claudin-1 proteins that were reversed with lysosome inhi
266 We investigated the mechanisms by which claudin-1 regulates E-cadherin expression and its effect
268 ductions in the expression of E-cadherin and claudin-1, responses that are standard characteristics o
269 ns appeared normal, immunohistochemistry for claudin 1 showed no reduction in protein amounts, and mo
270 audin-1 barrier via repression of HIF-1alpha/claudin-1 signaling, which was restored by transgenic ex
271 pathway, including MMP9 hemopexin domain or claudin-1 siRNA, enables an opioid peptide ([D-Ala2,N-Me
272 complexes of claudin-7, integrin alpha2, and claudin-1 that normally form in epithelial basolateral c
273 proteins (ie, zonula occludens-1, Occludin, Claudin-1) that critically regulate epithelial paracellu
278 in vivo Here, we report the generation of a claudin-1 transgenic mouse model with doxycycline-induci
285 ll borders of the superficial layer, whereas claudin-1 was localized mainly in the basal and wing cel
288 taining of a tissue microarray revealed that claudin-1 was overexpressed in melanoma, and aberrantly
289 g claudin-1 indicated that newly synthesized claudin-1 was present on the cell membrane (~45%), was i
290 in human melanoma, cells lacking endogenous claudin-1 were treated with 200 nM phorbol myristic acid
292 surface and interaction between Occludin and Claudin-1 which are thought to be required for tight jun
293 ion and integrity through down-regulation of claudin-1, which is a key component of tight junctions.
297 n-1beta (IL-1beta) causes rapid induction of claudin-1, with an expression pattern reciprocal to loss
298 and localization of tight junction proteins (claudin-1, ZO-1) were visualized by immunofluorescence.
300 n 1-fusion proteins of beta-actin, occludin, claudin-1, ZO-1, clathrin light chain A1, and caveolin-1