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1 on interactions between HCV and CD81 but not claudin 1.
2 f the barrier-forming tight junction protein claudin-1.
3 In contrast to NRC, Can 10 does not express claudin-1.
4 ger E-box binding homeobox-box1 (ZEB-1) with claudin-1.
5 tion of the tight junction proteins ZO-1 and claudin-1.
6 junction (TJ) proteins occludin, JAM-A, and claudin-1.
7 etween mutant BRAF and the loss of Cdx-2 and claudin-1.
8 ediated mechanism, independent of effects on claudin-1.
9 ial cell markers paired box protein PAX2 and claudin-1.
10 function and plasma membrane localisation of Claudin-1.
11 cyclin D1, c-Myc, COX-2, MMP-7, MMP-14, and Claudin-1.
12 localization, including ZO-1, occludin, and claudin-1.
13 en reported in four tight junction proteins (claudin 1, 14, 16, and zona occludens 2), nine gap junct
14 lls possess mRNAs encoding ZO-1, -2, and -3, claudin-1, -2, -4, and -8, occludin, and connexin-32.
18 the TJ-associated proteins actin, occludin, claudin-1, -3, and -5, and ZO-1 and -2 were analyzed by
22 junction adhesion molecule 1, occludin, and claudin-1/4 with minimal effects on the cytoplasmic plaq
23 ne phosphorylation and its dissociation from claudins 1/5, induces endothelial TJ disruption and its
25 ematical modeling shows that the majority of claudin-1 (76 +/- 5%) is stably localized at the tight j
26 ferentiation and effector functions, such as claudin-1, a Cdx-2 target gene encoding a critical tight
28 product has 91% identity to a mouse protein, claudin-1, a tight junction (TJ)-associated protein.
29 ubset tested expressed significant levels of Claudin-1, a tight junction protein needed for HCV infec
30 e selectively required for the expression of claudin-1, a tight junction protein that was recently id
35 is speculated that cholestasis is caused by Claudin-1 absence, leading to increased paracellular per
39 ression studies, certain claudins, including claudin-1 and -4, are postulated to increase, whereas ot
43 s against tight junction proteins, ZO-1, and claudin-1 and by measuring apical-basolateral movements
45 ccludin and enhanced membrane association of claudin-1 and claudin-2 by IL-15 required the presence o
50 nts, showed a similar pattern of increase in claudin-1 and HDAC-2 mRNA expression throughout all stag
52 y the observation of decreased expression of claudin-1 and nuclear beta-catenin in brain endothelial
53 B member I, and the tight-junction proteins claudin-1 and occludin have been identified as essential
54 our findings provide evidence for a role of claudin-1 and occludin in epidermal regeneration with po
56 meability selectively in ileum (up-regulated claudin-1 and occludin) and a significant reduction in B
61 croscopic analyses confirmed the presence of claudin-1 and ZO-1 in Z310 cells at cell-cell contact si
62 rmed that tight junction proteins (occludin, claudin-1 and zona occludens-1) are internalized through
64 in, p120 and beta-catenins, occludin, JAM-1, claudins 1 and 4, and ZO-1) in T84 epithelial cells.
65 of ZO-1 from its binding partners, occludin, claudin 1, and myosin 1C, coincident with opening of tjs
66 ter 6 hours of treatment with HGF, occludin, claudin-1, and beta-catenin were redistributed from the
67 in exchange, but increases exchange of ZO-1, claudin-1, and claudin-2, thereby causing the mobile fra
68 unction proteins zona occludens-1, occludin, claudin-1, and claudin-4, as well as that of desmosomal
70 tion of the TJ proteins, ZO-1, occludin, and claudin-1, and is associated with increased paracellular
71 l intercellular TJ proteins (occludin, ZO-1, claudin-1, and JAM) and subjacent AJ (beta-catenin and E
72 creases in expression of zonula occludens 1, claudin-1, and occludin in rectosigmoid mucosa; the effe
73 lls were transfected with a plasmid encoding Claudin-1, and stable Claudin-1-expressing clones were i
74 d Madin-Darby canine kidney cells, occludin, claudin-1, and ZO-1 were absent from cell-cell contacts
75 n-activated protein kinase (MAPK), occludin, claudin-1, and ZO-1 were recruited to the cell membrane,
76 ounts of the TJ proteins ZO-1, occludin, and claudin-1; and marked disorganization of the actin cytos
80 ly suppressed the mRNA and protein levels of claudin-1 but had only minor effects on the expression o
82 cell complex molecules such as annexin-2 and claudin-1, but also focal adhesion components such as DO
83 Because antibodies directed against CD81 and claudin-1, but not antibodies directed against scavenger
84 try factors CD81, scavenger receptor BI, and claudin-1; by interferon; and by reagents that inhibit N
87 bstitutions of these residues did not impair claudin-1 cell surface expression or lateral protein int
88 testinal permeability in vivo and changes in claudin-1, claudin-2, and myosin IXB genes expression, w
89 molecular weight complex containing at least claudin-1, claudin-2, and occludin; the difference in th
90 docytes used as a negative control expressed claudin-1, claudin-2, and protein gene product 9.5, whic
92 onstrate that EMT is associated with loss of claudin-1, claudin-2, occludin, and E-cadherin expressio
94 n Transwell permeable supports and expressed claudin-1, claudin-4, and claudin-8-key proteins for tig
95 hilic solutes, and the TJ proteins occludin, claudin-1, claudin-4, junctional adhesion molecule, and
96 significantly, whereas no obvious change of claudin-1, claudin-4, zonula occludens protein 1, and zo
97 s in ZO-2 expression, but not with occludin, claudin-1, claudin-5 or ZO-1 expression in ovine cerebra
99 measure the protein expression of occludin, claudin-1, claudin-5, zonula occludens (ZO)-1, and ZO-2,
101 ctions within the plasma membrane, including claudin-1-claudin-1 and claudin-1-CD81 interactions.
104 arrier composed of reactive astrocyte TJs of claudin 1 (CLDN1), CLDN4, and junctional adhesion molecu
106 evels of MIR29A and B, but reduced levels of Claudin-1 (CLDN1) and nuclear factor-kappaB-repressing f
107 d that E-cadherin is closely associated with claudin-1 (CLDN1) and occludin (OCLN) on the cell membra
109 immunosorbant assay using a recombinant CD81-claudin-1 (CLDN1) fusion protein to detect and quantify
112 ve expression cloning approach we identified claudin-1 (CLDN1), a tight junction component that is hi
114 ier and increased expression of TJ proteins, claudin-1 (CLDN1), claudin-23 (CLDN23), occludin, and Zo
115 Other cell surface molecules, such as CD81, Claudin-1 (CLDN1), Occludin (OCLN), SR-BI, and low-densi
128 e structural and functional roles of various claudin-1 domains in HCV entry, we applied a mutagenesis
131 audin-1 and a synthetic peptide based on the claudin-1 ECL-2 offered no protection to Caco-2 cells.
134 80), because peptides corresponding to other claudin-1 EL domains failed to influence TJ function.
137 oclonal antibody specific for the TJ protein claudin-1 eliminates chronic HCV infection without detec
138 tibodies and HCV particles increase CD81 and claudin-1 endocytosis, supporting a model wherein HCV st
141 hibitors restore cell-cell junctions, rescue claudin 1 expression, and abrogate growth and disseminat
143 ckdown of Rab3Gap1 prevented plasma membrane Claudin-1 expression and the formation of a barrier comp
144 urther show a functional correlation between claudin-1 expression and TSA-mediated regulation of inva
145 cells showed a positive correlation between claudin-1 expression and tumor growth and metastasis.
148 Furthermore, we demonstrate that changes in claudin-1 expression have significant effects on growth
150 t a novel post-transcriptional regulation of claudin-1 expression in colon cancer cells and further s
151 lecular mechanism(s) underlying dysregulated claudin-1 expression in colon cancer remains poorly unde
152 ver, the mechanisms underlying the increased claudin-1 expression in colorectal cancer remains unknow
153 is issue of Oncogene, Suh et al. reported on claudin-1 expression in hepatocellular carcinoma (HCC),
154 rt an inverse relationship between Smad4 and claudin-1 expression in human colorectal carcinoma tumor
155 t and widely used HDAC inhibitors, inhibited claudin-1 expression in multiple colon cancer cell lines
158 thermore, this Smad4-dependent inhibition of claudin-1 expression is independent of TGF-beta signalin
159 hibition of PKC signaling in cells with high claudin-1 expression resulted in decreased claudin-1 exp
160 ry human keratinocytes showed that decreased claudin-1 expression resulted in significantly impaired
162 HT29 colon cancer cell lines down-regulates claudin-1 expression through transcriptional repression
164 expressed claudin-1, or SW620 cells in which claudin-1 expression was repressed, to determine the eff
170 sed to eDHFR) and the C-terminal YV motif of claudin-1 (fused to GFP) in single microscope images at
172 ched controls, we assessed the filaggrin and claudin 1 genotypes, the phenotypes by dermatoscopy, and
177 Here, we report an increased expression of claudin-1 in human primary colon carcinoma and metastasi
179 tein kinase C (PKC) can affect expression of claudin-1 in rat choroid plexus cells, and we observed a
182 ata establish the function and regulation of claudin-1 in the perineurium as the major sealing compon
189 unolabeling of kidney proteins revealed that claudin-1 induction destabilized the SD protein complex
191 ays, AT1002 decreased ZO-1-occludin and ZO-1-claudin 1 interactions coincident with PKCalpha-dependen
193 data suggest Rab3Gap1 mediated exocytosis of Claudin-1 is an important component of epidermal barrier
194 Expression of the tight junction protein claudin-1 is dysregulated in colon tumors and associates
197 the expression of a tight junction protein, claudin-1, is increased during colon carcinogenesis and
198 e gene expression of claudins, in particular claudin-1, is markedly upregulated in the podocyte, acco
199 on of other TJ and AJ proteins such as ZO-1, claudin-1, JAM, beta-catenin, and E-cadherin were down-r
200 rearrangement of key TJ proteins: occludin, claudin-1, junctional adhesion molecule-A, and zonula oc
202 T pathway was significantly attenuated after claudin-1 knockdown, and protein levels of extracellular
208 key HCV receptor/coreceptor molecules CD81, claudin-1, low-density lipoprotein receptor (LDLr), occl
209 we propose that cell-cell contacts formed by claudin-1 may generate specialized membrane domains that
212 ond to CPE, while transfectants expressing a Claudin-1 mutant with the corresponding ECL-2 residue ch
213 dition, expression of cell adhesion proteins claudin-1, occludin, and e-cadherin are also increased.
216 SW480 colon cancer cells that overexpressed claudin-1, or SW620 cells in which claudin-1 expression
217 Ninety-five renal biopsies were stained for claudin-1 (PEC marker), CD44 (activated PECs), and LKIV6
218 During normal mouse epidermal development, Claudin-1 plasma membrane localisation and Rab3Gap1 cell
219 e expression of Smad4 in Smad4-deficient but claudin-1-positive SW480 or HT29 colon cancer cell lines
220 een HCV E2 and its two co-receptors CD81 and claudin-1 probably triggered the activation of AKT.
222 947 did not prevent the Smad4 suppression of claudin-1 protein expression in either SW480 or HT29 cel
223 genous occludin protein led to a recovery in claudin-1 protein level, relocation of the zonula occlud
224 kdown resulted in decreases in claudin-7 and claudin-1 proteins that were reversed with lysosome inhi
229 We investigated the mechanisms by which claudin-1 regulates E-cadherin expression and its effect
231 ductions in the expression of E-cadherin and claudin-1, responses that are standard characteristics o
232 ns appeared normal, immunohistochemistry for claudin 1 showed no reduction in protein amounts, and mo
233 pathway, including MMP9 hemopexin domain or claudin-1 siRNA, enables an opioid peptide ([D-Ala2,N-Me
234 complexes of claudin-7, integrin alpha2, and claudin-1 that normally form in epithelial basolateral c
235 proteins (ie, zonula occludens-1, Occludin, Claudin-1) that critically regulate epithelial paracellu
240 in vivo Here, we report the generation of a claudin-1 transgenic mouse model with doxycycline-induci
247 ll borders of the superficial layer, whereas claudin-1 was localized mainly in the basal and wing cel
250 taining of a tissue microarray revealed that claudin-1 was overexpressed in melanoma, and aberrantly
251 in human melanoma, cells lacking endogenous claudin-1 were treated with 200 nM phorbol myristic acid
253 surface and interaction between Occludin and Claudin-1 which are thought to be required for tight jun
254 ion and integrity through down-regulation of claudin-1, which is a key component of tight junctions.
256 n-1beta (IL-1beta) causes rapid induction of claudin-1, with an expression pattern reciprocal to loss
257 and localization of tight junction proteins (claudin-1, ZO-1) were visualized by immunofluorescence.
259 n 1-fusion proteins of beta-actin, occludin, claudin-1, ZO-1, clathrin light chain A1, and caveolin-1
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