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1 involving increased inflammation and loss of claudin-3.
2 udin-19 mRNA was 25 times more abundant than claudin-3.
3  site at amino acid 192 in the C terminus of claudin-3.
4 nd diminished junctional immunoreactivity of claudin-3.
5 d downregulated expression of genes encoding claudin 3, 4, and 7 and the luminal marker, cytokeratin
6                                              Claudin 3, a tight junction protein, is transiently inco
7 regimen, a novel and tissue-specific role of claudin-3, a tight junction integral protein, in inhibit
8                                      Loss of claudin-3 also predicted poor patient survival.
9 5 only in junctions of acinar cells, whereas claudin 3 and 4 are in both.
10 EB1, S100A8, amyloid beta precursor protein, claudin 3 and cadherin 1 (downregulated in MDA-MB-231) w
11 whereas the expression of 194 genes, such as claudin 3 and cell adhesion molecule 1, is significantly
12 family, and low to absent expression of both claudin 3 and E-cadherin.
13 junction (TJ) proteins in the ileum revealed claudin 3 and occludin expression to be increased overal
14                                              Claudin-3 and -4 are frequently overexpressed in ovarian
15                         Here, we showed that claudin-3 and -4 can be phosphorylated in ovarian cancer
16  presence of the high-affinity CPE receptors claudin-3 and -4 in both organs of rabbits, consistent w
17 present surface or secreted proteins such as claudin-3 and -4, HE4, mucin-1, epithelial cellular adhe
18 ptors on intestinal epithelial cells include claudin-3 and -4, members of a large family of tight jun
19 ity association of the PDZ domain of nNOS to claudin-3 and claudin-14, two tight junction tetraspan m
20                               In particular, claudin-3 and claudin-4 are frequently overexpressed in
21                                     However, claudin-3 and claudin-4 are the only family members capa
22 nterfering RNA (siRNA)-mediated knockdown of claudin-3 and claudin-4 expression in ovarian cancer cel
23 ely in breast cancer cells, correlating with claudin-3 and claudin-4 expression.
24 current ovarian tumors were found to express claudin-3 and claudin-4 genes at significantly higher le
25 profiling, we and others have recently found claudin-3 and claudin-4 genes to be highly expressed in
26 (CNS) revealed low or undetectable levels of claudin-3 and claudin-4 in all regions tested by Western
27 tudy was designed to study the expression of claudin-3 and claudin-4 in human prostate tissue as pote
28      Our previous studies have revealed that claudin-3 and claudin-4 proteins are highly overexpresse
29                   In contrast, expression of claudin-3 and claudin-4 was absent in adjacent normal br
30 issue Northern blot analysis, mRNAs for both claudin-3 and claudin-4 were expressed at high levels in
31             By immunohistochemical analysis, claudin-3 and claudin-4 were expressed frequently in met
32                       We found that although claudin-3 and claudin-4 were heteromerically compatible
33 estroy cancer cells expressing CPE receptors claudin-3 and claudin-4.
34 E) cells constitutively expressing wild-type claudin-3 and claudin-4.
35 ession of TJ proteins ZO-1, JAM-2, Occludin, Claudin-3 and Claudin-5, using in vitro cultures of the
36 y we investigated the level of expression of claudin-3 and/or claudin-4 in chemotherapy-naive and che
37                             The abundance of claudins-3 and -5 remained unchanged.
38                                       Rvp.1 (claudin-3) and CPE-R (claudin-4) are members of a larger
39 s 8, 18, and 19, CD133/1, telomerase, CD44H, claudin 3, and albumin (weakly).
40 e tight-junction molecules zona occludens-1, claudin 3, and claudin 5 and other pathways critically i
41 e able to heterotypically bind to claudin-1, claudin-3, and claudin-5.
42 blots revealed that expression of Claudin-7, Claudin-3, and Occludin, critical proteins that regulate
43              Although glucose transporter 1, claudin-3, and plasmalemma vesicular-associated protein
44 helial cells, in which zonal occludens-1 and claudin-3, apical tight-junction proteins, are mislocali
45       Overall, these novel findings identify claudin-3 as a therapeutic target for inhibiting overact
46                                              Claudin-3, claudin-10, and claudin-19 were detected in R
47 ts were unexplained by effects on claudin-2, claudin-3, claudin-19, occludin, and ZO-1, but changes i
48 audins expressed by the alveolar epithelium, claudin-3, claudin-4, and claudin-18 are the most promin
49 hrough immunohistochemical analysis of ApoJ, claudin-3, claudin-4, and epithelial cellular adhesion m
50 pression of other tight junctional proteins (claudin-3, claudin-4, claudin-5, occludin, and ZO-1) and
51                                              Claudin-3 (CLDN3) and claudin-4 (CLDN4) are the major st
52                                              Claudin-3 (CLDN3) is a tight junction protein that is ov
53 ered intestinal morphology, and dysregulated claudin-3 crypt expression.
54 , which were heterotypically compatible with claudin-3, did not heterotypically bind to claudin-4.
55 tercellular junctional proteins (e.g., ZO-1, claudin-3, E-cadherin) and the subapical cytoskeletal/mi
56 nal barrier function maturation by promoting claudin 3 expression.
57 ibit impaired barrier function and decreased claudin 3 expression.
58 es intestinal barrier maturation and induces claudin 3 expression.
59 e findings however contrasted an upregulated claudin-3 expression in other cancer types and implicate
60                 The persistent high level of claudin-3 expression in prostate adenocarcinoma and func
61 ases in the distribution of occludin but not claudin-3 in the B, EF, and B+EF groups.
62  from periportal to pericentral hepatocytes, claudin 3 is uniformly expressed, claudin 4 is absent, a
63 nstructs demonstrated that the C terminus of claudin-3 is an excellent substrate for cAMP-dependent p
64                                              Claudin-3 loss also upregulated the gp130/IL6/Stat3 sign
65 c and pharmacological studies confirmed that claudin-3 loss induces Wnt/beta-catenin activation, whic
66                                              Claudin-3-/- mice revealed dedifferentiated and leaky co
67 ndent manner, differentiated colon cancer in claudin-3-/- mice versus WT-mice.
68 nding normal glandular tissue, expression of claudin-3 mRNA remained high in the epithelium of prosta
69                     Our results suggest that claudin-3 phosphorylation by PKA, a kinase frequently ac
70 e blood-testis barrier to biotin, suggesting claudin 3 regulates the movement of small molecules acro
71 stinal tight junction proteins, occludin and claudin-3, showed decreases in the distribution of occlu
72 on in the first extracellular loop domain of claudin-3 to convert Asn(44) to the corresponding amino
73     In normal prostate tissue, expression of claudin-3 was localized exclusively within acinar epithe
74 icated by loss of the tight junction protein claudin-3 was not observed during acute infection despit
75                                              Claudin-3 was reduced in LSI animals with severe intesti
76 e first EL domain or the second EL domain of claudin-3 were able to heterotypically bind to claudin-1
77 ion in the ileum, VE-cadherin, occludin, and claudin-3, Western blot analyses were conducted.
78 n Sertoli cells, regulates the expression of claudin 3, which encodes a transient component of newly
79  caused a loss of the tight junction protein claudin-3, which was ameliorated by genetic ablation of

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