ライフサイエンスコーパス: claudin-2

1 ociated with "leaky" nephron segments (e.g., claudin-2).

2 vated expression of the pore-forming protein claudin-2.

3 by expression of the tight junction protein claudin-2.

4 ion of the epithelial tight junction protein claudin-2.

5 racellular water and Na(+) channel formed by claudin-2.

6 ion injury was more severe in the absence of claudin-2.

7 Rab14 results in increased TER and decreased claudin-2.

8 luding increased TER and decreased levels of claudin-2.

9 s by lysosomal degradation of the TJ protein claudin-2.

10 play size- and charge-selectivity typical of claudin-2.

11 rier through IL-10RA-dependent repression of claudin-2.

12 he transcripts for several other isotypes of claudins-2, -3, -7, -9, -14, and -15 were identified in

13 In MDCK cells (showing cation selectivity), claudins 2, 4, and 7 are powerful effectors of paracellu

14 in the gut are a crypt-to-villus decrease in claudin 2, a highly restricted expression of claudin 4 t

15 pithelium markedly induces the expression of Claudin-2, a cation-channel-forming tight junction prote

16 similar to the typical channel-type claudins claudin-2 and -15.

17 ysis of the interactions between chimeras of claudin-2 and -4 are consistent with the transmembrane d

18 association was found between expression of Claudin-2 and age, gender, grade, stage, or patients' su

19 In tight junctions, both claudin-2 and claudin-10b form paracellular cation-selec

20 ks deciliation-associated down-regulation of claudin-2 and gp135.

21 Starvation reduced the membrane presence of claudin-2 and increased its cytoplasmic, lysosomal local

22 Moreover, IL-22-mediated upregulation of Claudin-2 and loss of TEER can be suppressed with the tr

23 NA expression of the tight junction proteins claudin-2 and occludin.

24 and, LLC-PK1 cells express little endogenous claudin-2 and show anion selectivity.

25 The conductance of wild-type claudin-2 and the other cysteine mutants was only weakly

26 Furthermore, claudins 2 and 4 have reciprocal effects on epithelial b

27 dant expression of Na(+)/Pi cotransporter 2, claudin-2, and aquaporin 1.

28 rmeability in vivo and changes in claudin-1, claudin-2, and myosin IXB genes expression, while no cha

29 eight complex containing at least claudin-1, claudin-2, and occludin; the difference in the protein c

30 d as a negative control expressed claudin-1, claudin-2, and protein gene product 9.5, which are prote

31 his regulation requires occludin, claudin-1, claudin-2, and ZO-1.

32 Paracellular permeabilities conferred by claudin-2 are captured by P-SICM which demonstrates the

33 increase, whereas other claudins, especially claudin-2, are postulated to decrease the overall transc

34 Recent evidence has identified claudin-2 as constituting the cation-reabsorptive pathwa

35 y-associated, "leaky" tight junction protein claudin-2 at intercellular junctions.

36 consistent with the transmembrane domains of claudin-2 being responsible for dimerization, and mutati

37 r the expression and membrane association of claudin-2 but not claudin-1 in T84 cells.

38 nsistent with this, binding of claudin-1 and claudin-2, but not claudin-4, to S408A occludin tail is

39 substantial depletion of the leaky claudin, claudin-2, but not other tight junction components.

40 We aimed to map the pore-lining residues of claudin-2 by comprehensive cysteine-scanning mutagenesis

41 hanced membrane association of claudin-1 and claudin-2 by IL-15 required the presence of the IL-2Rbet

42 It is a VDRE required for the regulation of Claudin-2 by vitamin D.

43 In both cells, claudin-2 channels display conductances of ~90 pS.

44 echnique that detects flux across individual claudin-2 channels within the tight junction of cultured

45 lled, CPE-treated transfectants expressing a Claudin-2 chimera with a substituted ECL-2 from Claudin-

46 The results were unexplained by effects on claudin-2, claudin-3, claudin-19, occludin, and ZO-1, bu

47 Although the abundance of claudin-2 declined to undetectable levels in the ras-ove

48 hermore, the expression of junction protein, claudin-2, decreased.

49 Relative to wild-type, claudin-2-deficient mice experienced severe disease, inc

50 colitis severity and C. rodentium burden in claudin-2-deficient, but not transgenic, mice, demonstra

51 ally, CK2 inhibition reversed IL-13-induced, claudin-2-dependent barrier loss.

52 Removal of claudin-2 depressed the permeation of Na+ and resulted i

53 d cation selectivity compared with wild-type claudin-2 due to a decrease in Na(+) permeability, witho

54 vations are consistent with a model in which claudin-2 encodes a highly cation-permeable channel, whe

55 MDCK I cells lack claudin-2 endogenously, and knockdown of Rab14 in these

56 Knockdown of claudin-2 enhanced the development of TEER in matriptase

57 n and claudins are required for increases in claudin-2 exchange, suggesting assembly of a phosphoryla

58 the natural ECL-2 was replaced by ECL-2 from Claudin-2, exhibited no CPE-induced cytotoxicity.

59 he effects of calcium on the permeability of claudin-2, expressed in an inducible MDCK I cell line.

60 ane fraction immunoblotting); iii) increased claudin 2 expression at 6 hours and decreased claudin 4

61 U0126 treatment also induced claudin-2 expression and decreased TER in a high resista

62 t least in part, by an inability to regulate claudin-2 expression and incorporation into junctions.

63 ase into MDCK strain II cells also inhibited claudin-2 expression and increased TER.

64 increased gut permeability through increased claudin-2 expression and related to local and systemic r

65 treatment of MDCK strain II cells inhibited claudin-2 expression and transiently increased TER.

66 A significant association was found between Claudin-2 expression and VDR and TGR5 expression.

67 Absence of VDR decreased Claudin-2 expression by abolishing VDR/promoter binding.

68 that the colonic microenvironment regulates claudin-2 expression in a manner dependent on signaling

69 Furthermore, genetic silencing of claudin-2 expression in Caco-2, a colon cancer cell line

70 found that vitamin D receptor (VDR) enhanced Claudin-2 expression in colon and that bile salt recepto

71 sally associated with tumor growth as forced claudin-2 expression in colon cancer cells that do not e

72 portantly, we demonstrate that the increased claudin-2 expression in colorectal cancer is causally as

73 We also report similar increases in claudin-2 expression in inflammatory bowel disease-assoc

74 RK 1/2 signaling pathway negatively controls claudin-2 expression in mammalian renal epithelial cells

75 In mice, HNF-1alpha was required for claudin-2 expression in the villus epithelium of the ile

76 In contrast, IL-13-dependent claudin-2 expression increases paracellular cation flux

77 We conclude that Claudin-2 expression is significantly associated with bi

78 on using a total of 309 patient samples that claudin-2 expression is significantly increased in color

79 In addition, claudin-2 expression is specifically decreased in the co

80 inal epithelial permeability by upregulating Claudin-2 expression through the JAK/STAT pathway.

81 Claudin-2 expression was examined by immunohistochemistr

82 uced EGFR activation significantly inhibited claudin-2 expression while simultaneously inducing cellu

83 Knocking down Claudin-2 expression with small interfering RNA reverses

84 he channels are gated, strictly dependent on claudin-2 expression, and display size- and charge-selec

85 chain kinase (MLCK) activation and increased claudin-2 expression, respectively, in cultured intestin

86 herin and claudin-7 expression and decreased claudin-2 expression.

87 Claudin-2 forms gated paracellular channels and allows s

88 We conclude that claudin-2 forms gated paracellular channels and speculat

89 of the tight junction proteins occludin and claudin-2 from intercellular junctions.

90 mplicate Rab14 in specialized trafficking of claudin-2 from the recycling endosome.

91 In conclusion, claudin-2 functions as a paracellular channel to Na+ to

92 The 5'-flanking region of the claudin-2 gene contains binding sites for intestine-spec

93 function of HNF-1alpha in the regulation of claudin-2 gene expression.

94 rrelated with up-regulation of claudin-1 and claudin-2 gene transcription.

95 Here, we examined the expression of Claudin-2 in EAC and precancerous lesions and its associ

96 sed murine models to investigate the role of claudin-2 in maintaining energy efficiency in the kidney

97 is associated with atypical localization of claudin-2 in pancreatic acinar cells.

98 ther, these results uncover a novel role for claudin-2 in promoting colon cancer, potentially via EGF

99 ated with increased intestinal expression of claudin-2 in septic wild-type mice, which was further in

100 n of the pore-forming tight junction protein claudin-2 in STAT6(-/-) mice.

101 pithelial cells led to significant decreased Claudin-2 in VDR(-/-) and VDR(DeltaIEC) mice.

102 y, short hairpin RNA STAT6 knockdown reduced claudin-2 induction and transepithelial resistance decre

103 audin-8 is expressed, it replaces endogenous claudin-2, inserting in its place into existing tight ju

104 In the pancreas, claudin 2 is only detected in junctions of the duct epit

105 Claudin-2 is a structural component of tight junctions i

106 Claudin-2 is a tight junction protein that mediates para

107 Claudin-2 is a unique member of the claudin family of tr

108 The loss of claudin-2 is complemented by inhibition of lysosomal fun

109 Despite loss of the tight junction protein claudin-2, KO mice had preserved functional integrity of

110 erexpression of PKCiota results in increased claudin-2 levels.

111 ssociated BEC barrier function by activating claudin-2-mediated paracellular pore pathways.

112 but not transgenic, mice, demonstrating that claudin-2-mediated protection is the result of enhanced

113 In the proximal tubule (PT) of the kidney, claudin-2 mediates paracellular sodium reabsorption.

114 educed the activated and basal expression of claudin-2 messenger RNA and protein expression.

115 levels of claudin-1 and increased levels of claudin-2 mRNAs.

116 We found that claudin-2-null mice conserve sodium to the same extent a

117 nimals, oxygen consumption in the kidneys of claudin-2-null mice was markedly increased, resulting in

118 at EMT is associated with loss of claudin-1, claudin-2, occludin, and E-cadherin expression within 72

119 ed expression of the tight junction proteins claudin-2, occludin, and ZO-1.

120 f EpCAM with claudin-7 and claudin-1 but not claudin-2 or claudin-4.

121 and aPKC interact to regulate trafficking of claudin-2 out of the lysosome-directed pathway.

122 osomal function, suggesting that Rab14 sorts claudin-2 out of the lysosome-directed pathway.

123 Conversely, transgenic claudin-2 overexpression reduced disease severity.

124 tagenesis and chemical derivatization of the claudin-2 pore.

125 This suggests that claudin-2 pores are multimeric and that Asp(65) lies clo

126 Our data showed that VDR-enhances Claudin-2 promoter activity in a Cdx1 binding site-depen

127 Both Cdx1 and Cdx2 activated the claudin-2 promoter in the human intestinal epithelial ce

128 uced transcriptional activation of the human claudin-2 promoter.

129 5-AGATAACAAAGGTCA-3 in the Cdx1 site of the Claudin-2 promoter.

130 7 expression at 24 hours; and iv) increased claudin 2 protein at 48 hours.

131 Similar results were seen in human NEC, with claudin 2 protein increased.

132 more, treatment of IL-22 in mice upregulates Claudin-2 protein in colonic epithelial cells.

133 tight junction components demonstrates that claudin-2 protein levels are decreased.

134 We find that matriptase enhances the rate of claudin-2 protein turnover, and that this is mediated in

135 active ERK 1/2 levels, induced expression of claudin-2 protein, and decreased TER by approximately 20

136 ssociated with down-regulation of endogenous claudin-2 protein.

137 on in colon cancer cells that do not express claudin-2 resulted in significant increases in cell prol

138 In the liver, claudin 2 shows a lobular gradient increasing from perip

139 olecules and also triggers IL-13 expression, claudin-2 synthesis, and increased paracellular cation f

140 ent evidence suggests potential functions of claudin-2 that are relevant to neoplastic transformation

141 t increases exchange of ZO-1, claudin-1, and claudin-2, thereby causing the mobile fractions of these

142 tibodies were produced against peptides from claudins 2 through 5.

143 nd butyrate represses permeability-promoting claudin-2 tight-junction protein expression through an I

144 adherin and claudin-7 and high expression of claudin-2, to a "tight" epithelium with increased E-cadh

145 racellular loop 2 of a modified, CPE-binding Claudin-2, together with high-resolution native and pore

146 e, suggesting that the effect is specific to claudin-2 trafficking.

147 aracellular pathway of ion permeation across claudin-2-transfected Madin-Darby canine kidney type I c

148 adherin, zonula occluden 1 (ZO-1), occludin, claudin-2, tumor necrosis factor alpha (TNF-alpha), and

149 MDCK I Tet-off cells stably transfected with claudin-2 Tyr(67) mutants.

150 Thus, IL-22-induced claudin-2 upregulation drives diarrhea and pathogen clea

151 he cation-selective, pore-forming TJ protein claudin-2 was observed after cell starvation.

152 the tight junction integral membrane protein claudin-2 was preferentially isolated as a homodimer, wh

153 Notably, the contribution of claudin-2, which has been linked to IL-13, does not medi

154 total conductance and Na(+) permeability of claudin-2, without causing changes in tight junction str