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 ction that requires the PDZ-binding motif of Claudin-2.

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

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

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

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

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

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

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

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

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

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

15 strands and higher order meshworks formed by claudins 2, 7, 15, and 19.

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

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

18 gs indicate that signaling downstream from a Claudin-2/Afadin complex enables the efficient formation

19 Afadin associates with Claudin-2, an interaction that requires the PDZ-binding

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

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

22 Moreover, combining Claudin-2 and Afadin as prognostic markers better predic

23 cer tumors revealed that high levels of both Claudin-2 and Afadin in primary tumors were associated w

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

25 The tight junction proteins claudin-2 and claudin-10a form paracellular cation and a

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

27 We find claudin-2 and claudin-12 form partially redundant, indep

28 CLE had immediate increases in expression of claudin-2 and decreases in occludin.

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

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

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

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

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

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

35 Immunohistochemical analysis of Claudin-2 and/or Afadin expression in 206 metastatic bre

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

37 ith RU having significantly lower Claudin 1, Claudin 2, and E-Cadherin expression than the SI and LI.

38 audin 2, increased binding of caveolin-1 and claudin 2, and increased trafficking of claudin 2 to the

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

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

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

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

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

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

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

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

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

48 e cation pore-forming transmembrane protein, claudin-2, at tight junctions through upregulation of th

49 rier integrity through modulation of the AKT/claudin-2 axis.

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

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

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

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

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

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

56 Further, inhibition of claudin-2 by targeting casein kinase 2 (CK2) also amelio

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

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

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

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

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

62 The tight junctional pore-forming protein claudin-2 (CLDN-2) mediates paracellular Na(+) and water

63 Claudin-2 (CLDN2) expression is upregulated in IBD; howe

64 caused by adenoviral-mediated expression of claudin-2 (Cldn2), a tight junction protein that forms p

65 paired proximal tubular Ca(2+) reabsorption (claudin-2 [CLDN2]-deficient Cldn2(-/-) mice) was equival

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

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

68 rs used transgenic mouse models to show that claudin-2 deficiency attenuated colitis progression as w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 SNP was associated with increased intestinal claudin-2 expression in patients with IBD.

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

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

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

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

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

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

102 Claudin-2 expression was examined by immunohistochemistr

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

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

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

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

107 Mechanistically, IFN-lambda2/3 suppresses Claudin-2 expression, thereby promoting barrier formatio

108 tinal IL-10 expression and downregulated the claudin-2 expression.

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

110 Claudin-2 forms gated paracellular channels and allows s

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

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

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

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

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

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

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

118 On knockout, claudin-10a was replaced by claudin-2 in all proximal tubule segments.

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

120 that interact with the PDZ-binding motif of Claudin-2 in liver metastatic breast cancer cells, inclu

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

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

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

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

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

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

127 Expression of claudin-2 increased from crypt to villus tip (P < .001)

128 nal permeability and increased expression of claudin 2, increased binding of caveolin-1 and claudin 2

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

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

131 y examined the role of Afadin as a potential Claudin-2-interacting partner that promotes breast cance

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

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

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

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

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

137 ow demonstrate that the PDZ-binding motif of Claudin-2 is necessary for anchorage-independent growth

138 The tight junction protein claudin-2 is upregulated in inflammatory bowel disease,

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

140 Moreover, elevated claudin-2 levels and paracellular electrolyte flux in TC

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

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

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

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

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

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

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

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

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

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

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

152 hibits flux across cation channels formed by claudins 2 or 15.

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

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

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

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

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

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

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

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

161 5-AGATAACAAAGGTCA-3 in the Cdx1 site of the Claudin-2 promoter.

162 Claudin-2 promotes breast cancer liver metastasis by ena

163 7 expression at 24 hours; and iv) increased claudin 2 protein at 48 hours.

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

165 b-cellular fractionation localized increased claudin 2 protein to the cytoskeleton.

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

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

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

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

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

171 calcium and magnesium hyper-reabsorption by claudin-2 redistribution.

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

173 act as a shuttle for the internalization of claudin 2 seen in experimental NEC.

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

175 Co-immunoprecipitation of caveolin-1 with claudin 2 suggests that caveolin-1 may act as a shuttle

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

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

178 Cebpd-deficient mice showed upregulation of Claudin-2 that correlated with increased intestinal perm

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

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

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

182 and claudin 2, and increased trafficking of claudin 2 to the cytoskeleton.

183 shikanth et al. examined the contribution of claudin-2 to immune-mediated colitis.

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

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

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

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

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

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

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

191 Gene and protein expression of claudin 2 was increased in experimental NEC.

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

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

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

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