ライフサイエンスコーパス: intestinal epithelia

1 vectorial thiamine transport (e.g. renal and intestinal epithelia).

2 ctively induced the expression of IL-10R1 on intestinal epithelia.

3 and subsequent recruitment of neutrophils by intestinal epithelia.

4 both the apical and basolateral membranes of intestinal epithelia.

5 a-induced IL-8 expression in polarized model intestinal epithelia.

6 activates proinflammatory gene expression in intestinal epithelia.

7 ent to drive PMN transmigration across model intestinal epithelia.

8 ability of PMNL to transmigrate across model intestinal epithelia.

9 tracheal epithelial cells but is absent from intestinal epithelia.

10 IL-8 secretion when added apically to model intestinal epithelia.

11 2 and alphaEbeta7 expression and homing into intestinal epithelia.

12 its CCh-stimulated chloride secretion across intestinal epithelia.

13 secretion in physiologically polarized model intestinal epithelia.

14 ndependent 37-kDa nonglycosylated protein on intestinal epithelia.

15 on, and induction of PEEC secretion in model intestinal epithelia.

16 sion of a panel of inflammatory mediators by intestinal epithelia.

17 mediated chloride (Cl-) secretion (CaMCS) in intestinal epithelia.

18 larized TNF-alpha receptor types I and II on intestinal epithelia.

19 a-receptor expression was observed on native intestinal epithelia.

20 t increases the paracellular permeability of intestinal epithelia.

21 hat PP2Calpha is expressed in airway and T84 intestinal epithelia.

22 iption in hepatocytes and in respiratory and intestinal epithelia.

23 ce expressed on both model and natural human intestinal epithelia.

24 sive pancreatic beta-cells, hepatocytes, and intestinal epithelia.

25 and fuel the extraordinary tissue renewal of intestinal epithelia.

26 tent, lymphocytes transmigrated across fetal intestinal epithelia.

27 were added to the surfaces of fetal oral and intestinal epithelia.

28 cture and remodeling of AJs and TJs in model intestinal epithelia.

29 neration of reactive oxygen species (ROS) in intestinal epithelia.

30 ile enhancing PMN-adhesive interactions with intestinal epithelia.

31 the effects of GSIs in normal and cancerous intestinal epithelia.

32 about its function and expression in normal intestinal epithelia.

33 tributor to total CaCC current in airway and intestinal epithelia.

34 1 to derive mice deficient for all miRNAs in intestinal epithelia.

35 deletion also elevated NF-kappaB activity in intestinal epithelia.

36 ly active MLCK (CA-MLCK) specifically within intestinal epithelia.

37 exchanger 3 (Nhe3) at the apical membrane of intestinal epithelia.

38 ces the regulatory pathways of the mammalian intestinal epithelia.

39 cytes and Caco2-BBE monolayers as a model of intestinal epithelia.

40 major intermediate filament proteins in the intestinal epithelia.

41 ressed in many tissues, including kidney and intestinal epithelia.

42 ake of inorganic phosphate (Pi) in renal and intestinal epithelia.

43 uman T84 epithelial cells were used as model intestinal epithelia.

44 taching and effacing (A/E) histopathology on intestinal epithelia.

45 l paracellular flux has been demonstrated in intestinal epithelia.

46 -mediated electrogenic chloride secretion in intestinal epithelia.

47 tant apical route for Cl(-) secretion across intestinal epithelia.

48 estals beneath themselves upon attachment to intestinal epithelia.

49 for K20 in maintaining keratin filaments in intestinal epithelia.

50 erminants that mediate such changes in model intestinal epithelia.

51 s demonstrate apical localization of Ctr1 in intestinal epithelia across three mammalian species and

52 (TLR5) is the dominant means by which model intestinal epithelia activate proinflammatory gene expre

53 phenotype and composition of the gastric and intestinal epithelia also suggests that epithelial cell-

54 ing nontransformed human cells, normal mouse intestinal epithelia and adenomas, human cancer cell lin

55 Stxs appear to translocate across intestinal epithelia and affect sensitive endothelial ce

56 tegrin are present on the luminal surface of intestinal epithelia and are potentially accessible as r

57 eterminants of barrier function in polarized intestinal epithelia and are regulated by Rho guanosine

58 ed glycoproteins are present in normal human intestinal epithelia and could play a role in cholera.

59 eletion of the NF-kappaB RelA gene in murine intestinal epithelia and determine its function in homeo

60 Caco-2 cells as a model of human intestinal epithelia and EPEC-infected C57BL/6J mouse mo

61 ally delayed tumor appearance in Apc-mutated intestinal epithelia and greatly prolonged mice survival

62 ndance of the CCK-2 receptor was assessed in intestinal epithelia and IEC-6 intestinal epithelial cel

63 that cell-free HIV traversed fetal oral and intestinal epithelia and infected HIV-susceptible CD4(+)

64 is expressed in the basolateral membrane of intestinal epithelia and is associated with beta1 integr

65 (MCT-1) is apically polarized in model human intestinal epithelia and is involved in butyrate uptake

66 CXCR3 is expressed in mouse and human intestinal epithelia and lamina propria.

67 M-C is abundantly expressed basolaterally in intestinal epithelia and localizes to desmosomes but not

68 egulating basolateral cargo transport in the intestinal epithelia and postsynaptic cargo transport in

69 cells of the V(delta)1 subset predominate in intestinal epithelia and respond to MICA and MICB (MHC c

70 trate the activation of NF-kappaB by IL-6 in intestinal epithelia and the down-regulation of NF-kappa

71 s of VDR ablation on NF-kappaB activation in intestinal epithelia and the role of enteric bacteria on

72 if LIGHT is capable of signaling directly to intestinal epithelia and to define the mechanisms and co

73 es in the development or function of KPT and intestinal epithelia and to gain insight into the functi

74 ponent in wound healing and proliferation in intestinal epithelia and when acetylated by acetylsalicy

75 t determinant of damage-induced apoptosis in intestinal epithelia, and unlike bcl-2, which regulates

76 There was variable hyperplasia of intestinal epithelia, and urothelium of the urinary blad

77 Intestinal epithelia are in intimate contact with subepi

78 of IELs is induced by close interaction with intestinal epithelia as a consequence of homing.

79 tic regulation of cell death and division in intestinal epithelia, as well as for protection from dev

80 s reported here revealed that, as in natural intestinal epithelia, beta1 integrin was strictly polari

81 g pathway is required for maintenance of the intestinal epithelia; blocking this pathway reduces the

82 iation was very similar in the chloragog and intestinal epithelia but differed subtly in the kidneyli

83 als that Salmonella typhimurium activates in intestinal epithelia, but likely led to attenuation of s

84 an intracellular [Ca(2+)] increase in model intestinal epithelia, but not with their ability to inva

85 are involved in the infection of biliary and intestinal epithelia by C. parvum.

86 d4-2 may regulate TRPV6 protein abundance in intestinal epithelia by controlling TRPV6 ubiquitination

87 in dose- and time-dependent manner in model intestinal epithelia (Caco-2 BBE cell monolayers), 2) th

88 dient across apical plasma membrane in model intestinal epithelia (Caco2-BBE monolayers).

89 In contrast to the fetal oral/intestinal epithelia, cell-free HIV transmigration throu

90 t shock proteins (hsps) confer protection to intestinal epithelia cells (IECs), we studied whether SC

91 s results from sequential genetic changes in intestinal epithelia commencing with inactivation of the

92 t these mutants exhibit reduced adherence to intestinal epithelia compared with isogenic wild-type st

93 In addition to MHC class I and II antigens, intestinal epithelia constitutively express the nonclass

94 In response to luminal leptin, model intestinal epithelia critically activate the NF-kappaB,

95 wever, the effect of interferon-gamma on the intestinal epithelia di-tripeptide hPepT1 transporter ha

96 nt of actin (but not tubulin) in biliary and intestinal epithelia directly adjacent to C. parvum.

97 feb (DeltaIEC) mice exhibited grossly normal intestinal epithelia, except for a defect in Paneth cell

98 These data indicate that human intestinal epithelia express CD73, which is apically pol

99 The apical membrane of intestinal epithelia expresses intermediate conductance

100 ce of the CCK-2 receptor was demonstrated in intestinal epithelia following 14 Gy gamma-radiation by

101 Hypergastrinemia increases regeneration of intestinal epithelia following diverse forms of injury.

102 of growth factors affect the regeneration of intestinal epithelia following injury, but the effects o

103 ntestinal trefoil factor (ITF/TFF3) protects intestinal epithelia from a range of insults and contrib

104 tein were not significantly altered in small intestinal epithelia from Apc(mNLS/mNLS) mice.

105 To determine the function of guanylin in intestinal epithelia, guanylin null mice were generated

106 as a physiological regulator of apoptosis in intestinal epithelia has been investigated.

107 nt phosphatase inhibitor, but its effects on intestinal epithelia have not been examined.

108 of cell-associated virus into fetal oral and intestinal epithelia, HIV-infected macrophages and lymph

109 dicate that in this in vitro model system of intestinal epithelia, human sIgA and IgG contribute to t

110 We show that IL-6 receptors are present in intestinal epithelia in a polarized fashion.

111 Lastly, examination of inflamed intestinal epithelia in human biopsies revealed up-regul

112 ical in protecting against primary tumors of intestinal epithelia in mice.

113 m as applied to neutrophils migrating across intestinal epithelia in response to a chemoattractant.

114 a role of KLF5 in promoting proliferation of intestinal epithelia in response to LPA.

115 hain fatty acids supplemented to model human intestinal epithelia in vitro and human tissue ex vivo r

116 olarized distribution of the NKCC protein on intestinal epithelia, indicate that NKCC may be associat

117 is study suggests that STEC interaction with intestinal epithelia induces neutrophil recruitment to t

118 These secretagogues are released from the intestinal epithelia into the intestinal lumen and syste

119 ce of pathogenic Escherichia coli strains to intestinal epithelia is essential for infection.

120 he regulation and function of keratin in the intestinal epithelia is largely unknown.

121 When tumors form in intestinal epithelia, it is important to know whether th

122 e the primary route by which MNV crosses the intestinal epithelia of BALB/c mice.

123 like the intestine of normal subjects, small-intestinal epithelia of cystic fibrosis patients and cys

124 LPS mutants have differential effects on the intestinal epithelia of orally inoculated catfish.

125 ation, was increased and mislocalized in the intestinal epithelia of the beta1 integrin-deleted mice

126 stimulation of Salmonella uptake across the intestinal epithelia of the infected host.

127 model expressing a truncated form of OVA in intestinal epithelia of the terminal ileum and colon.

128 GE'), was investigated in the pancreatic and intestinal epithelia of transgenic mice.

129 t neutrophil migration across model T84 cell intestinal epithelia produced transient separation of ep

130 hat mediates paracellular water transport in intestinal epithelia, rendering them "leaky".

131 Salt and water secretion from intestinal epithelia requires enhancement of anion perme

132 Conditional inactivation of Pnn within intestinal epithelia resulted in significant downregulat

133 induces profound transcriptional changes in intestinal epithelia resulting in the recruitment of neu

134 sured at the brush-border membrane of intact intestinal epithelia results from a close functional rel

135 ng of intraepithelial lymphocytes (IEL) into intestinal epithelia seems to be guided by signals from

136 and inflammatory tolerance of the mammalian intestinal epithelia specifically.

137 This effect was significantly reversed in intestinal epithelia stably expressing anti-sense to hsp

138 these adhesins have not been demonstrated in intestinal epithelia, the colonic microflora includes st

139 y unappreciated 6-keto-PGF1alpha receptor on intestinal epithelia, the ligation of which results in a

140 affect global cAMP-mediated responses in the intestinal epithelia, thereby decreasing secretory respo

141 In the intestinal epithelia, these bacteria induce secretion of

142 ed exclusively on the basolateral surface of intestinal epithelia, thus providing a molecular basis f

143 ignaling regulates the susceptibility of the intestinal epithelia to damage caused by C. rodentium.

144 asolateral, but not apical, surface of model intestinal epithelia to elicit IL-8 secretion.

145 l studies revealed that exposure of cultured intestinal epithelia to hypoxia (pO(2), 20 torr; 24-48 h

146 Thus, we hypothesized that exposure of intestinal epithelia to hypoxia may modulate PMN-epithel

147 Cells in intestinal epithelia turn over rapidly due to damage fro

148 horylates and inactivates CFTR in airway and intestinal epithelia, two major sites of disease, is not

149 iously showed that aPKC is down-regulated in intestinal epithelia under inflammatory stimulation.

150 reduced C. parvum attachment to biliary and intestinal epithelia up to 70%.

151 Many of the studies of small intestinal epithelia use as models T84 cells.

152 and bacterial infection inactivate Foxo3a in intestinal epithelia via the PI3K pathway and inactivate

153 expression on apoptotic cell death in mouse intestinal epithelia was assessed using homozygously nul

154 n across adult oral and neonatal/infant oral/intestinal epithelia, we established ex vivo organ tissu

155 t shock proteins (hsp) are cytoprotective in intestinal epithelia, we hypothesized that IL-11-conferr

156 rstand the regulation of the A2b receptor in intestinal epithelia, we studied the effects of interfer

157 In newborn mutants lacking GSLs at day P0, intestinal epithelia were indistinguishable from those i

158 Morphologically normal areas of intestinal epithelia were uniformly negative for cyclin

159 iking pattern was observed in esophageal and intestinal epithelia, where expression was limited to th

160 ly expressed in mammalian tissues, including intestinal epithelia, where they facilitate fluid secret

161 ms of GH inhibition of chloride secretion in intestinal epithelia, which may be relevant to therapeut

162 occludin in these processes, we established intestinal epithelia with stable occludin knockdown.

163 ), potently induced gene remodeling in model intestinal epithelia with the specific pattern of expres