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 for K20 in maintaining keratin filaments in intestinal epithelia.

3 erminants that mediate such changes in model intestinal epithelia.

4 ile enhancing PMN-adhesive interactions with intestinal epithelia.

5 and subsequent recruitment of neutrophils by intestinal epithelia.

6 both the apical and basolateral membranes of intestinal epithelia.

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

8 activates proinflammatory gene expression in intestinal epithelia.

9 ent to drive PMN transmigration across model intestinal epithelia.

10 ability of PMNL to transmigrate across model intestinal epithelia.

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

12 2 and alphaEbeta7 expression and homing into intestinal epithelia.

13 its CCh-stimulated chloride secretion across intestinal epithelia.

14 secretion in physiologically polarized model intestinal epithelia.

15 ndependent 37-kDa nonglycosylated protein on intestinal epithelia.

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

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

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

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

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

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

22 t increases the paracellular permeability of intestinal epithelia.

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

24 iption in hepatocytes and in respiratory and intestinal epithelia.

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

26 gated transcriptional profiles of LT-treated intestinal epithelia.

27 sal and 45.9% (IQR, 19.7-66.6; P < 0.001) in intestinal epithelia.

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

29 mice is most toxic to the high cell turnover intestinal epithelia.

30 tracheal epithelial cells but is absent from intestinal epithelia.

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

32 and fuel the extraordinary tissue renewal of intestinal epithelia.

33 tent, lymphocytes transmigrated across fetal intestinal epithelia.

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

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

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

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

38 about its function and expression in normal intestinal epithelia.

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

40 1 to derive mice deficient for all miRNAs in intestinal epithelia.

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

42 o-2 Transwell cultures as a model system for intestinal epithelia.

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

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

45 ces the regulatory pathways of the mammalian intestinal epithelia.

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

47 major intermediate filament proteins in the intestinal epithelia.

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

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

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

51 l paracellular flux has been demonstrated in intestinal epithelia.

52 -mediated electrogenic chloride secretion in intestinal epithelia.

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

54 estals beneath themselves upon attachment to intestinal epithelia.

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

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

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

58 In small and large intestinal epithelia and adenomas, 14-3-3o expression wa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 n alginate/chitosan MPs delivered protein to intestinal epithelia and reduced clinical and histologic

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

76 ACAMs on extracellular vesicles (EV) shed by intestinal epithelia and that CEACAM-laden EV increase i

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

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

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

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

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

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

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

84 ivates residual channels on the surface when intestinal epithelia are exposed to glucocorticoids at b

85 Intestinal epithelia are in intimate contact with subepi

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

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

88 is the key CaSR activator in mouse and human intestinal epithelia at physiological levels in stool.

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

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

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

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

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

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

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

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

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

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

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

100 ion of sperm flagellar 1, or CLAMP, in human intestinal epithelia cells (IECs).

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

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

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

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

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

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

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

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

109 Intestinal epithelia express two long myosin light-chain

110 The apical membrane of intestinal epithelia expresses intermediate conductance

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

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

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

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

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

116 with MC4R agonists were carried out on human intestinal epithelia, GLP-1 and PYY contents of secretio

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

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

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

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

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

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

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

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

125 e improvement of CFTR function in airway and intestinal epithelia in patients with CF and one or two

126 f ELX/TEZ/IVA on CFTR function in airway and intestinal epithelia in patients with CF and one or two

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

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

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

130 erived organoids and in APC-deficient murine intestinal epithelia in vivo.

131 T) modulates the expression of many genes in intestinal epithelia, including carcinoembryonic cell ad

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

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

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

135 Absorption of dietary phosphate (Pi) across intestinal epithelia is a regulated process mediated by

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

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

138 In contrast to MLCK1, MLCK2 expressed in intestinal epithelia is predominantly associated with ba

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

140 d in the glandular stomach epithelia and not intestinal epithelia like other enteric picornaviruses.

141 elts are basal of the tight junctions as the intestinal epithelia mature.

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

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

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

145 The intestinal epithelia of patients with IBD exhibited incr

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

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

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

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

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

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

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

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

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

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

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

157 and inflammatory tolerance of the mammalian intestinal epithelia specifically.

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

159 proposed as an alternative Cl(-) channel in intestinal epithelia that can compensate for CFTR loss-o

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

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

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

163 In the intestinal epithelia, these bacteria induce secretion of

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

165 EZ/IVA) improves CFTR function in airway and intestinal epithelia to 40-50% of normal in patients wit

166 le range [IQR], 27.5-72.4; P < 0.001) and in intestinal epithelia to 41.8% of normal (IQR, 25.1-57.6;

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

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

169 he well-established role of inflammasomes in intestinal epithelia to highlight principles of epitheli

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

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

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

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

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

175 During development, intestinal epithelia undergo dramatic morphogenesis medi

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

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

178 deling host-pathogen interactions with human intestinal epithelia using enteroid monolayers on permea

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

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

181 a-MSH immunoreactivity in the human intestinal epithelia was predominantly localized to L ce

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

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

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

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

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

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

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

189 molecules (CEACAMs) on the surface of small intestinal epithelia, where they serve as critical bacte

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

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

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