ライフサイエンスコーパス: enterocyte

1 axis and buffers Cu levels in the cytosol of enterocytes.

2 mulation of intracellular vesicles in villus enterocytes.

3 impaired viability and maturation of villus enterocytes.

4 leading to the buildup of bile acids within enterocytes.

5 cell cycle programs of adult stem cells and enterocytes.

6 ribution, trafficking, and turnover in human enterocytes.

7 ved in membrane fusion of apical vesicles in enterocytes.

8 owed by the uptake of hydrolyzed products by enterocytes.

9 positive regulator of FXR expression in the enterocytes.

10 Insig proteins in the sterol homeostasis of enterocytes.

11 tion of microvillar assembly and polarity in enterocytes.

12 vities of SREBP-2 or HMGR in Insig-deficient enterocytes.

13 FGF15/19 levels in mouse intestine and human enterocytes.

14 ay a key role in the elimination of infected enterocytes.

15 ults in massive triglyceride accumulation in enterocytes.

16 emonstrated that TTC7A is expressed in human enterocytes.

17 promoter in IEC-6 cells and in rat duodenal enterocytes.

18 e progenitor cells differentiate into midgut enterocytes.

19 that differentiate as midgut versus hindgut enterocytes.

20 li (MV) from the surface of small intestinal enterocytes.

21 (mOct1) in Caco-2 cells, and human and mouse enterocytes.

22 of bacterial binding to porcine gut villous enterocytes.

23 ated that OCT1 is basolaterally localized in enterocytes.

24 nal stem cells, epithelial cells, and mature enterocytes.

25 nnate immune response to gliadin peptides in enterocytes.

26 sms whereby Shiga toxin interacts with human enterocytes.

27 ytes, specific hypothalamic neurons, and gut enterocytes.

28 septate junctions, on the apical side of the enterocytes.

29 lateral (BL) localization in human and mouse enterocytes.

30 rter NPC1l1 to block cholesterol uptake into enterocytes.

31 pothesis that S Typhi preferentially targets enterocytes.

32 zebrafish model and in cultured human Caco-2 enterocytes.

33 gns with transcriptional variation of Lct in enterocytes.

34 infecting bacteria on the apical surface of enterocytes.

35 midgut morphology with dramatically enlarged enterocytes.

36 LUT1 appeared at the basolateral membrane of enterocytes.

37 ma TG excursion and accumulated lipid in the enterocytes.

38 (II) absorption through the DMT1 channels of enterocytes.

39 echanistic studies were performed in primary enterocytes.

40 The mean number of IELs per 100 enterocytes (95% CI) in specimens was 14.7 (11.8-17.6) i

41 ll (Caco-2; TC-7) and large (T84) intestinal enterocytes a polarization-dependent mechanism that can

42 e posteriorly and differentiate into hindgut enterocytes, a group of the progenitor cells, unexpected

43 ification of digested triacylglycerol in the enterocytes, a process catalyzed by acyl-CoA:monoacylgly

44 te another virulence-associated event (intra-enterocyte accumulation).

45 ), stimulated proliferation and migration of enterocytes adjacent to the colonic wounds in a process

46 cellular level, LDs failed to form in iF2KO enterocytes after acute oil challenge and instead accumu

47 umin simultaneously in biliary epithelia and enterocytes after transfer of OT-I T cells.

48 fluid-ion homeostasis and differentiation of enterocytes along the crypt-villus axis.

49 he mouse lactase gene (Lct), which occurs in enterocytes along the proximal-to-distal axis of the sma

50 ibute to the transport of folates across the enterocyte, along with the contribution of the enterohep

51 ty acids).alpha-Retinol is esterified in the enterocyte and transported in the blood analogous to ret

52 wo BMP ligands, Dpp and Gbb, are produced by enterocytes and act in conjunction to promote ISC self-r

53 Marked clones consist entirely of enterocytes and are all lost from villus tips within day

54 E) pathogens adhere intimately to intestinal enterocytes and efface brush border microvilli.

55 cellular signaling governs processes in both enterocytes and endothelial cells.

56 tent intestinal stem cells that generate new enterocytes and enteroendocrine cells in response to tis

57 HRVs infect differentiated enterocytes and enteroendocrine cells, and viroplasms an

58 red for efficient access to small intestinal enterocytes and for the optimal delivery of heat-labile

59 ciated protein, which accumulates in colonic enterocytes and goblet cells.

60 pes that comprise the intestinal epithelium (enterocytes and goblet, enteroendocrine, and Paneth cell

61 that modulates fatty acid (FA) metabolism in enterocytes and hepatocytes, also modulates HSC FA utili

62 ith rapamycin, DCLK1 and IL-25 expression in enterocytes and IL-13 expression in mesenchyme were dimi

63 the mucosa (including enteroendocrine cells, enterocytes and immune cells) and the microbiome interac

64 an enteric pathogen which attaches itself to enterocytes and induces attachment and effacing (A/E) le

65 ession was detected in developing intestinal enterocytes and liver hepatocytes.

66 cid were identified as metabolites formed in enterocytes and released at the serosal side of the mode

67 We report that mTOR supports absorptive enterocytes and secretory Paneth and goblet cell functio

68 the Arp2/3 complex in vesicle trafficking in enterocytes and suggest that defects in cytoplasmic F-ac

69 nstrated that the mutations cause defects in enterocytes and T cells that lead to severe apoptotic en

70 w hypothesize that TLR4 induces autophagy in enterocytes and that TLR4-induced autophagy plays a crit

71 hether glucose modulates apelin secretion by enterocytes and the effects of apelin on intestinal gluc

72 e of polarized epithelia, such as intestinal enterocytes and tubule and duct epithelia.

73 ncrease in the abundance of Paneth cells and enterocytes, and broad activation of an antimicrobial pr

74 ong lipopolysaccharide, was unable to invade enterocytes, and demonstrated decreased ability to infec

75 erovars can adhere to and invade M cells and enterocytes, and it has been assumed that S Typhi also p

76 lles or methyl-beta-cyclodextrin in cultured enterocytes, and it is required for HDL activation of en

77 namely via ferroportin-dependent efflux from enterocytes, and thus offers potential as a novel oral i

78 ed immunodeficiency include abnormalities of enterocyte apicobasal polarity, increased apoptosis of i

79 arises through a coupling mechanism in which enterocyte apoptosis breaks feedback inhibition of stem

80 reduced GvHD-related mortality, IL-6 levels, enterocyte apoptosis, and histopathology scores.

81 paired enterocyte tight junctions, increased enterocyte apoptosis, and reduced enterocyte proliferati

82 increased endoplasmic reticulum (ER) stress, enterocyte apoptosis, and the release of circulating HMG

83 Within the gut, Salmonella-infected enterocytes are expelled into the lumen, limiting pathog

84 hed, but processes regulating LD dynamics in enterocytes are poorly understood.

85 to-blood group antigens (HBGAs) expressed on enterocytes are proposed receptors for rotaviruses and c

86 Enterocytes are specialized to absorb nutrients from the

87 Enterocytes are the only cell type that must balance the

88 and in vivo-polarised absorptive epithelia (enterocytes) are considered to be non-phagocytic towards

89 the ratio of intraepithelial lymphocytes to enterocytes, as well as changes in the microbiota, can b

90 a19/Delta19)Apoe(-/-) mice was high and that enterocytes assembled and secreted more chylomicrons.

91 cholesterol levels associated with increased enterocyte ATP-binding cassette transporter A1 (Abca1) e

92 ouse and human was associated with increased enterocyte autophagy.

93 red intestinal epithelial cells and in mouse enterocytes blocked AIEC-induced inhibition of ATG5 and

94 In the enterocyte brush border, protocadherin function requires

95 sphingolipid S1P and is highly expressed in enterocytes but downregulated in colon cancer.

96 is localized in the apical (AP) membrane of enterocytes, but the literature is ambiguous about OCT1

97 across the apical membrane of the intestinal enterocyte by divalent metal-ion transporter 1 (DMT1) an

98 R) 30C and MIR130A in T84 cells and in mouse enterocytes by activating nuclear factor-kappaB.

99 es ISC self-renewal and differentiation into enterocytes by elaborating Notch signaling, and ISC comm

100 e apelin regulates carbohydrate flux through enterocytes by promoting AMPKalpha2 phosphorylation and

101 ctivity drives progenitors toward absorptive enterocytes by repressing secretory differentiation prog

102 forced coating, while transiting through the enterocytes by surface adsorption of apoproteins and pho

103 Treatment of human enterocytes (CaCo-2 cells) with recombinant human PCSK9

104 ons were analysed using MTT assay on the gut enterocyte cell line Caco-2 and they showed no toxicity

105 In Caco-2/TC7 enterocytes, ceramide effects on insulin-dependent AKT p

106 Enterocyte Cl(-) channels represent an attractive class

107 e profile and an increased ability to infect enterocytes compared with the wild type, but it had no i

108 hway components, Tnks activity in absorptive enterocytes controls the proliferation of neighboring IS

109 te using experimental mouse models and human enterocyte cultures the potential utility of (R)-BPO-27

110 was positively associated with biomarkers of enterocyte damage and microbial translocation.

111 nal cells in situ prior to any indication of enterocyte damage and that ricin rapidly reaches the kid

112 In critically ill patients, enterocyte damage is frequent, and it is significantly a

113 al fatty acid-binding protein is a marker of enterocyte damage, and plasma citrulline concentration i

114 Moreover, hyperactive immunity and increased enterocyte death resulted in the highest bacterial load

115 s required for the differentiation of midgut enterocytes derived from hindgut progenitors.

116 tion was a permanent state and dominant over enterocyte differentiation in plasticity experiments.

117 is involved in the regulation of intestinal enterocyte differentiation.

118 ration and a dramatic increase in markers of enterocyte differentiation.

119 epithelial absorption of these molecules via enterocytes, diffusive distribution over the lamina prop

120 Gpat3(-/-) enterocytes displayed a compensatory increase in the syn

121 erior midgut, both terminally differentiated enterocyte (EC) and enteroendocrine (EE) cells are gener

122 ells causes their rapid differentiation into enterocytes (EC) or entero-endocrine cells (EE).

123 ophila intestinal stem cells (ISCs) generate enterocytes (ECs) and enteroendocrine (ee) cells.

124 stem cells to produce enteroblasts (EBs) and enterocytes (ECs) that regenerate the gut.

125 epithelial sodium channel (ENaC) subunits in enterocytes (ECs) to maintain osmotic and ISC homeostasi

126 , that coregulate expression of the locus of enterocyte effacement (LEE) genes in a metabolite-depend

127 haracterized by the presence of the locus of enterocyte effacement (LEE) genomic island, which encode

128 so contributes to expression of the locus of enterocyte effacement (LEE) in an EA-dependent manner.

129 A subset of STEC strains carry the Locus of Enterocyte Effacement (LEE) pathogenicity island (PAI),

130 ty island 1 (SPI-1), SPI-2, and the locus of enterocyte effacement (LEE) T3SSs.

131 EHEC includes the genes within the locus of enterocyte effacement (LEE) that are largely organized i

132 of virulence factors encoded by the locus of enterocyte effacement (LEE), as well as Shiga toxin.

133 III secretion system encoded in the locus of enterocyte effacement (LEE), but lack the virulence fact

134 opathogenic Escherichia coli (EPEC) locus of enterocyte effacement (LEE)-encoded effectors EspF and M

135 III secretion system encoded by the locus of enterocyte effacement (LEE).

136 mal pathogenicity island called the locus of enterocyte effacement (LEE).

137 e III secretion system borne on the locus of enterocyte effacement pathogenicity island.

138 that the highly conserved non-LEE (locus of enterocyte effacement)-encoded effector F (NleF) shows b

139 by definition all strains carry the locus of enterocyte effacement, the effector repertoires of diffe

140 The locus of enterocyte effacement-encoded regulator (Ler) of enterop

141 -neuronal cell types in the gut wall such as enterocytes, enteroendocrine and immune cells and are th

142 n handling of four main cell types: duodenal enterocytes, erythrocyte precursors, macrophages, and he

143 The enterocyte expresses two fatty acid-binding proteins (FA

144 ake an initial choice between a secretory or enterocyte fate.

145 ed a fractionation method to separate mature enterocytes from crypt cells and analyzed gene expressio

146 s mitochondrial respiration while protecting enterocytes from ROS-driven macromolecule damage and con

147 However, enterocyte function depends not only on the number of ce

148 rishing microbiota to restore IL-22-mediated enterocyte function.

149 e-expression of constitutively active FXR in enterocytes (FXR(-/-)iVP16FXR) and corresponding control

150 anscription factors GATA4 and GATA6 regulate enterocyte gene expression and control regional epitheli

151 CDX1 activates the expression of enterocyte genes, but it is not clear how the concomitan

152 o direct lineage differentiation into mature enterocytes, goblet cells and Paneth cells.

153 reduced, changes in expression of markers of enterocytes, goblet cells, and proliferative cells were

154 by differentiated intestinal cell lineages (enterocytes, goblet cells, Paneth cells, tuft cells and

155 We found that in the absence of ArpC3, enterocytes had defects in the organization of the endol

156 Here we address how polarized enterocytes harboring actin-rich apical microvilli under

157 l bacterial adherence and internalization in enterocytes have been documented in Crohn disease, celia

158 acquisition, homeostasis, and hematopoiesis (enterocytes, hepatocytes, macrophages, hematopoietic cel

159 th factor and epidermal growth factors cause enterocyte hypertrophy and hyperplasia, allowing greater

160 cterized by a preserved iron transfer in the enterocytes (i.e., cells with low iron turnover) and iro

161 als are only capable of transforming ISC and enterocyte identity during a defined window of metamorph

162 OVA mice with mice that express ovalbumin in enterocytes (iFABP-OVA mice).

163 h celiac disease had a median of 50 IELs/100 enterocytes in D1 and a median of 48 IELs/100 enterocyte

164 particular, act as growth factors for crypt enterocytes in patients with celiac disease (CD).

165 ween Caco-2 cells and in vivo differentiated enterocytes in relation to MV effacement.

166 nger oleoylethanolamide (OEA) is released by enterocytes in response to fat intake and indirectly sig

167 ful cultivation of multiple HuNoV strains in enterocytes in stem cell-derived, nontransformed human i

168 Increased proliferation of crypt enterocytes in the intestine of CD patients is mediated

169 In contrast to MNV, reovirus infects enterocytes in the intestine.

170 bundantly expressed in the apical surface of enterocytes in the small intestine.

171 r (ASBT; also known as SLC10A2) expressed on enterocytes in the terminal ileum.

172 ve imaging technologies, we demonstrate that enterocytes in vitro and in vivo rapidly depolarize thei

173 late macropinocytosis and deliver toxin into enterocytes in vitro and in vivo; intact bacteria are no

174 ggest that S Typhi may preferentially target enterocytes in vivo.

175 The effect of NLRC3 is most dominant in enterocytes, in which it suppresses activation of the mT

176 cretory cells converted them into functional enterocytes, indicating prolonged responsiveness of mark

177 alimentary lipid micelles to polarized human enterocytes induces an immediate autophagic response, ac

178 Healthy enterocytes inhibit stem cell division through E-cadheri

179 utilized by Fpn-KO mice and was retained in enterocytes, irrespective of the iron source.

180 The intestinal enterocyte is a key regulatory point for copper absorpti

181 We find that BMP production in enterocytes is inhibited by BMP signaling itself, and th

182 arrangement necessary for EHEC attachment to enterocytes is mediated by the type 3 secretion system w

183 Here, Btnl1 expressed by murine enterocytes is shown to shape the local TCR-Vgamma7(+) g

184 Examination of enterocytes isolated from infected mice revealed that a

185 Consistently, enterocytes isolated from mice infected with C. rodentiu

186 din reduces iron efflux from the basolateral enterocyte, it is uncertain whether luminal enhancers of

187 he brush border membrane of small intestinal enterocytes, it is unclear whether function of SGLT1 is

188 osus treatment also increased microvilli and enterocyte lengths and decreased lipid droplet size in t

189 d in lipid and lipoprotein metabolism at the enterocyte level.

190 ith very long villi resulting from increased enterocyte lifespan and also demonstrate greater tumor s

191 n CN3718 uses NanI sialidase for adhering to enterocyte-like Caco-2 cells.

192 that Caco-2 cells (a naturally CPE-sensitive enterocyte-like cell line) can be protected from CPE-ind

193 rtant for the adherence of C. perfringens to enterocyte-like cells, NanI sialidase is now emerging as

194 independent ploidy reduction of cells in the enterocyte lineage through a process known as amitosis.

195 ne fail to thrive during weaning and exhibit enterocyte lipid accumulation and reduced plasma TGs.

196 ses the conductance of Cl(-) channels at the enterocyte luminal membrane, which include the cystic fi

197 Unlike common enterocytes, M cells lack an organized apical brush bord

198 Glutamine is a fundamental fuel for enterocytes, maintaining intestinal mucosal health.

199 that the recycling endosomal compartment in enterocytes maintains a homeostatic TLR9 intracellular d

200 knockdown cells had increased expression of enterocyte markers, decreased expression of cycling gene

201 line concentration is a marker of functional enterocyte mass.

202 Epigenetic divergence within enterocytes may contribute to the functional specializat

203 er accumulation and/or redistribution within enterocytes may influence iron transport, and high hepat

204 Moreover, these findings suggest that enterocytes may regulate whole-body metabolism, and that

205 is cytoprotective effect was associated with enterocyte-mediated phosphoinositide 3-kinase (PI3K)/gly

206 permeability was mediated by an increase in enterocyte membrane TLR-4 expression and a TLR-4-depende

207 CD36 is abundant on apical enterocyte membranes in the proximal small intestine, wh

208 ains the intestinal homeostasis by enhancing enterocyte migration and attenuating inflammation.

209 characterized by TLR4-mediated inhibition of enterocyte migration and reduced mucosal healing.

210 lved, TLR4-induced autophagy led to impaired enterocyte migration both in vitro and in vivo, which in

211 at the negative consequences of autophagy on enterocyte migration play an essential role in its devel

212 LPS represses MFG-E8 expression and disrupts enterocyte migration via a miR-99b dependent mechanism.

213 ation of intestinal MFG-E8 and impairment of enterocyte migration.

214 umulation of triglyceride-filled vesicles in enterocytes, mislocalization of apolipoprotein B, and lo

215 19 expression was induced in polarized human enterocyte-models and mouse organoids by basolateral inc

216 In enterocytes of AEG-1KO mice, we observed increased activ

217 amage can result in massive telomere loss in enterocytes of aGVHD patients.

218 uction of SGLT1-mediated glucose uptake into enterocytes of duodenum and jejunum (P < 0.001).

219 eal, we observe morphological changes in the enterocytes of larval zebrafish, including elongation of

220 In this study, we demonstrate that enterocytes of patients with refractory intestinal aGVHD

221 Restoring PGRP-SC2 expression in enterocytes of the intestinal epithelium, in turn, preve

222 The epithelial enterocytes of the intestine are responsible for absorbi

223 Enterocytes of the small intestine accumulate mannose-co

224 etary triglycerides (TG) are absorbed by the enterocytes of the small intestine after luminal hydroly

225 required for dietary fat absorption into the enterocytes of the small intestine.

226 PPAR-alpha activation in the enterocyte on HDL and chylomicron formation.

227 nterocytes in D1 and a median of 48 IELs/100 enterocytes (P = .7) in D2.

228 In cultured human and murine hepatocytes and enterocytes, pharmacological activation of AMPK inhibite

229 polyunsaturated phosphatidylcholines in the enterocyte plasma membrane and reduced Niemann-Pick C1-l

230 r 1 (ATP8B1) enables Cdc42 clustering during enterocyte polarization.

231 ribbons," indicative of dedifferentiation of enterocyte precursors into Lgr5(+) stems.

232 e that the highly proliferative, short-lived enterocyte precursors serve as a large reservoir of pote

233 tem cells, but it is unknown if the abundant enterocyte progenitors that express the Alkaline phospha

234 The effects of gliadin on crypt enterocyte proliferation and activation of innate immuni

235 n tissues from these mice also had increased enterocyte proliferation and transcription factor nuclea

236 large T-antigen solely in villi had ectopic enterocyte proliferation with increased villus apoptosis

237 ta loads, interleukin-22 (IL-22) production, enterocyte proliferation, and antimicrobial gene express

238 cimates gut microbiota, resulting in loss of enterocyte proliferation, leading to microbiota encroach

239 increased enterocyte apoptosis, and reduced enterocyte proliferation, leading to NEC.

240 y partially reversing the effects of TcdB on enterocyte proliferation, migration, and apoptosis, ther

241 Individual apoptotic enterocytes promote divisions by loss of E-cadherin, whi

242 ation and apoptosis in transgenic mice whose enterocytes re-enter the cell cycle.

243 in the gut, involving cytoplasm ejection and enterocyte regrowth.

244 sease (MVID) is a congenital disorder of the enterocyte related to mutations in the MYO5B gene, leadi

245 tin to ensure microvillus depolarization and enterocyte remodeling upon injury.

246 both in vitro and in vivo, which in cultured enterocytes required the induction of RhoA-mediated stre

247 Our previous studies demonstrated that enterocytes respond to the pharmacological blockade of c

248 Deficiency of both Insigs in enterocytes resulted in constitutive activation of SREBP

249 insulin signaling and lipid accumulation in enterocytes, resulting in host lethality.

250 eration of Apc-deficient (but not wild-type) enterocytes, revealing an unexpected opportunity for the

251 In enterocytes, scavenger receptor class B, type 1 (SR-B1,

252 for de novo lipogenesis (DNL) and stimulates enterocyte secretion of apoB48.

253 Enterocytes sense highly elevated levels of (conjugated)

254 reatment, we found that Lpcat3 deficiency in enterocytes significantly reduced polyunsaturated phosph

255 on and morphogenesis, the protective role of enterocyte sloughing in enteric ischemia-reperfusion and

256 found to promote energy homeostasis via gut enterocyte sNPF receptors, which appear to maintain gut

257 In summary, our study reveals that enterocyte specific Raptor is required for initiating a

258 ntial of the TC-7 model for defining dynamic enterocyte-specific changes during infection.

259 Enterocyte-specific NF-kB has a beneficial role in sepsi

260 of this study was to investigate the role of enterocyte-specific NF-kB in sepsis through selective ab

261 t P9, E. coli K1 bacteria gain access to the enterocyte surface in the mid-region of the small intest

262 ier in vitro accelerates toxin access to the enterocyte surface.

263 creted protein EspZ is postulated to promote enterocyte survival by regulating the T3SS and/or by mod

264 nd promotes the proliferation of tumorigenic enterocytes that just lost expression of the APC tumor s

265 al cells from diverse tissues, including the enterocytes that line the intestinal tract, remodel thei

266 Enterocytes, the intestinal absorptive cells, have to de

267 ctococcus lactis enhanced adherence to human enterocytes through extracellular matrix protein and bac

268 latter indicates an impact on clearance into enterocytes through SERT.

269 ed NEC in mice, while IL-17 release impaired enterocyte tight junctions, increased enterocyte apoptos

270 igand for PXR in vivo, and IPA downregulated enterocyte TNF-alpha while it upregulated junctional pro

271 ed as a reductionistic model of the immature enterocyte to investigate mechanism.

272 initial physiological response of intestinal enterocytes to dietary lipid.

273 response of palmitic acid-treated Caco-2/TC7 enterocytes to insulin.

274 ATP7B buffers Cu levels in enterocytes to maintain a range necessary for formation

275 element-binding protein (SREBP) activity in enterocytes to support increased lipid metabolism.

276 within transformed colonic epithelial cells (enterocytes) to promote early tumor development.

277 Induction of rhomboid in the dying enterocyte triggers activation of the EGF receptor (Egfr

278 soluble gp130, tumor necrosis factor [TNF]), enterocyte turnover (intestinal fatty acid binding prote

279 inal fatty acid binding protein, a marker of enterocyte turnover and other inflammatory biomarkers, i

280 nd local tissue inflammation, have preserved enterocyte turnover and T-helper type 17 cells with mini

281 ry biomarkers, but the acute-phase response, enterocyte turnover, monocyte activation, and fibrosis b

282 may regulate whole-body metabolism, and that enterocyte urate metabolism could potentially be targete

283 onset metabolic syndrome in mice lacking the enterocyte urate transporter Glut9 (encoded by the SLC2A

284 Glut9-deficient mice develop impaired enterocyte uric acid transport kinetics, hyperuricaemia,

285 ntrol differentiation of stem-like cells and enterocytes via the homeobox gene CDX1.

286 . cloacae colonized pigs, HuNoV infection of enterocytes was confirmed, however infection of B cells

287 Expression of PMCA1b in enterocytes was decreased in 4.1(-/-) mice.

288 te cholesterol transport by polarised Caco-2 enterocytes was demonstrated.

289 By single-cell analysis of dedifferentiating enterocytes, we observed the generation of Paneth-like c

290 For studies using organoids, primary enterocytes were isolated from the intestine and transfe

291 Enterocytes were lost, and goblet cells were increased.

292 intestinal epithelial T84 cells and in mouse enterocytes were measured using quantitative reverse-tra

293 r, when mouse intestine and human Caco-2/TC7 enterocytes were treated with the saturated fatty acid,

294 1R is located on the basolateral membrane of enterocytes, where it co-localizes with PMCA1b (plasma m

295 transcription of the Slc6a19 gene in villus enterocytes, whereas high levels of SOX9 repress express

296 nstrate that only a subpopulation of colonic enterocytes which are characterized by apical dislocatio

297 s in the crypt and differentiate into mature enterocytes while moving along the crypt-villus axis.

298 MPA-MG was subsequently re-esterified in the enterocyte with oleic acid (most likely originating from

299 characterized by the proliferation of crypt enterocytes with an inversion of the differentiation/pro

300 TC-7 cell line also mimicked ex vivo derived enterocytes with regard to MV effacement, enabling a bet