ライフサイエンスコーパス: enterocyte

1 serve to increase the functional capacity of enterocyte.

2 endocrine, tuft and goblet cells, as well as enterocytes.

3 HDAC3 inhibition induces their expression in enterocytes.

4 necessary, to induce PC differentiation into enterocytes.

5 f ferrous iron across the apical membrane of enterocytes.

6 er mediating basolateral manganese uptake in enterocytes.

7 formation of inclusions in neonatal Myo5b KO enterocytes.

8 ke) cells and, except in duodenum, in mature enterocytes.

9 teroblasts, enteroendocrine cells (EEs), and enterocytes.

10 for differentiation of AMPs and PCs into new enterocytes.

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

12 pothesis that S Typhi preferentially targets enterocytes.

13 midgut morphology with dramatically enlarged enterocytes.

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

15 rter NPC1l1 to block cholesterol uptake into enterocytes.

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

17 gns with transcriptional variation of Lct in enterocytes.

18 infecting bacteria on the apical surface of enterocytes.

19 LUT1 appeared at the basolateral membrane of enterocytes.

20 ma TG excursion and accumulated lipid in the enterocytes.

21 echanistic studies were performed in primary enterocytes.

22 mulation of intracellular vesicles in villus enterocytes.

23 , which failed to further differentiate into enterocytes.

24 impaired viability and maturation of villus enterocytes.

25 leading to the buildup of bile acids within enterocytes.

26 cell cycle programs of adult stem cells and enterocytes.

27 ribution, trafficking, and turnover in human enterocytes.

28 ved in membrane fusion of apical vesicles in enterocytes.

29 ing pathway partially restored the number of enterocytes.

30 oronavirus 2 (SARS-CoV-2) replication within enterocytes.

31 le acid uptake and lowering FXR induction in enterocytes.

32 s, including differentiated Krt20(+) surface enterocytes.

33 gth on the surface of crypt, but not villus, enterocytes.

34 ipid homeostasis and chylomicron assembly in enterocytes.

35 lls (PCs), but not to differentiate PCs into enterocytes.

36 sensitive CncC/Nrf2 signaling pathway within enterocytes.

37 g in their cellular siblings, the absorptive enterocytes(1).

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

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

40 te of BA action is the terminal ileum, where enterocytes actively reuptake BAs and express high level

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

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

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

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

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

46 terleukin 18, a pro-Th1 cytokine produced by enterocytes, also contributes to the downregulation of C

47 ional signature is shared in small intestine enterocytes among coronavirus receptors (ACE2, DPP4, ANP

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

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

50 ssential for Mn excretion by hepatocytes and enterocytes and could be an effective target for pharmac

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

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

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

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

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

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

57 iR-200C prevents the decrease in occludin in enterocytes and intestine tissues of mice with colitis,

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

59 which is accomplished through crosstalk with enterocytes and other immune cells.

60 creases iron release to plasma by absorptive enterocytes and recycling macrophages.

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

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

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

64 -3p, which reduces expression of occludin by enterocytes and thereby increases TJ permeability.

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

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

67 ents and tight junctions expression in human enterocytes, and IL-10, IFN-gamma and FoxP3 expression t

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

69 n lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells.

70 EV-A71 is able to be actively replicated in enterocytes, and that the exosome pathway is involved in

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

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

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

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

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

76 specific transport pathways of bile acid in enterocytes are described and the recent finding of lymp

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

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

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

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

81 s (ROS) produced by the NADPH oxidase Nox in enterocytes, are required for p38 activation in enterocy

82 hila midgut enterocytes disrupted the normal enterocyte arrangement.

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

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

85 riking expression of ACE2 on the small bowel enterocyte brush border supports intestinal infectivity

86 In the enterocyte brush border, protocadherin function requires

87 upon exit from stem-cell-containing crypts, enterocytes build thousands of microvilli, each supporte

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

89 in a formulation that optimizes uptake into enterocytes but prevents entry into the blood is propose

90 a10 also localized to the apical membrane of enterocytes, but mice with Slc30a10 deficiency in small

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

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

93 Regulation of lipid absorption by enterocytes can influence metabolic status in humans and

94 ctivity, and Upd3 and Rhomboid production in enterocytes, catalyzing feedforward ISC hyperplasia.

95 ding SARS-CoV-2 and porcine CoVs, can infect enterocytes, cause diarrhea, and be shed in the feces.

96 rd regulatory module promotes and stabilizes enterocyte cell identity; disruption of the HNF4-SMAD4 m

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

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

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

100 Inclusions in Myo5b KO enterocytes contained VAMP4 and Pacsin 2 (Syndapin 2).

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

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

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

104 Restricted to the colon, enterocyte damage and mucosal immune dysfunction play a

105 INR had higher blood levels of the enterocyte damage marker Intestinal fatty acid binding p

106 lon and correlated to circulating markers of enterocyte damage.

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

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

109 yperproliferation and expansion of ISCs, but enterocyte differentiation was impaired, based on loss o

110 mice implicated Notch signaling in inducing enterocyte differentiation.

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

112 is involved in the regulation of intestinal enterocyte differentiation.

113 exit from the regenerative state and driving enterocyte differentiation.

114 onomers into microvillar core bundles during enterocyte differentiation.

115 mechanism by which BMP/SMAD signaling drives enterocyte differentiation.

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

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

118 tly, expression of VopA in Drosophila midgut enterocytes disrupted the normal enterocyte arrangement.

119 sion was only partially elevated in duodenal enterocytes due to a low proliferation level measured by

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

121 its activity restricts cell fate towards the enterocyte (EC) lineage.

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

123 ey supervises the identity of differentiated enterocytes (ECs) in the adult Drosophila midgut.

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 ture differentiation of Drosophila ISCs into enterocytes (ECs).

127 terized by the presence of both the locus of enterocyte effacement (LEE) and the plasmid-encoded bund

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

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

130 irulence factors encoded within the locus of enterocyte effacement (LEE) pathogenicity island, includ

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

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

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

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

135 o EHEC and C. rodentium possess the locus of enterocyte effacement (LEE), which is the canonical viru

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

137 The locus of enterocyte effacement (LEE)-encoded type 3 secretion sys

138 the host's intestinal environment, locus of enterocyte effacement (LEE)-encoded virulence genes are

139 studies showed global increases in Locus for Enterocyte Effacement (LEE)-negative STEC infection.

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

141 nce genes, notably those within the locus of enterocyte effacement (LEE).

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

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

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

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

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

147 PACSIN2 KO enterocytes exhibit reduced numbers of microvilli and de

148 ycoprotein decreases bumped kinase inhibitor enterocyte exposure, resulting in reduced in vivo effica

149 that multiple colonic cell types, especially enterocytes, express ACE2 and are permissive to SARS-CoV

150 of the HNF4-SMAD4 module results in loss of enterocyte fate in favor of progenitor and secretory cel

151 erocytes, are required for p38 activation in enterocytes following infection or wounding, and for ISC

152 postulated that inclusions in Myo5b KO mouse enterocytes form through invagination of the apical brus

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

154 mal bacterial loads are sufficient to invade enterocytes from the apical side and trigger loss of bar

155 f ACE2 and TMPRSS2 is elevated in absorptive enterocytes from the inflamed ileal tissues of Crohn dis

156 ontributes to brush border morphogenesis and enterocyte function under native in vivo conditions, we

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

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

159 ion is associated with perturbed zonation of enterocyte genes induced at the villus tip.

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

161 pparent influence on the relative numbers of enterocytes, goblet cells or Paneth cells.

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

163 tein (L-Fabp) modulates lipid trafficking in enterocytes, hepatocytes, and hepatic stellate cells (HS

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

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

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

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

168 Rotaviruses bind to enterocytes in a genotype-specific manner via histo-bloo

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

170 The origin of inclusions in small-intestinal enterocytes in microvillus inclusion disease is currentl

171 ling is activated in adult Drosophila midgut enterocytes in response to diverse stresses including pa

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

173 FGF15 is induced by FXR in ileal enterocytes in response to increased amounts of intestin

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

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

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

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

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

179 Healthy enterocytes inhibit stem cell division through E-cadheri

180 pose that Nox-ROS-Ask1-MKK3-p38 signaling in enterocytes integrates multiple different stresses to in

181 Nutrient-transporting enterocytes interact with their luminal environment usin

182 or controls systemic growth from a subset of enterocytes-interstitial cells-by promoting food intake

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

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

185 minase-related growth factor A (Adgf-A) from enterocytes is necessary for extracellular adenosine to

186 Ask1-p38 signaling in enterocytes is required upon infection to promote full i

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

188 Examination of enterocytes isolated from infected mice revealed that a

189 meability, compared with mice given vehicle; enterocytes isolated from mice given IL1B had increased

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

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

192 tural IELs)-that is dispersed throughout the enterocyte layer of the small intestine and that modulat

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

194 s CPE-induced pore formation and activity in enterocyte-like Caco-2 cells, reducing the cytotoxicity

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

196 maintenance of adherence capability to human enterocyte-like cell lines, was evaluated.

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

198 drives ISC daughter cells towards absorptive enterocyte lineage ensuring epithelial growth.

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

200 ntrol the binary fate decision (secretory vs enterocyte lineage) by repressing genes regulated by ATO

201 ates their specification toward secretory vs enterocyte lineages (binary fate).

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

203 ntestinal cells, which we call lysosome-rich enterocytes (LREs), internalize dietary protein via rece

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

205 fferentiation was impaired, based on loss of enterocyte markers and functions.

206 utant mice displayed increased expression of enterocyte markers, but reduced expression of the goblet

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

208 Epigenetic divergence within enterocytes may contribute to the functional specializat

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

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

211 and immune cell subsets, including BEST4(+) enterocytes, microfold-like cells, and IL13RA2(+)IL11(+)

212 bits marked enrichment at the distal tips of enterocyte microvilli, the site of IMAC function, and is

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

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

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

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

217 19 expression was induced in polarized human enterocyte-models and mouse organoids by basolateral inc

218 Increase of Axin protein in enterocytes non-autonomously enhanced stem cell division

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

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

221 kage and an increased lesion burden in cecal enterocytes of colonized mice.

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

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

224 k et al. (2019) demonstrate that specialized enterocytes of the developing vertebrate intestine are e

225 The epithelial enterocytes of the intestine are responsible for absorbi

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

227 utrient transporters found on the absorptive enterocytes of the small intestine.

228 drug exposure in the gastrointestinal lumen, enterocytes, or systemic circulation?

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

230 a implicate lipin 2/3 as a control point for enterocyte phospholipid homeostasis and chylomicron biog

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

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

233 criptional cell state, leading to a proximal enterocyte population enriched for genes within oxidativ

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

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

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

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

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

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

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

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 est that apical bulk endocytosis in Myo5b KO enterocytes resembles activity-dependent bulk endocytosi

246 Here, we investigated enterocyte responses to AHR agonists in coffee and measu

247 how that genetic disruption of CALML4 within enterocytes results in brush border assembly defects tha

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

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

250 Enterocytes secreted Unpaired proteins and thereby stimu

251 Enterocytes sense highly elevated levels of (conjugated)

252 Tipe0(-/-) enterocytes show basal induction of the Clu(+) regenerat

253 inactivating mutations in myosin Vb (Myo5B), enterocytes show large inclusions lined by microvilli.

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

255 In differentiated enterocytes, SLC30A10 localized to the apical/luminal do

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

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

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

259 Enterocyte-specific activation of CncC stimulated the pr

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

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

262 Enterocyte TAGs are stored transiently as cytosolic lipi

263 to identify Hodor, an ionotropic receptor in enterocytes that sustains larval development, particular

264 of TIPE0 in mice results in injury-resistant enterocytes, that are hyperproliferative, yet have regen

265 Enterocytes, the intestinal absorptive cells, have to de

266 riggers electrical responses in neighbouring enterocytes through P2Y(2) and nodose ganglion neurones

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

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

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

270 ro-proliferative signals are transduced from enterocytes to AMPs.

271 initial physiological response of intestinal enterocytes to dietary lipid.

272 f how ANKS4B targets to the apical domain of enterocytes to drive brush border assembly and identifie

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 ntiate in response to damage to generate new enterocytes, transiently depleting their pool.

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

278 rker expression, although the expressions of enterocyte-, tuft- and goblet-cell specific markers are

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

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

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

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

283 action, making the role of lipin proteins in enterocytes unclear.

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

285 hin the intestine, the nutrient-transporting enterocytes utilize the intermicrovillar adhesion comple

286 TAG synthesis in small intestinal enterocytes utilizes 2-monoacylglycerol and does not req

287 ion, influence host mucosal immune cells and enterocytes via butyrate production, or contribute to sy

288 for the first time that ABCB1 is involved in enterocyte vitamin K efflux in both cell and mouse model

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

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

291 cs on sorted intestinal stem cells and adult enterocytes, we identified candidate genes, which change

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

293 and analyzed by histology and real-time PCR; enterocytes were isolated by laser capture microdissecti

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

295 rush borders, we sought to determine whether enterocytes were resource (i.e., actin monomer) limited

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

297 he leading role of bile acid absorption into enterocytes, where bile acids are delivered to basolater

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

299 ession of CCL20 and CCL25 by small intestine enterocytes, while it increases the expression of CXCL9/

300 gonad, which activates JAK-STAT signaling in enterocytes within this intestinal portion.