ライフサイエンスコーパス: colonocyte

1 by epithelial cells lining the colon (i.e., colonocytes).

2 c phenotype as opposed to that of the mature colonocyte.

3 of absorbed fluids to avoid intoxication of colonocytes.

4 so increased CCN1 expression in NCM460-NK-1R colonocytes.

5 reduced gp96 expression and cytotoxicity in colonocytes.

6 everal miRNAs, including miR-31-3p, in human colonocytes.

7 n IV messenger RNA in the ileum and cultured colonocytes.

8 ) (PGE(2)) expression and apoptosis in human colonocytes.

9 pressure in SW620 or primary human malignant colonocytes.

10 ated kinase (3.3+/-0.4-fold) in premalignant colonocytes.

11 nd especially the vitamin level in the local colonocytes.

12 n identified at the apical membrane of human colonocytes.

13 ke at the luminal (apical) membrane of human colonocytes.

14 f cell types, including normal and malignant colonocytes.

15 n with subsequent release of IL-8 from human colonocytes.

16 the TxB-mediated proinflammatory pathway in colonocytes.

17 ation increased paracellular permeability of colonocytes.

18 tracellular NTR1 trafficking in human NCM460 colonocytes.

19 ause of its impact on the differentiation of colonocytes.

20 meostasis of these vitamins in the localized colonocytes.

21 taF508 CFTR at the luminal membrane of crypt colonocytes.

22 s - GTP + Ras - GDP)] was >3 SD above normal colonocytes.

23 tyrate constitutes the major energy fuel for colonocytes.

24 e release of IL-8 from non-transformed human colonocytes.

25 roduction of carcinogens or direct damage to colonocytes.

26 plasma membranes were prepared from isolated colonocytes.

27 umnar enterocytes and therefore model normal colonocytes.

28 PKC-beta11 were found compared with control colonocytes.

29 ce, corresponding to the normal migration of colonocytes.

30 ansport in primary cultures of rabbit distal colonocytes.

31 pecificity to inflamed colonocytes/crypt top colonocytes.

32 tly localized to the basolateral membrane of colonocytes.

33 ll growth with reduced sensitivity of normal colonocytes.

34 xpression and inhibited barrier formation of colonocytes.

35 properties, which induce apoptosis in tumor colonocytes.

36 sis, especially toward cellular nutrition of colonocytes.

37 rier-mediated uptake system for TPP in human colonocytes.

38 and high-affinity TPP uptake system in human colonocytes.

39 the uninvolved colonic mucosa and the fecal colonocytes.

40 ed on rectal brushings or from abraded fecal colonocytes.

41 F receptor-mediated MAPK activation in human colonocytes.

42 pressing NK-1R (NCM460-NK-1R) and in primary colonocytes.

43 protein, Musashi1 (MSI1), in cultured human colonocytes.

44 tosis and respond similarly to the wild-type colonocytes.

45 in histone H3 in NCM460-NK-1R and/or primary colonocytes.

46 released KPV on or within the closed area of colonocytes.

47 aluating the effects of E(2) in noncancerous colonocytes.

48 lasma membrane TxA binding proteins on human colonocytes.

49 omponents in unprocessed human feces include colonocytes (~107 per gram of wet stool), archaea (~108

50 ice raises intracellular polyamine levels in colonocytes, accelerating epithelial renewal.

51 e and manganese stimulated primary and SW620 colonocyte adhesion to collagen.

52 ection activates signals governing malignant colonocyte adhesion.

53 d butyrate, the extent of their oxidation in colonocytes affects their capacity to modulate gene expr

54 Colonocyte and tumor homogenates or membranes were probe

55 + absorption, presumably by acidification of colonocytes and activation of apical Na+/H+ exchangers.

56 ve genes such as Cyp1a1/CYP1A1 in YAMC mouse colonocytes and Caco-2 human colon cancer cell lines.

57 yrate stimulated the proliferation of normal colonocytes and cancerous colonocytes when the Warburg e

58 of PAR(2) and trypsin IV in enterocytes and colonocytes and caused a 2-fold increase in Ca(2+) respo

59 es, including gradients of progenitor cells, colonocytes and goblet cells within intestinal crypts.

60 me-dependent manner in cultured NCM460 human colonocytes and in human intestinal xenografts.

61 with gp96 antibody decreased TxA binding to colonocytes and inhibited TxA-induced cell rounding.

62 yrate is the primary energy source of normal colonocytes and is metabolized to acetyl-CoA, which was

63 tenin is active in hyperproliferating native colonocytes and is similar to that recorded during the e

64 by quantitative polymerase chain reaction in colonocytes and leukocytes of 2 different sets of UC pat

65 ly hsp25 and hsp72, are expressed by surface colonocytes and may have a role in protecting intestinal

66 so inhibited sustained protease signaling to colonocytes and nociceptive neurons that naturally expre

67 Following antibiotic treatment, K8(-/-) colonocytes and organ cultures become less resistant to

68 nt dendrimer NPs accumulated in endosomes of colonocytes and polymeric NPs accumulated in neurons, si

69 GFP was depleted from the plasma membrane of colonocytes and redistributed to early endosomes, consis

70 n of cleaved Notch, villin, and claudin 5 in colonocytes and significantly reduced the permeability o

71 ateral membrane of terminally differentiated colonocytes and that integrin alpha5 staining may be red

72 compared gene expression profiles in murine colonocytes and their c-Myc-transformed counterparts, wh

73 ted in vitro function consistent with mature colonocytes, and a positive short circuit current respon

74 stimulates PLC-gamma as well as c-Src in rat colonocytes, and indicate that PLC-gamma is a direct sub

75 -deficient murine embryo fibroblasts, murine colonocytes, and isogenic human HNPCC tumor cell lines t

76 on both luminal and basolateral membranes of colonocytes, and, in other cell systems, this receptor h

77 l villus epithelial cells; low in absorptive colonocytes; and not significantly different in the dist

78 G protein alpha subunits in rat colonocytes, colonocyte antipodal plasma membranes, and colonic neopl

79 S-sensitive, SCFA-dependent transport in the colonocyte apical membrane contributes to pHo regulation

80 protein family, which is expressed on human colonocyte apical membranes as well as in the cytoplasm.

81 l factor expression in the ileum, as well as colonocyte apoptosis and microbiota-driven chronic infla

82 The relationship between colonocyte apoptosis and p38/p53-dependent pathways was

83 The signaling pathway for colonocyte apoptosis following toxin A exposure involves

84 epatocytes, lack of K8 confers resistance to colonocyte apoptosis in a microflora-dependent manner.

85 mice deficient in ITF showed an increase in colonocyte apoptosis unaccompanied by changes in express

86 tty acid fiber fermentation product, induces colonocyte apoptosis via a nonmitochondrial, Fas-mediate

87 d apoptosis and increased toxin A-associated colonocyte apoptosis.

88 ated protein kinase (p38) in toxin A-induced colonocyte apoptosis.

89 est-studied effectors of Shigella entry into colonocytes are the invasion plasmid antigens IpaC and I

90 colon tumor cell lines compared with normal colonocytes, as well as in colon tumors from human clini

91 ocalization of PKC isozymes in mouse and rat colonocytes at different developmental stages were deter

92 confirmed the location of S. flexneri within colonocytes at the mouth of crypts.

93 The main colonocyte binding protein for TxA was identified as gly

94 pH and osmolarity, which are known to affect colonocyte biology per se.

95 G4) to activate ErbB4 and define its role in colonocyte biology.

96 se, whereas ErbB4 overexpression in cultured colonocytes blocks TNF-induced apoptosis in a ligand-dep

97 Compared with control colonocytes [bromodeoxyuridine (BrdUrd), 2.2+/-1.2%], az

98 exotoxins, TcdA and TcdB, which target host colonocytes by binding to unknown cell surface receptors

99 B signals acute proinflammatory responses in colonocytes by transactivation of the EGFR and activatio

100 find that expression of oncogenic ras in HD3 colonocytes causes increased alpha2-6 sialylation of bet

101 Compared with a mouse colonocyte cell line that expresses high levels of wild-

102 the molecular mechanisms of folate action on colonocyte cell proliferation, gene expression, and colo

103 lanin-1 receptor activation by ligand causes colonocyte Cl- secretion.

104 2 microRNA cluster, which was upregulated in colonocytes coexpressing K-Ras and c-Myc.

105 xpression of G protein alpha subunits in rat colonocytes, colonocyte antipodal plasma membranes, and

106 entifying epithelial specificity to inflamed colonocytes/crypt top colonocytes.

107 s transient overexpression in Myc-transduced colonocytes decreased cell accumulation.

108 t WIF1; overexpression of miR-203 in primary colonocytes decreased WIF1 mRNA and protein levels.

109 Complex II knockdown in colonocytes decreases the efficiency of H(2)S clearance

110 demonstrate that chronic sulfide exposure of colonocyte-derived cells leads to lower Mic60 and Mic19

111 ion were markedly attenuated in p53-silenced colonocytes, despite active p38.

112 Consistent with increased colonocyte differentiation and apoptosis, inhibition of

113 that 5-hmC regulates gene expression during colonocyte differentiation and controls gene expression

114 However, whether or not 5-hmC regulates colonocyte differentiation is unknown.

115 Hedgehog (IHH), a canonical driver of normal colonocyte differentiation, exists in a bivalent chromat

116 These findings are indicative of colonocyte differentiation, which was confirmed by immun

117 d in promoting a retinoid-induced program of colonocyte differentiation.

118 ding of the cellular mechanisms that promote colonocyte differentiation.

119 e thiosulfonate-treated early passage p53-/- colonocytes do not form tumors when injected into immuno

120 rmal crypt and to clonal expansion of mutant colonocytes during tumorigenesis.

121 lonocytes, suggesting a role for keratins in colonocyte energy metabolism and homeostasis.

122 iii) whether IL-1alpha, released by injured colonocytes, exacerbated experimental IBD.

123 Moreover, colonocytes exposed to toxin A produced reactive oxygen

124 ng antibody markedly attenuated apoptosis in colonocytes exposed to toxin A.

125 Mouse and rat colonocytes express PKC alpha, beta II, delta, epsilon,

126 We found that NCM460, non-transformed human colonocytes, express a functional high affinity NT recep

127 Normal colonocytes expressed all DNA-PK proteins.

128 Colonocytes expressed PAR2 mRNA and responded to PAR2 ag

129 rate was increased and increased numbers of colonocytes expressing proliferating cell nuclear antige

130 However, compared to normal colonocytes, expression of these genes is lower, and the

131 thelial cells that express ZnR, particularly colonocytes, face frequent changes in extracellular pH t

132 Reduced mitochondrial activity in colonocytes facilitates AMPKalpha2-dependent inflammatio

133 Colonocytes from newborn (7-9 days old), weanling (25-28

134 Despite increased luminal BA, colonocytes from WD-fed mice exhibited decreased express

135 could provide a mechanism for modulation of colonocyte function by dietary and systemic extracellula

136 himurium and Shigella flexerii also increase colonocyte galanin-1 receptor expression, whose activati

137 In colonocytes, Galpha subunits are localized primarily in

138 Importantly, microarray analysis of colonocyte gene expression profiles discerned fundamenta

139 genes to help decipher the global changes in colonocyte gene expression profiles in carcinogen-inject

140 Specific colonocyte genes were significantly downregulated.

141 ation of a similar subset of goblet cell and colonocyte genes, and GATA6 was found to occupy active l

142 Individual cells, including colonocytes, goblet cells, and inflammatory cells, could

143 We conclude that human colonocyte gp96 serves as a plasma membrane binding prot

144 Upon activation in colonocytes, GPR109A potentiates anti-inflammatory pathw

145 rowth factor (EGF) receptor (EGFR) regulates colonocyte growth and differentiation and is overexpress

146 Coincident with colonocyte growth arrest/differentiation, PKC isozyme ex

147 itu hybridization showed that the neoplastic colonocytes had increased expression of PHS-2 (n = 4).

148 TLR5-associated signaling in non-transformed colonocytes has not been investigated.

149 olgi proteomes of YIPF6 and TVP23B-deficient colonocytes have a common deficiency of several critical

150 Human colonocytes have the potential to serve as targets for c

151 ole in maintaining physiologic expression of colonocyte hsp25 and hsp72.

152 the pathways that underlie the mechanism of colonocyte hyperplasia and the normalization of the colo

153 Colonocyte hyperproliferation was associated with a 4.3

154 n K8(-/-) and K8(+/+) isolated colon crypts (colonocytes) identified apoptosis as a major altered pat

155 Thus, mast cells signal to colonocytes in a paracrine manner by release of tryptase

156 rplasia, and binding of the pathogen to host colonocytes in adults, with similar findings in neonatal

157 in order to predict metabolic signatures of colonocytes in both healthy and disease states.

158 the existence of a cluster of BEST4+ mature colonocytes in humans.

159 ive stress during chronic inflammation, e.g. colonocytes in inflammatory bowel diseases, and the mult

160 tly increased amounts of SI, LPH, and ApN in colonocytes in most SBS patients with large variation an

161 Expression of miR-137 was restricted to the colonocytes in normal mucosa and inversely correlated wi

162 aling as well as cell proliferation in human colonocytes in response to NT.

163 ing pathways mediating postmitotic events in colonocytes in situ, and suggest that diminished activit

164 plore the interplay between gut bacteria and colonocytes in the human large intestine and study the m

165 hat E(2) alters the growth of nontransformed colonocytes in vitro and that, through an ERbeta-mediate

166 difficile toxin A causes marked apoptosis of colonocytes in vivo and in vitro, which contributes to t

167 laying a role in terminal differentiation of colonocytes, in situ hybridization of normal colonic epi

168 pression of PDE10 in normal and precancerous colonocytes increases proliferation and activates TCF tr

169 ients without IBD (controls), and of HCT-116 colonocytes incubated with 5-aza-2'-deoxycytidine (5-AZA

170 r of transcription 3 (STAT3) in NCM460 human colonocytes incubated with interleukin-6.

171 Spontaneous transformation of p53-/- colonocytes is only observed using late passage cells, a

172 Knockdown of dynamin-2 (Dnm2), the major colonocyte isoform, and Dnm inhibition attenuated PAR(2)

173 ucosa was mirrorred in the mucus layer fecal colonocytes isolated from AOM rat stool and the degree o

174 Herein we report that SW48 colonocytes lacking alpha2-6 sialylation exhibit beta1 i

175 Yet Kras-transformed mouse colonocytes lacking p53 formed indolent, poorly vascular

176 release of proinflammatory mediators at the colonocyte level.

177 The contribution of major changes in the colonocyte luminal environment in pathological processes

178 Transport of butyrate across the colonocyte luminal membrane is mediated by the monocarbo

179 When mast cells were co-cultured with colonocytes, mast cell degranulation increased paracellu

180 Thus, in non-transformed human colonocytes, MEK activation following flagellin/TLR5 eng

181 To test whether PKM1/2 alter colonocyte metabolism, we created a knockdown of PKM2 an

182 During homeostasis, differentiated colonocytes metabolized butyrate likely preventing it fr

183 hat immunocytochemical analysis of retrieved colonocytes might enable accurate detection of colorecta

184 ukocyte telomeres and increased gammaH2AX in colonocytes might reflect oxidative damage secondary to

185 Importantly, DALDA-induced colonocyte migration was completely ablated by shStat3 k

186 hermore, Stat3 is required for DALDA-induced colonocyte migration.

187 pithelial resistance of monolayers of normal colonocytes (NCM 460) by diminishing the mRNA expression

188 by C. difficile toxin A or IL-1beta in human colonocyte NCM460 cells in a dose-dependent fashion.

189 ockade on toxin A-induced apoptosis of human colonocytes (NCM460) and of PGE(2) or toxin A on the Fas

190 trafficking in transfected HEK293 cells and colonocytes (NCM460) that endogenously express TGR5.

191 Thus, in human colonocytes, NK-1R-induced EGFR and MAPK activation and

192 We speculate that the increase in colonocyte number is related to decreased levels of cGMP

193 ble to identify preneoplastic changes in the colonocytes of the azoxymethane (AOM)-treated rat model

194 Colonocytes of UC patients show premature shortening of

195 gammaH2AX intensity is higher in colonocytes of UC patients than in controls and is not d

196 Exposure of K8(-/-) colonocytes or colon organ ("organoid") cultures, but no

197 e is expressed in the apical membrane of rat colonocytes, our data support the view that, in rat dist

198 ithelial restitution, the rapid migration of colonocytes over mucosal wounds.

199 When applied to the basolateral surface of colonocytes, PAR2 agonists and mast cell supernatant dec

200 that the 5-hmC distribution in primary human colonocytes parallels the distribution found in differen

201 this may play an important role in promoting colonocyte participation in host defense and pathogen cl

202 ly modified mice exhibit distinct changes in colonocyte phenotype and therefore have utility as model

203 Rabbit distal colonocytes possess inhibitor-sensitive Cl- permeabiliti

204 icate that CGN-induced inflammation in human colonocytes proceeds through a pathway of innate immunit

205 Previously, we reported that normal colonocytes produce the memory CD4(+) T cell-directed ch

206 DALDA also enhanced colonocyte proliferation (Ki-67 staining) by 350%.

207 adenoma and carcinoma formation by enhancing colonocyte proliferation and impairing differentiation.

208 al cells and fibroblasts directly stimulated colonocyte proliferation.

209 Due to the Warburg effect, cancerous colonocytes rely on glucose as their primary energy sour

210 2) influences the physiology of noncancerous colonocytes, resulting in fewer preneoplastic lesions.

211 ha stimulated mPGES-1 transcription in human colonocytes, resulting in increased amounts of mPGES-1 m

212 vestigate methods and conditions for optimum colonocyte retrieval.

213 e maintenance protein 2 (MCM2) expression in colonocytes retrieved from the faecal surface.

214 Herein, we show that in colonocytes, rictor/mammalian target of rapamycin comple

215 expression in colon biopsies and exfoliated colonocyte RNA in feces and fecal microbial community co

216 Comparing murine primary colonic EECs with colonocytes showed expression of intercellular Ca(2+) st

217 In addition, Gatm(c/c) colonocytes showed increased metabolic stress in respons

218 al epithelial cells in the pancreas, surface colonocytes, small intestinal villi, and gastric isthmus

219 accounts for the intraluminal, mucosal, and colonocyte spaces.

220 tro experiments, human nontransformed NCM460 colonocytes stably transfected with NK-1R (NCM460-NK-1R

221 -2 expression in human nontransformed NCM460 colonocytes stably transfected with the human NK-1R (NCM

222 We used non-transformed human NCM460 colonocytes stably transfected with the human NK-1R (NCM

223 Human NCM460 colonocytes stably transfected with the human NK-1R (NCM

224 e we show that by generating cytoplasts from colonocytes, standard fusion techniques can be used to t

225 SP exposure of NCM460-NK-1R colonocytes stimulated phosphorylation of the antiapopto

226 Likewise, human NCM460 colonocytes subjected to shRNA-mediated IER3 knockdown e

227 CFA-MCT1-HMGCS2 axis is disrupted in K8(-/-) colonocytes, suggesting a role for keratins in colonocyt

228 pressed by a variety of cell types including colonocytes, suggesting that MIP-3alpha may regulate add

229 but required secosteroid treatment of intact colonocytes, suggesting the involvement of a soluble fac

230 Colonocyte telomeres shorten with age almost twice as ra

231 ed peptide bound more strongly to dysplastic colonocytes than to adjacent normal cells with 81% sensi

232 ence of carrier-mediated mechanisms in human colonocytes that are capable of absorbing some of the vi

233 a metabolic barrier formed by differentiated colonocytes that consume butyrate and stimulate future s

234 ttle characterization has been done in human colonocytes, the target tissue of colon carcinogenesis.

235 , or claudin 5 was not detected in RAG1(-/-) colonocytes; their loss correlated with increased intest

236 al production of PGI(2) promotes survival of colonocytes through PPAR delta activation.

237 f primary human colon cancer cells and SW620 colonocytes to collagen and endothelial cells.

238 The transition from normal colonocytes to colorectal cancer correlates with increas

239 aves protease-activated receptor 2 (PAR2) on colonocytes to increase paracellular permeability.

240 Sustained exposure of colonocytes to SP activates NF-kappaB and stimulates IL-

241 ergy metabolism of colonic epithelial cells (colonocytes) toward beta-oxidation.

242 In addition, Src isolated from colonocytes treated with 1,25(OH)2D3, demonstrated an in

243 where it plays an important role in linking colonocyte turnover and differentiation to luminal conte

244 rotection induced by ethanol exists in human colonocytes under in vitro conditions independent of muc

245 ently, active caspase-3 increases in surface colonocytes undergoing apoptosis/anoikis and causes epit

246 it inhibited the proliferation of cancerous colonocytes undergoing the Warburg effect.

247 s found to induce apoptosis in parental SW48 colonocytes (unsialylated), whereas ST6Gal-I expressors

248 OX-2 expression and PGE2 production in human colonocytes via activation of the JAK2-STAT3/5 pathway.

249 imulates expression of miR-21 and miR-155 in colonocytes, via Akt and NF-kappaB, to down-regulate PTE

250 Functional activity of elevated FasL on colonocytes was assessed by coculture of colonocytes wit

251 complex class II (MHCII) expression by these colonocytes was required to elicit sustained IL-22 signa

252 We found that the L(d) obtained from rectal colonocytes was well correlated with colon tumorigenicit

253 In HEK293 cells and non-transformed human colonocytes, we observed that G protein-coupled receptor

254 tive fluorescence microscopy in living mouse colonocytes, we show that docosahexaenoic acid (DHA), a

255 ZnR/GPR39-dependent Ca(2+) responses in HT29 colonocytes were maximal at pH 7.4 but were reduced by a

256 olarized monolayers of T(84) and HT29/cl.19A colonocytes were preincubated with IFN-gamma prior to st

257 Detached necrotic colonocytes were present in the lumen, with inflammatory

258 Mouse colonocytes were treated with 50 micromol/L DHA or linol

259 feration of normal colonocytes and cancerous colonocytes when the Warburg effect was prevented from o

260 is phenotype, allowing increased invasion of colonocytes where cefepime concentrations were reduced.

261 to mediate toxin-induced VEGF production in colonocytes, which can further stimulate human intestina

262 on surface, and instability of HIF-1alpha in colonocytes, which indicated increased epithelial oxygen

263 ase C (GCC), the principle source of cGMP in colonocytes, which is overexpressed in colorectal cancer

264 degranulated mast cells increased [Ca2+]i in colonocytes, which was prevented by a tryptase inhibitor

265 Incubation of HCT-116 colonocytes with 5-AZA up-regulated miR-124 and reduced

266 Coculture of human colonocytes with endothelial cells and fibroblasts direc

267 on colonocytes was assessed by coculture of colonocytes with Fas bearing Jurkat T cells.

268 vealed that treatment of T84 and HT29/cl.19A colonocytes with spermidine increased both TCPTP protein

269 ic tumor for 6 wk but eliminated from normal colonocytes within days.

270 or EGFR to the cell surface of pre-cancerous colonocytes within the epithelium of dysplastic crypts i

271 g and increases apoptosis/anoikis of surface colonocytes without affecting the crypt architecture.

272 NTR1 trafficking to plasma membrane in human colonocytes, without affecting NTR1 internalization.

273 ased apoptotic activity in young adult mouse colonocytes (YAMC), a nonmalignant cell line, in a dose-