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 tracellular NTR1 trafficking in human NCM460 colonocytes.

4 reduced gp96 expression and cytotoxicity in colonocytes.

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

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

7 pressure in SW620 or primary human malignant colonocytes.

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

9 nd especially the vitamin level in the local colonocytes.

10 n identified at the apical membrane of human colonocytes.

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

12 f cell types, including normal and malignant colonocytes.

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

14 the TxB-mediated proinflammatory pathway in colonocytes.

15 ation increased paracellular permeability of colonocytes.

16 ause of its impact on the differentiation of colonocytes.

17 meostasis of these vitamins in the localized colonocytes.

18 taF508 CFTR at the luminal membrane of crypt colonocytes.

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

20 ll growth with reduced sensitivity of normal colonocytes.

21 tyrate constitutes the major energy fuel for colonocytes.

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

23 roduction of carcinogens or direct damage to colonocytes.

24 plasma membranes were prepared from isolated colonocytes.

25 umnar enterocytes and therefore model normal colonocytes.

26 PKC-beta11 were found compared with control colonocytes.

27 ce, corresponding to the normal migration of colonocytes.

28 ansport in primary cultures of rabbit distal colonocytes.

29 xpression and inhibited barrier formation of colonocytes.

30 sis, especially toward cellular nutrition of colonocytes.

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

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

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

34 the uninvolved colonic mucosa and the fecal colonocytes.

35 ed on rectal brushings or from abraded fecal colonocytes.

36 F receptor-mediated MAPK activation in human colonocytes.

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

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

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

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

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

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

43 lasma membrane TxA binding proteins on human colonocytes.

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

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

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

47 ection activates signals governing malignant colonocyte adhesion.

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

49 Colonocyte and tumor homogenates or membranes were probe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 2 microRNA cluster, which was upregulated in colonocytes coexpressing K-Ras and c-Myc.

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

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

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

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

101 Consistent with increased colonocyte differentiation and apoptosis, inhibition of

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

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

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

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

106 ding of the cellular mechanisms that promote colonocyte differentiation.

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

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

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

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

111 Moreover, colonocytes exposed to toxin A produced reactive oxygen

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

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

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

115 Normal colonocytes expressed all DNA-PK proteins.

116 Colonocytes expressed PAR2 mRNA and responded to PAR2 ag

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

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

119 Reduced mitochondrial activity in colonocytes facilitates AMPKalpha2-dependent inflammatio

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

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

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

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

124 In colonocytes, Galpha subunits are localized primarily in

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

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

127 Specific colonocyte genes were significantly downregulated.

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

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

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

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

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

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

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

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

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

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

138 Colonocyte hyperproliferation was associated with a 4.3

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 release of proinflammatory mediators at the colonocyte level.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 Colonocytes of UC patients show premature shortening of

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

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

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

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

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

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

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

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

182 Rabbit distal colonocytes possess inhibitor-sensitive Cl- permeabiliti

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

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

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

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

187 al cells and fibroblasts directly stimulated colonocyte proliferation.

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

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

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

191 vestigate methods and conditions for optimum colonocyte retrieval.

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

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

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

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

196 -2 expression in human nontransformed NCM460 colonocytes stably transfected with the human NK-1R (NCM

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

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

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

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

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

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

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

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

205 Colonocyte telomeres shorten with age almost twice as ra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

236 Coculture of human colonocytes with endothelial cells and fibroblasts direc

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

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

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

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

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

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