ライフサイエンスコーパス: crypt

1 zone (PDZ) around the implantation chamber (crypt).

2 lates bound to the metal encapsulated in the crypt.

3 generating 2 daughter crypts from 1 parental crypt.

4 the migration of cells within the colorectal crypt.

5 cells (IESCs) positioned at the base of each crypt.

6 h genes in the villus but Bcl-2 alone in the crypt.

7 sion, in which 2 crypts fuse into 1 daughter crypt.

8 tentiate Wnt signalling in the proliferating crypt.

9 use downward invasion of mutant cells in the crypt.

10 tional and architectural features of in vivo crypts.

11 yposis coli (Apc) inactivation in intestinal crypts.

12 fusion windows while supporting the in vitro crypts.

13 lonocytes and goblet cells within intestinal crypts.

14 nally controls fatty acid oxidation (FAO) in crypts.

15 R3C1 bind to the CLDN1 promoter in rat colon crypts.

16 blet cells, resulting in enlarged intestinal crypts.

17 dney tips, as well as homeostatic intestinal crypts.

18 o epithelial cells distributed along colonic crypts.

19 high degree of plasticity within intestinal crypts.

20 s units with stem cells at the bottom of the crypts.

21 crypts and apoptosis occurring in villi and crypts.

22 match the dimensions and density of in vivo crypts.

23 ls cultured for 12 d to form mature in vitro crypts.

24 ents of growth factors are formed across the crypts.

25 lowest at night, when hemocytes entered the crypts.

26 environmental niches, the luminal mucosa and crypts.

27 ed growth of small intestine villi and colon crypts.

28 n mutant and normal epithelial stem cells in crypts(1).

29 ris(amide) complex [K(crypt)][Tb(NR(2))(3)] (crypt = 2.2.2-cryptand), 1-Tb, reacts with dinitrogen in

30 (crypt)}2{[(R2N)3Sc]2[mu-eta(1):eta(1)-N2]} (crypt = 2.2.2-cryptand, R = SiMe3), has been isolated fr

31 ing of the N(2) unit in the same crystal, [K(crypt)](2){[(R(2)N)(3)Gd](2)[mu-eta(x):eta(x)-N(2)]} (x

32 rm the end-on bridging dinitrogen complex [K(crypt)](2){[(R(2)N)(3)Tb](2)[mu-eta(1):eta(1)-N(2)]}, 2-

33 DFT calculations on [Nd(II) (crypt)](2+) ], the first Nd(II) cryptand complex, assign

34 h metal with an end-on dinitrogen bridge, {K(crypt)}2{[(R2N)3Sc]2[mu-eta(1):eta(1)-N2]} (crypt = 2.2.

35 f up to 20 K, as observed for the complex [K(crypt-222)][(Cp(Me4H)2Tb)2(mu-[Formula: see text])].

36 O}(10) intermediate, key to formation of [Cs(crypt-222)][(TIMEN(Mes))Fe(NO)], (5) featuring a metalac

37 e characterization of the compound [K([2.2.2]crypt)](4) [In(8) Sb(13) ], which proves to contain a 1:

38 In this work, we introduce the [K(2,2,2-crypt)](4){(Ge(9))(2)[eta(6)-Ge(PdPPh(3))(3)]} complex t

39 clones down to 20% of the cellularity of the crypt (~50 of 250 cells).

40 e results showed that the number of aberrant crypts, aberrant crypt foci (ACF) and crypts/focus in ra

41 xhibited similar distributions of villus and crypt afferents as control mice, suggesting surgery did

42 ed mice, with the number of Paneth cells per crypt also significantly reduced.

43 The intestinal crypt and its stem cells are dependent on the Wnt pathwa

44 We observed a decrease in PC/crypt and lysozyme intensity in the first week after ITx

45 ined for PC (lysozyme) and apoptosis, and PC/crypt and lysozyme intensity were scored.

46 position of these cells along the intestinal crypt and their capacity for multipotency.

47 Most crypt and villus afferent terminals along the entire pro

48 decreased crypt proliferation and increased crypt and villus apoptosis.

49 Crypt and villus cells were isolated, incubated with flu

50 testinal epithelium is a repetitive sheet of crypt and villus units with stem cells at the bottom of

51 results in Wnt hyperactivation in intestinal crypts and accelerates CRC progression to adenocarcinoma

52 tudied expansion of organoids generated from crypts and adenomas, stimulated by HGF or EGF, that were

53 t epithelium, with proliferation confined to crypts and apoptosis occurring in villi and crypts.

54 deletion reduces proliferation in intestinal crypts and compromises regeneration capacity.

55 t Lgr5-negative cells can regenerate colonic crypts and give rise to Lgr5 (+) stem cells.

56 NRG1 robustly stimulates proliferation in crypts and induces budding in organoids, in part through

57 f neutrophil infiltration in less than 5% of crypts and no crypt destruction, erosions, ulcerations,

58 ressed mainly in the epithelial cells of the crypts and only marginally in the villi.

59 dent mechanisms that radioprotect intestinal crypts and that ATM inhibition promotes GI syndrome afte

60 ar beta-catenin throughout the length of the crypts and up-regulation of Axin2, a canonical Wnt targe

61 lial tissues, most notably in the intestinal crypts, and is highly up-regulated in many colorectal, h

62 t axin associates with LRP5/6 in CR-infected crypts, and this association was correlated with increas

63 e of these changes was revealed by rescue of crypt apoptosis and Wnt pathway gene expression upon tre

64 damage observed by shortened villi, loss of crypt architecture and intense inflammatory cell infiltr

65 ucin-producing goblet cells, loss of defined crypt architecture and the resulting acute inflammatory

66 h MVs prevented colon shortening and loss of crypt architecture.

67 lonal expansions outside the confines of the crypt are rare, we observed widespread millimeter-scale

68 mucosa, in close proximity to proliferative crypts, are a source of WNT and RSPONDIN ligands, wherea

69 The cultured in vitro crypt arrays successfully recapitulated the architecture

70 higher number of apoptotic Paneth cells per crypt at 45I-30R (16.4% [7.1-32.1] vs 10.6% [0.0-25.4]).

71 how that nine individuals buried in an elite crypt at Pueblo Bonito, the largest structure in the can

72 ATM inhibition also increased cell death in crypts at 4 h in Cdkn1a(p21(CIP/WAF1))-/-, earlier than

73 eled expression of WNT2b and WNT4 in colonic crypts at days 6 and 12 post-infection with Citrobacter

74 ls of nuclear beta-catenin in the intestinal crypt, augmenting CRC tumorigenesis in an adenomatous po

75 to replicate cell differentiation along the crypt axis.

76 ithelial integrity, and spared cell death in crypt base columnar cells compared to TAI-CONV irradiati

77 n of the Wnt pathway via Apc inactivation in crypt base columnar intestinal stem cells (ISC) led to t

78 t with the stem cell compartment and loss of crypt base columnar ISCs, which expressed both MHC class

79 the crypt progenitor cells in vivo, lack of crypt base columnar stem cell markers, and a failure of

80 nes in intestinal crypt epithelia, including crypt base columnar stem cells and Paneth cells, and in

81 the small intestine, where it is enriched in crypt base columnar stem cells, one of the most active s

82 Recruitment to the crypt base region resulted in direct T cell engagement w

83 We observed that Gpr182 is expressed at the crypt base throughout the small intestine, where it is e

84 dhesion molecule MAdCAM-1 clustered near the crypt base, preferentially regulating crypt compartment

85 The colonic epithelial turnover is driven by crypt-base stem cells that express the R-spondin recepto

86 Paneth cells and increased cell death at the crypt bottom in inflamed ileum samples.

87 As that were differentially expressed in the crypt bottom, creating an SC signature for normal coloni

88 Intestinal stem cells (ISCs) are confined to crypt bottoms and their progeny differentiate near crypt

89 ally differentiated Paneth cell daughters at crypt bottoms.

90 athway, reduced cell proliferation, and less crypt branching than adenomas of mice given the control

91 ed in vitro crypt organoid proliferation and crypt budding was abrogated by the Wnt inhibitor IWP2.

92 ncreased microvilli length on the surface of crypt, but not villus, enterocytes.

93 ee virions were present in 10% of intestinal crypts by 10-12 days.

94 Duodenal lamina propria crypt CD4 T cells were decreased in CG, and stayed low f

95 ptor Il11ra1, and recombinant IL-11 enhances crypt cell regenerative potential.

96 hile ATR inhibition may potentiate arrest in crypt cells after TBI.

97 Crypt cells rapidly absorbed labeled fatty acids, and me

98 Intestinal crypt cells residing in the +4 and higher positions exhi

99 -Seq analysis of freshly isolated intestinal crypt cells showed that Bccip deletion caused an overwhe

100 r the first time found to be expressed in GI crypt cells, and SHP2 expression in the crypt Osx+ cells

101 age is characterized by a loss of intestinal crypt cells, intestinal barrier disruption and transloca

102 , two bona fide GI stem cell markers, at the crypt cells.

103 WR-2721 in promoting survival of intestinal crypt clonogens after morbid irradiation.

104 e number of Lgr5EGFP-positive stem cells per crypt compared with IgG-treated mice, with the number of

105 sed numbers of MSI1(+) cells in regenerating crypts compared to those of control mice.

106 ar the crypt base, preferentially regulating crypt compartment invasion and ISC reduction without aff

107 Reduction of these Ln(III) -in-crypt complexes using KC(8) in THF forms the neutral Ln(

108 m from microbial dysbiosis and proliferative crypt damage.

109 Ablation of both genes resulted in rapid crypt death.

110 n permits the hemocytes to be drawn into the crypts, delivering chitin.

111 rom baseline to week 12 in villous height-to-crypt depth (VHCD) ratio.

112 WD also increased crypt depth and colon cell proliferation.

113 deletion showed significantly lower colonic crypt depth and lower numbers of secretory cell lineages

114 Digital quantitative villous height: crypt depth ratio (VH: CrD) measurements revealed signif

115 efined as a Marsh 3 lesion or villous height:crypt depth ratio below 3.0.

116 Median villous height to crypt depth ratio in distal duodenal biopsies was not si

117 symptoms and villous atrophy (villous height:crypt depth ratio of </=2.0) were assigned randomly to g

118 ps in change from baseline in villous height:crypt depth ratio, numbers of intraepithelial lymphocyte

119 end point was a change in the villous height:crypt depth ratio.

120 tinal histological scores (villous height-to-crypt depth ratio; VHCD); intraepithelial lymphocyte cou

121 No changes in villus height/crypt depth were observed.

122 sed on BrdU incorporation, villus height and crypt depth, and cell number.

123 wered to detect changes in villous height to crypt depth, and stopped at planned interim analysis on

124 bpd(-/-) mice show decreased villous height, crypt depth, crypt to villi ratio and expression of the

125 Villous height to crypt depth, video capsule endoscopy enteropathy score,

126 acterial community composition and increased crypt depth.

127 Wild-type and DRA-knockout (KO) mice and crypt-derived colonoids were used as models for intestin

128 Injection of mice with TNF or incubation of crypt-derived enteroids with TNF reduced their expressio

129 nfiltration in less than 5% of crypts and no crypt destruction, erosions, ulcerations, or granulation

130 MSC therapy reduced crypt dropout in the small intestine and promoted elevat

131 and were protected from immune infiltration, crypt dropout, and ulcers following administration of de

132 e intestinal submucosa and expand around the crypts during the third week of life in mice, independen

133 -Ires-CreERT2) mice, we monitored individual crypt dynamics over multiple days with single-cell resol

134 acterial metabolites and/or drugs on colonic crypt dynamics.

135 Homozygous loss of Apc alone resulted in crypt elongation, activation of the Wnt signature and ac

136 tiation, upon exit from stem-cell-containing crypts, enterocytes build thousands of microvilli, each

137 egulation of Wnt pathway genes in intestinal crypt epithelia, including crypt base columnar stem cell

138 gr5, a gene previously considered a specific crypt epithelial stem cell marker.

139 increased IEC apoptosis, hyperproliferative crypts, epithelial barrier dysfunction, and chronic infl

140 cells both in vitro and in vivo and that the crypt epithelium also expressed IL-6.

141 Using normal colonic crypt epithelium as a comparator, we identify enhancers

142 testinal stem cells but drives Wnt-uncoupled crypt expansion.

143 YAMC and intestinal crypts expressed lower levels of XIAP, cIAP1, cIAP2, and

144 ifying the mechanisms that regulate rates of crypt fission and fusion could provide insights into int

145 As counteracting processes, crypt fission and fusion could regulate crypt numbers du

146 pondin-3 (RSPO3), which occurs by increasing crypt fission and inhibiting crypt fixation.

147 In the adult intestine, crypt fission is observed at a low frequency.

148 duced goblet-like cell maturation, increased crypt fission, and accelerated the development of tumors

149 sed maturation of goblet-like cells, reduced crypt fission, and developed fewer tumors.

150 usion, an almost exact reverse phenomenon of crypt fission, in which 2 crypts fuse into 1 daughter cr

151 s by increasing crypt fission and inhibiting crypt fixation.

152 that the number of aberrant crypts, aberrant crypt foci (ACF) and crypts/focus in rats of the KJT + A

153 ed DNA methylation changes in human aberrant crypt foci (ACF), the earliest putative precursor to CRC

154 xpression levels, and the number of aberrant crypt foci in the colon endothelium.

155 Aberrant crypt foci, luminal microbiota, and DNA alterations (col

156 e number of mutagen-induced aberrant colonic crypt foci.

157 errant crypts, aberrant crypt foci (ACF) and crypts/focus in rats of the KJT + AOM group were signifi

158 by Bmi1-Cre(ER) to give rise to regenerating crypts following gamma irradiation.

159 at Hmga1 drives hyperproliferation, aberrant crypt formation and polyposis in transgenic mice.

160 tive PDZ formation and implantation chamber (crypt) formation, compromising pregnancy success.

161 In vitro crypts formed from primary human intestinal epithelial s

162 en ceramide reduced the number of intestinal crypt-forming enteroids without affecting their structur

163 multiply via fission, generating 2 daughter crypts from 1 parental crypt.

164 om 46 IBD patients and compared these to 412 crypts from 41 non-IBD controls from our previous public

165 ome sequencing to analyse hundreds of normal crypts from 42 individuals.

166 We whole-genome sequenced 446 colonic crypts from 46 IBD patients and compared these to 412 cr

167 We isolated intestinal crypts from C57BL/6 mice, cultured enteroids, incubated

168 -) mice did not expand to the same extent as crypts from Cd44(+/+) mice on stimulation with HGF, but

169 Intestinal crypts from Cd44(-/-) mice did not expand to the same ex

170 m Lkb1(Lgr5-KO) mice lost ISCs compared with crypts from control mice.

171 from LGR5(+) stem cell-containing intestinal crypts from healthy subjects, represents a technological

172 However, most crypts from Lkb1(Lgr5-KO) mice contained functional ISCs

173 Some intestinal crypts from Lkb1(Lgr5-KO) mice lost ISCs compared with c

174 Finally, regenerating crypts from patient biopsies showed increased expression

175 erse phenomenon of crypt fission, in which 2 crypts fuse into 1 daughter crypt.

176 We discovered the existence of crypt fusion, an almost exact reverse phenomenon of cryp

177 s 4.1 +/- 0.9% of all crypts were undergoing crypt fusion.

178 epithelium is a structured organ composed of crypts harboring Lgr5+ stem cells, and villi harboring d

179 first acid-free anionic oxoborane, [K(2.2.2-crypt)][(HCDippN)(2)BO] (1) (Dipp = 2,6- (i)Pr(2)C(6)H(3

180 ding the first anionic thioxoborane [K(2.2.2-crypt)][(HCDippN)(2)BS] (2), isoelectronic with thiocarb

181 -6 signaling in the gut epithelium regulates crypt homeostasis through the Paneth cells and the Wnt s

182 pleted in the small intestines, which showed crypt hyperplasia and dissociation of villous epithelium

183 . rodentium infection, manifested by reduced crypt hyperplasia, reduced epithelial expression of IL-6

184 ind that prior to the development of colonic crypt hyperplasia, T3SS-mediated intimate attachment is

185 Previous work showed that during colonic crypt hyperplasia, type III secretion system (T3SS)-medi

186 and MTG16-knockout intestines had increased crypt hyperproliferation and expansion of ISCs, but ente

187 The percentage of mice possessing dysplastic crypt in the recovery protocol among WT and Cld-1 Tg gro

188 xes (Ln=Nd, Sm; OTf=SO(3) CF(3) ) react with crypt in THF to form the THF-soluble complexes [Ln(III)

189 Examining 819 crypts in 4 mice, we found that 3.5% +/- 0.6% of all cry

190 Loss of MCL1 retained intestinal crypts in a hyperproliferated state and prevented the di

191 irradiation reduced numbers of proliferating crypts in Ah(Cre)/Met(fl/fl)/LacZ mice.

192 upled to cell proliferation rates within the crypts in all conditions.

193 ive crypts in WT DSS Recovery and dysplastic crypts in Cld-1 Tg Recovery.

194 ound healing pathways, and maintained viable crypts in colon explants from patients with inflammatory

195 re present in around 1% of normal colorectal crypts in middle-aged individuals, indicating that adeno

196 The method was applied to colonic crypts in Mus musculus, and enabled detection of mutant

197 D21(+)/CD35(+) myeloid cells surrounding the crypts in the colon mucosa.

198 N ligands, whereas EGF is expressed far from crypts in the villus epithelium.

199 malized cell-cell adhesion, and formation of crypts in tissue cultures.

200 by increasing the number of S phase cells in crypts in wild-type but not Cdkn1a(p21(CIP/WAF1))-/- mic

201 d DSS recovery protocol showing regenerative crypts in WT DSS Recovery and dysplastic crypts in Cld-1

202 e formation of chemical gradients across the crypts, including those of growth and differentiation fa

203 Crypts incubated with EGF or HGF expanded into self-orga

204 We established organoids from duodenal crypts, incubated them with labeled palmitate or acetate

205 c AhR knockout increases basal stem cell and crypt injury-induced cell proliferation and promotes col

206 Compared with villus afferents, crypt innervation exhibited a muted proximal-to-distal d

207 To convert these immature crypts into fully polarized, functional units with a bas

208 conclude that cell proliferation within the crypt is the primary force that drives cell migration al

209 Cell proliferation within small intestinal crypts is the principal driving force for cell migration

210 three-dimensional organoid assay in colonic crypts isolated from CR-infected mice revealed elevated

211 Dark maroon [K(crypt)](+) , [K(18-c-6)](+) , and [Cs(crypt)](+) salts o

212 markers, transiently arose from hypertrophic crypts known to facilitate regeneration.

213 neration of which is fueled by proliferative crypt Lgr5(+) intestinal stem cells (ISCs).

214 Shigella quickly colonizes epithelial crypt-like invaginations and demonstrates the essential

215 The large intestine, with its array of crypts lining the epithelium and diverse luminal content

216 s of chemical gradients along the intestinal crypt long axis can be generated, enabling scalable cult

217 r encoding RSPO1-Fc had significantly deeper crypts, longer villi, with increased EdU labeling, indic

218 th ATM inhibition prior to TBI was increased crypt loss within the intestine epithelium.

219 receptor 43-GLP-1 pathway in the intestinal crypts may be involved in the pathogenesis of normalizat

220 the colon demonstrated a rapid disruption of crypt morphology, aberrant proliferation, cell-death act

221 During postnatal development, crypts multiply via fission, generating 2 daughter crypt

222 of nonpeptidergic neurons innervated mucosal crypts, myenteric ganglia, and submucosa.

223 Ablation of crypt neurons in zebrafish resulted in increased suscept

224 ses, crypt fission and fusion could regulate crypt numbers during the lifetime of a mouse.

225 ority of gut colonization determines colonic crypt occupancy.

226 inal stem cells are located at the bottom of crypts of Lieberkuhn, where they express markers such as

227 increase in goblet cell numbers in the colon crypts of Zfp36(DeltaIEC) mice.

228 were only found in some individuals, in some crypts or during certain periods of life.

229 Using mouse in vitro crypt organoid and in vivo models, this study first demo

230 stem cell markers, and a failure of in vitro crypt organoid growth.

231 to IL-6 significantly reduced in vitro basal crypt organoid proliferation and budding, and in vivo si

232 dies demonstrated that IL-6-induced in vitro crypt organoid proliferation and crypt budding was abrog

233 st demonstrated that exogenous IL-6 promoted crypt organoid proliferation and increased stem cell num

234 livery of rhabdoviruses induces apoptosis in crypt OSNs via the interaction of the OSN TrkA receptor

235 n GI crypt cells, and SHP2 expression in the crypt Osx+ cells is critical for self-renewal and prolif

236 Ln(II) -in-crypt triflate complexes [Ln(II) (crypt)(OTf)(2) ].

237 to form the THF-soluble complexes [Ln(III) (crypt)(OTf)(2) ][OTf] with two triflates bound to the me

238 Simultaneous fabrication of 3875 crypts over a single membrane was developed.

239 as a tendency towards a larger decline in PC/crypt (P = 0.08) and lysozyme intensity (P = 0.08) in W1

240 Villus height and crypt perimeter were significantly decreased in colon ti

241 We measured villus height, crypt perimeter, and relative densities of enterochromaf

242 Mesenchymal cells in the crypt play indispensable roles in the maintenance of int

243 Different intestinal crypt populations dedifferentiate to provide new ISCs, b

244 loss of the proliferative capability of the crypt progenitor cells in vivo, lack of crypt base colum

245 iation-induced apoptotic death of intestinal crypt progenitor/stem (ICPS) and villus stromal cells th

246 ia cecal ligation and puncture had decreased crypt proliferation and increased crypt and villus apopt

247 GS Wnt in vivo reveals that adult intestinal crypt proliferation can be promoted by agonism of Fzd5 a

248 of villous epithelium-specific gene APOA4 to crypt proliferation gene Ki67, showed a similar signific

249 organized cell compartments, each decreasing crypt proliferation in the basal regions to negligible v

250 ared with unmanipulated littermates, whereas crypt proliferation was decreased.

251 contrast, depletion of stromal Rspo3 impairs crypt regeneration, even upon mild injury.

252 Since MSI1 has been shown to be crucial for crypt regeneration, this finding elucidates a pro-prolif

253 , these cells are recruited to contribute to crypt regeneration.

254 s]) that are localized to the SI villous and crypt region.

255 Pathological crypt remodeling plus extracellular S1P-signaling caused

256 d in the upper intestine, with enrichment in crypt-resident progenitor cells.

257 DZ creates a permeability barrier around the crypt restricting immune cells and harmful agents from m

258 oon [K(crypt)](+) , [K(18-c-6)](+) , and [Cs(crypt)](+) salts of the [Sc(NR2 )3 ](-) anion are formed

259 sis to form the monomeric Sc(2+) complex, [K(crypt)][Sc(NR2)3], was observed.

260 them and cover the scaffold surface with the crypt-shaped structures.

261 ) c-Cbl(+/+) mice, APC(Delta14/+) c-Cbl(+/-) crypts showed nuclear beta-catenin throughout the length

262 r of cartilage and an important regulator of crypt stem cell biology.

263 ubtypes, while maintenance of the intestinal crypt stem cell compartment involves only a limited subs

264 igases NEDD4 and NEDD4L are expressed in the crypt stem cell regions and regulate ISC priming by degr

265 trengthen cell-cell adhesion in normal adult crypt stem cells and colon cancer cells.

266 eneration of gastrointestinal organoids from crypt stem cells opens up the possibility of new researc

267 LGR5 ablation in colon cancer cells and crypt stem cells resulted in loss of cortical F-actin, r

268 Both receptors are coexpressed in intestinal crypt stem cells, bind to R-spondins (RSPOs) with high a

269 Enhanced proliferation of crypt stem cells, induction of anti-oxidant defence, sub

270 es of Wnt and RSPO ligands in the intestinal crypt stem-cell niche.

271 In profiling miRNA expression in SC-enriched crypt subsections isolated from fresh, normal surgical s

272 initrogen complex was not observed with this crypt system, but it did occur with the 18-crown-6 (crow

273 The isolated Ln(II) tris(amide) complex [K(crypt)][Tb(NR(2))(3)] (crypt = 2.2.2-cryptand), 1-Tb, re

274 (+) PDGFRA(lo) population present just below crypts that secretes the BMP antagonist Gremlin1.

275 rsible formation of an (N(2))(3-) complex [K(crypt)][(THF)(R(2)N)(2)Gd](2)[mu-eta(2):eta(2)-N(2)], 9-

276 then swim to pores and down into the deeper crypt tissues that they ultimately colonize.

277 show decreased villous height, crypt depth, crypt to villi ratio and expression of the proliferation

278 Expression of claudin-2 increased from crypt to villus tip (P < .001) and was up-regulated in C

279 tation and sequencing analyses of intestinal crypts to identify genes regulated by MTG16.

280 Sm(III) ions into the 2.2.2-cryptand ligand (crypt) to explore their reductive chemistry.

281 ng KC(8) in THF forms the neutral Ln(II) -in-crypt triflate complexes [Ln(II) (crypt)(OTf)(2) ].

282 red design principles to recapitulate native crypt-villi topography and luminal flow, Nikolaev et al.

283 B maintains a Cu gradient along the duodenal crypt-villus axis and buffers Cu levels in the cytosol o

284 I)/DLL1(HI) mesenchymal population lines the crypt-villus axis and is the source of the epidermal gro

285 sorption for each of the compounds along the crypt-villus axis, as well as confirming a proximal-dist

286 progenitors, compared with other cells along crypt-villus axis.

287 d populations of mesenchymal cells along the crypt-villus axis.

288 bottoms and their progeny differentiate near crypt-villus junctions.

289 ne expression thus accounting for a deranged crypt/villus axis development in CD.

290 chymal cells located at the large intestinal crypt, we established a novel method through which cells

291 In the context of the colorectal crypt, we see that mutations in APC can lead directly to

292 ntiation and dedifferentiation in intestinal crypts, we discuss here how self-renewing and other tiss

293 At the top of the crypts, we find a previously unknown absorptive cell, ex

294 Both villus and crypt were found to express Vdr and VDR target genes.

295 n 4 mice, we found that 3.5% +/- 0.6% of all crypts were in the process of fission, whereas 4.1 +/- 0

296 Their intestinal crypts were isolated and cultured as organoids.

297 Normal appearing single crypts were laser microdissected in placebo- and sulinda

298 cess of fission, whereas 4.1 +/- 0.9% of all crypts were undergoing crypt fusion.

299 une cells) that traffic into the light-organ crypts, where the population of V. fischeri cells reside

300 ote long-term health and self-renewal of the crypts which were assayed in situ by confocal fluorescen