ライフサイエンスコーパス: intestinal stem cell

1 SRY-box transcription factor 9, a marker of intestinal stem cells.

2 , but little is known about its functions in intestinal stem cells.

3 olic and proliferative signals in Drosophila intestinal stem cells.

4 ed changes in 5-mC during differentiation of intestinal stem cells.

5 regulator of postnatal epigenetic changes in intestinal stem cells.

6 n enteroblasts to control niche signaling to intestinal stem cells.

7 roy is produced specifically by fast-cycling intestinal stem cells.

8 monstrated that Hopx is a specific marker of intestinal stem cells.

9 ay reduces the proliferative capacity of the intestinal stem cells.

10 reported that Bmi1 is a potential marker for intestinal stem cells.

11 that TLR4 is expressed on the Lgr5-positive intestinal stem cells.

12 turnover based on the asymmetric division of intestinal stem cells.

13 diate, and cell-autonomous target of Sox2 in intestinal stem cells.

14 f APC in governing the homeostasis of normal intestinal stem cells.

15 ly LGR4 is essential for the self-renewal of intestinal stem cells.

16 monolayer systems derived from human primary intestinal stem cells.

17 sential to maintain Wnt pathway activity and intestinal stem cells.

18 reted proteins that amplify Wnt signaling in intestinal stem cells.

19 d state and prevented the differentiation of intestinal stem cells.

20 um undergoes constant regeneration driven by intestinal stem cells.

21 ated the activity of the JAK-STAT pathway in intestinal stem cells.

22 The larval Drosophila midgut lacks dedicated intestinal stem cells.

23 hieved by Pol III inhibition specifically in intestinal stem cells.

24 LGR5-expressing cells can give rise to adult intestinal stem cells(3,4), it remains unclear whether t

25 How the niche regulates intestinal stem cell activity in both mammals and flies

26 5 reporter mice, we show that maintenance of intestinal stem cells after damage is severely impaired

27 uiescence, proliferation and regeneration of intestinal stem cells after injury.

28 fecundity, the more active and more numerous intestinal stem cells also increase female susceptibilit

29 s issue, O'Brien et al. demonstrate that fly intestinal stem cells alter their division patterns in r

30 g to groups of immune response, ion channel, intestinal stem cell and other growth signaling regulato

31 f TNF signaling in Wnt/beta-catenin-mediated intestinal stem cell and progenitor cell expansion in CD

32 In CD patients, intestinal stem cell and progenitor cell Wnt/beta-cateni

33 formation caused by loss of Apc and control intestinal stem cell and secretory cell homeostasis by d

34 Using transcriptomics on sorted intestinal stem cells and adult enterocytes, we identifi

35 ver, upregulated uncoupling protein UCP4C in intestinal stem cells and enteroblasts is sufficient to

36 Clevers and his associates identified intestinal stem cells and established conditions to grow

37 ally overexpressed in colon cancer cells and intestinal stem cells and is required for colon cancer c

38 ioning of the H3K79me2 mark in Lgr5(+) mouse intestinal stem cells and mature intestinal villus epith

39 small intestinal crypts, which contain both intestinal stem cells and mature villus cells.

40 e the impact of conditional Hey2 deletion on intestinal stem cells and microvascular compartment radi

41 ration, leading to hyperplasia, expansion of intestinal stem cells and niche cells, and formation of

42 ellular matrix to support in vitro growth of intestinal stem cells and organoids.

43 ted receptor delta (PPAR-delta) signature in intestinal stem cells and progenitor cells (non-intestin

44 plitude oscillations of circadian rhythms in intestinal stem cells and progenitor cells, indicating a

45 Although required for Lgr5+ intestinal stem cells and regeneration, Bcl9/9l deletion

46 Transcript profiles in isolated LGR5(+) intestinal stem cells and secretory and absorptive proge

47 tionship between proliferative and quiescent intestinal stem cells and support a model in which intes

48 ates the DNA damage response and survival of intestinal stem cells and support the concept that pharm

49 tion of the base-resolution DNA methylome in intestinal stem cells and their differentiated descendan

50 tect extensive dynamic epigenetic changes in intestinal stem cells and their progeny during the suckl

51 study the effect of TGF-beta on the Lgr5(+) intestinal stem cells and their progeny in intestinal ad

52 rogenitor cell populations to maintain adult intestinal stem cells and to regulate cell fate choice t

53 ates an isoform-specific function of CD44 in intestinal stem cells and tumorigenesis.

54 estinal stem cells and progenitor cells (non-intestinal stem cells), and pharmacological activation o

55 DVL signals in the nucleus of intestinal stem cells, and its forced expression leads t

56 formation of epithelial colonies from single intestinal stem cells, and rapid photodegradation is use

57 Intestinal stem cells are closely associated with a dive

58 While intestinal stem cells are critical for this regeneration

59 Adult intestinal stem cells are located at the bottom of crypt

60 n mouse models of intestinal cancer, LGR5(+) intestinal stem cells are major sources of cancer follow

61 educes their numbers, whereas the numbers of intestinal stem cells are unaffected by nematode infecti

62 The differences between fetal and adult intestinal stem cells are unclear, and understanding thi

63 etion of miR-34a/b/c increased the number of intestinal stem cells as well as Paneth and Goblet cells

64 g to decreases in the number and activity of intestinal stem cells as well as villus size and density

65 c stem cell activity, the sex differences in intestinal stem cell behaviour arise from intrinsic mech

66 summarize our current understanding of small intestinal stem cell biology and the current tools avail

67 ality of the dataset, and led to insights on intestinal stem cell biology, cell type-specific organel

68 Lats1/2 deletion leads to loss of intestinal stem cells but drives Wnt-uncoupled crypt exp

69 identified both proliferative and quiescent intestinal stem cells, but the molecular circuitry contr

70 stinal tissues of mice, PRC2 maintains small intestinal stem cells by promoting proliferation and pre

71 Notch signaling controls the fate of intestinal stem cells by regulating the expression of He

72 d it in CaCo-2 cells, a human cell line with intestinal stem cell characteristics.

73 al cells and proliferative exhaustion of the intestinal stem cell compartment compared with controls

74 we demonstrate that MSI2 is expressed in the intestinal stem cell compartment, that its expression is

75 g a potential role of Cftr in regulating the intestinal stem cell compartment.

76 ration and preventing differentiation in the intestinal stem cell compartment.

77 al epithelium play a major role in governing intestinal stem cell compartmentalization, differentiati

78 mice displayed complete loss of Lgr5+/Olfm4+intestinal stem cells, compromised Wnt signaling and imp

79 form mature human intestinal epithelium with intestinal stem cells contributing to the crypt-villus a

80 mediated transcription, thereby resulting in intestinal stem cell depletion and Wnt-uncoupled progeni

81 Human intestinal stem cell-derived enteroid monolayers co-cult

82 ors associated with the endocrine lineage of intestinal stem cell development.

83 mportant gene regulation cascade controlling intestinal stem cell development.

84 Thus, apparently similar intestinal stem cells differ regionally in cell producti

85 reveal a mechanism regulating intestinal stem cell differentiation and epithelial repa

86 ion and lineage-generating capacity of small intestinal stem cells, disrupting the supply of differen

87 ever, the molecular mechanisms that regulate intestinal stem cell division and epithelial homeostasis

88 al center protein kinase Misshapen restricts intestinal stem cell division by repressing the expressi

89 growth factors necessary to replicate adult intestinal stem cell division has led to the establishme

90 n stem cell progeny (ECs and EBs) stimulates intestinal stem cell division through modulation of JAK/

91 (neuroblast) and adult (female germline and intestinal stem cell) Drosophila melanogaster asymmetric

92 lly occurring mutations in Drosophila midgut intestinal stem cells during aging and find high-frequen

93 1) is up-regulated in and required for adult intestinal stem cells during metamorphosis.

94 nvolved in the T3-induced formation of adult intestinal stem cells during metamorphosis.

95 e developed a technique to follow changes in intestinal stem cell dynamics in human epithelial tissue

96 Clonal descendants of Cdx2(null) small intestinal stem cells enter the gastric differentiation

97 nbiased approach recovered most of the known intestinal stem cells/enteroblast and EE markers, highli

98 identified 22 distinct clusters representing intestinal stem cells, enteroblasts, enteroendocrine cel

99 blet and Paneth cell function, ion channels, intestinal stem cells, epidermal growth factor receptor

100 The cells expressed markers for intestinal stem cells, epithelial cells, and mature ente

101 reports that genetic removal of YAP enhances intestinal stem cell expansion and regeneration.

102 Zeilstra et al. report studies showing that intestinal stem cells express a specific CD44 variant th

103 has suboptimal Wnt pathway activity causing intestinal stem cell failure and that enhanced expressio

104 Our data indicate that human intestinal stem cells form de novo during development.

105 EVI and MDS/EVI are required for adult intestinal stem cell formation during postembryonic vert

106 The intestinal stem cell fuels the highest rate of tissue tu

107 Its role in the regulation of intestinal stem cell function and differentiation, howev

108 ceptor complexes and play a critical role in intestinal stem cell function in flies and mice.

109 ch pathway as a key regulator of gastric and intestinal stem cell function.

110 Moreover, these mice show signs of impaired intestinal stem cell function.

111 stablish that the loss of DNA methylation at intestinal stem cell gene enhancers causes inappropriate

112 anscription factor that controls the Lgr5(+) intestinal stem cell gene expression program.

113 teroids (HIEs), which are derived from human intestinal stem cells, grown ex vivo, and then different

114 In addition to the Lgr5 marker, intestinal stem cells have been associated with other ma

115 d interaction of proliferating and quiescent intestinal stem cells have been debated since their disc

116 Although Lgr5(+) intestinal stem cells have been expanded in vitro as org

117 te the importance of Wnt signaling for adult intestinal stem cell homeostasis and colorectal cancer,

118 our understanding of metabolic regulation in intestinal stem cell homeostasis.

119 vious Wnt pathway activity, that perpetuates intestinal stem cell identity in response to Wnt/R-spond

120 (a Wnt target gene) is a master regulator of intestinal stem cell identity.

121 For the first time mouse small intestinal stem cells in intact live crypts are identifi

122 Proliferation of intestinal stem cells in MCL1-deficient mice required WN

123 dly, Wnt3 was dispensable for maintenance of intestinal stem cells in mice, indicating a redundancy o

124 port that Lin-28 is highly enriched in adult intestinal stem cells in the Drosophila intestine.

125 ich stimulates the division and expansion of intestinal stem cells in two distinct proliferative phas

126 nt of intestinal organoids from single adult intestinal stem cells in vitro recapitulates the regener

127 roliferative phenotype seen in Apc defective intestinal stem cells in vivo.

128 In the adult Drosophila midgut, intestinal stem cells interpret a nutrient cue to "break

129 Self-renewal of intestinal stem cells is controlled by Wingless/Wnt-beta

130 s is required upon infection to promote full intestinal stem cell (ISC) activation and regeneration,

131 ll populations have been reported to possess intestinal stem cell (ISC) activity during homeostasis a

132 Ca(2+) signalling as a central regulator of intestinal stem cell (ISC) activity in Drosophila.

133 interference (RNAi) screen for regulators of intestinal stem cell (ISC) activity in the Drosophila mi

134 of WNT ligands but their origin and role in intestinal stem cell (ISC) and epithelial repair remains

135 Intestinal stem cell (ISC) are believed to contribute to

136 SH3PX1 restrains intestinal stem cell (ISC) division through an endocytos

137 ale undergoes major deterioration, driven by intestinal stem cell (ISC) division, while lower ISC act

138 n fruit flies, juvenile hormone (JH) induces intestinal stem cell (ISC) driven absorptive epithelial

139 This is characterized by intestinal stem cell (ISC) expansion as shown by an inos

140 nits of the Osa-containing complex result in intestinal stem cell (ISC) expansion as well as enteroen

141 g pathways, energy metabolism also regulates intestinal stem cell (ISC) function.

142 e to tissue damage is crucial in maintaining intestinal stem cell (ISC) homeostasis.

143 quired for the initiation and maintenance of intestinal stem cell (ISC) hyperproliferation following

144 ne silencing and activation are critical for intestinal stem cell (ISC) maintenance and differentiati

145 hway activity and that Gish is essential for intestinal stem cell (ISC) maintenance under stress cond

146 Both are necessary for intestinal stem cell (ISC) maintenance, and R-spondins a

147 The intestinal stem cell (ISC) marker LGR5 is a receptor for

148 chromatin remodeler Kismet/CHD7/CHD8 limits intestinal stem cell (ISC) number and proliferation with

149 We apply this model to the adult intestinal stem cell (ISC) of Drosophila, the fate of wh

150 Intestinal stem cell (ISC) plasticity is thought to be r

151 Although quiescent intestinal stem cell (ISC) populations have been describ

152 apid advance in identifying the once elusive intestinal stem cell (ISC) populations that fuel the con

153 Epidermal growth factor (EGF) maintains intestinal stem cell (ISC) proliferation and is a key co

154 or stress and it is exclusively required for intestinal stem cell (ISC) proliferation during tissue r

155 hat Src is necessary and sufficient to drive intestinal stem cell (ISC) proliferation during tissue s

156 ) signaling in enteroblasts (EBs) to promote intestinal stem cell (ISC) proliferation in Drosophila m

157 naling is also involved in the modulation of intestinal stem cell (ISC) proliferation in response to

158 ndocrine cells acting as local regulators of intestinal stem cell (ISC) proliferation through modulat

159 Wnt/beta-catenin signaling controls intestinal stem cell (ISC) proliferation, and is aberran

160 ease rates of Drosophila melanogaster midgut intestinal stem cell (ISC) proliferation, it is largely

161 be both necessary and sufficient to trigger intestinal stem cell (ISC) proliferation.

162 oupled receptor 5 (Lgr5)(+) cells within the intestinal stem cell (ISC) region.

163 ium-derived BMP serves as a niche signal for intestinal stem cell (ISC) self-renewal in Drosophila ad

164 vated Wnt/beta-catenin signaling and greater intestinal stem cell (ISC) self-renewal.

165 t RAC1 is required for expansion of the LGR5 intestinal stem cell (ISC) signature, progenitor hyperpr

166 ining G protein-coupled receptor 5 (LGR5)(+) intestinal stem cell (ISC) survival through NOD2 activat

167 roendocrine (EE) cells are generated from an intestinal stem cell (ISC).

168 via Apc inactivation in crypt base columnar intestinal stem cells (ISC) led to their rapid accumulat

169 th cells, a key constituent of the mammalian intestinal stem-cell (ISC) niche, augment stem-cell func

170 ized that genes shared between NF-kappaB and intestinal stem cell (ISCs) signatures might identify co

171 ells: slow cycling, injury-resistant reserve intestinal stem cells (ISCs) and actively proliferative

172 ology is the intrinsic immortality of normal intestinal stem cells (ISCs) and culture systems that ma

173 pent enterocytes (ECs) relies on division of intestinal stem cells (ISCs) and differentiation of thei

174 sophila, we identified expression of RalA in intestinal stem cells (ISCs) and progenitor cells of the

175 Little is known about the maintenance of intestinal stem cells (ISCs) and progenitors during immu

176 Here we show that NMS induces expansion of intestinal stem cells (ISCs) and their differentiation t

177 idgut, the Snail homolog Esg is expressed in intestinal stem cells (ISCs) and their transient undiffe

178 Intestinal stem cells (ISCs) are confined to crypt botto

179 In Drosophila, intestinal stem cells (ISCs) are essential for homeostat

180 Intestinal stem cells (ISCs) are highly proliferative ce

181 Intestinal stem cells (ISCs) are maintained by a niche m

182 Functions of intestinal stem cells (ISCs) are regulated by diet and m

183 testinal epithelium, but specific effects on intestinal stem cells (ISCs) are undefined.

184 However, the population of putative small intestinal stem cells (ISCs) at position +4 from the cry

185 We address the mechanism by which adult intestinal stem cells (ISCs) become localized to the bas

186 ce, we confirm the regenerative potential of intestinal stem cells (ISCs) but find limited roles for

187 ds, Dpp and Gbb, which drive an expansion of intestinal stem cells (ISCs) by promoting their symmetri

188 t, the surrounding visceral muscle maintains intestinal stem cells (ISCs) by stimulating Wingless (Wg

189 Intestinal stem cells (ISCs) drive small intestinal epit

190 We found that intestinal stem cells (ISCs) expressed Slit2 and its sin

191 tissue in the human body thanks to a pool of intestinal stem cells (ISCs) expressing Lgr5 The intesti

192 Drosophila intestinal stem cells (ISCs) generate enterocytes (ECs)

193 Identification of intestinal stem cells (ISCs) has relied heavily on the u

194 Intestinal stem cells (ISCs) in the adult Drosophila mel

195 Intestinal stem cells (ISCs) in the adult Drosophila mid

196 Here, we show that after severe depletion, intestinal stem cells (ISCs) in the Drosophila midgut ar

197 Intestinal stem cells (ISCs) in the Drosophila posterior

198 cells and quiescent Bmi1(+) cells behave as intestinal stem cells (ISCs) in vivo.

199 Ablation of LGR5(+) intestinal stem cells (ISCs) is associated with rapid re

200 Here, we show that mTORC1 signaling in intestinal stem cells (ISCs) is instead upregulated duri

201 Rapidly cycling LGR5+ intestinal stem cells (ISCs) located at the base of cryp

202 Intestinal stem cells (ISCs) maintain regenerative capac

203 Intestinal stem cells (ISCs) maintain the midgut epithel

204 Drosophila adult midgut intestinal stem cells (ISCs) maintain tissue homeostasis

205 factor 4 (KLF4) activates certain quiescent intestinal stem cells (ISCs) marked by Bmi1-Cre(ER) to g

206 ctron transport chain (ETC) complexes in the intestinal stem cells (ISCs) of Drosophila.

207 In insects and vertebrates, intestinal stem cells (ISCs) regenerate the GI epitheliu

208 cellular cues that regulate the apoptosis of intestinal stem cells (ISCs) remain incompletely underst

209 egulating the proliferation and apoptosis of intestinal stem cells (ISCs) remain incompletely underst

210 sponses and the impact of these responses on intestinal stem cells (ISCs) remain unclear.

211 Intestinal stem cells (ISCs) undergo symmetric division

212 romatin remodelling proteins are enriched in intestinal stem cells (ISCs), although their function in

213 ich is fueled by proliferative crypt Lgr5(+) intestinal stem cells (ISCs).

214 in PRC2-null villus cells, remain silent in intestinal stem cells (ISCs).

215 istance in colorectal cancer (CRC) cells and intestinal stem cells (ISCs).

216 Notch signaling maintains intestinal stem cells (ISCs).

217 Lgr5 marks mitotically active intestinal stem cells (ISCs).

218 issues in Drosophila melanogaster, including intestinal stem cells (ISCs).

219 and the current tools available for studying intestinal stem cells (ISCs).

220 is known about the effects of L-arginine on intestinal stem cells (ISCs).

221 gut is constantly replenished by multipotent intestinal stem cells (ISCs).

222 d continuous regeneration supported by crypt intestinal stem cells (ISCs).

223 ting and regenerating Paneth cells (PCs) and intestinal stem cells (ISCs).

224 rrent concept is that there are two pools of intestinal stem cells (ISCs): an actively cycling pool t

225 the intestinal epithelium is coordinated by intestinal stem cells (ISCs); dietary and metabolic fact

226 ted by Wnt signaling and highly expressed by intestinal stem cells [ISCs] and adenomas) affects intes

227 on of Yorkie, the Yap1 oncogene ortholog, in intestinal stem cells leads to wasting of the ovary, fat

228 to maintain its integrity, and Lgr5-positive intestinal stem cell (Lgr5(+)ISC) resilience following c

229 ploiting Bellymount's capabilities, we track intestinal stem cell lineages and gut microbial coloniza

230 These cells derive from the columnar intestinal stem cell located at position 0 and the trans

231 nt self renewal and differentiation of adult intestinal stem cells maintains a functional intestinal

232 AM10 deletion on cell fate specification and intestinal stem cell maintenance.

233 Although essential for intestinal stem-cell maintenance and adenoma formation,

234 Identification of Lgr5 as the intestinal stem cell marker as well as the growth factor

235 (LRIG1) is a pan-ErbB negative regulator and intestinal stem cell marker down-regulated in many malig

236 The intestinal stem cell marker lgr5 was identified as a nov

237 nd fluorescent in situ hybridization for the intestinal stem cell marker Lgr5, we demonstrate that TL

238 ning G-protein-coupled receptor 5 (LGR5), an intestinal stem cell marker, is known to exhibit tumor s

239 Olfactomedin 4 (OLFM4) has emerged as an intestinal stem-cell marker, but its biological function

240 n nuclear localization, and induction of the intestinal stem cell markers Lgr5 and Musashi-1 and the

241 ve LIN28B expression increases expression of intestinal stem cell markers LGR5 and PROM1 in the prese

242 re, we examined the effect of disrupting the intestinal stem cell niche by inducible deletion of the

243 The intestinal stem cell niche provides cues that actively m

244 The human intestinal stem cell niche supports self-renewal and epi

245 analysis of Foxl1-positive telocytes in the intestinal stem cell niche, and, finally, the current ch

246 stinal tumor suppressor by regulation of the intestinal stem cell niche.

247 al function, PCs serve as a component of the intestinal stem cell niche.

248 ells completely or permanently; defining the intestinal stem-cell niche requires clarity with respect

249 pletely rescues lin-28-associated defects in intestinal stem cell number and division pattern.

250 lt in increased crypt cell proliferation and intestinal stem cell number.

251 Although Lgr5-positive intestinal stem cell numbers remained constant in Msi1-o

252 ic population of adult midgut organ-boundary intestinal stem cells (OB-ISCs) is regulated by the neig

253 augments the numbers and function of Lgr5(+) intestinal stem cells of the mammalian intestine.

254 pling drugs also extend lifespan and inhibit intestinal stem cell overproliferation due to aging or e

255 anding the regulatory mechanisms controlling intestinal stem cell physiology is of great importance.

256 al gut tube-contribute actively to the adult intestinal stem cell pool.

257 In particular, the small intestinal stem cell populations identified as the crypt

258 n the patterned epithelium represents unique intestinal stem-cell precursors.

259 l fate specification, and the maintenance of intestinal stem cell/progenitor populations.

260 The overexpression of msi promoted intestinal stem cell proliferation, which increased surv

261 of EGFR signaling cell autonomously controls intestinal stem cell proliferation, with implications fo

262 ap polypeptide levels are necessary to drive intestinal stem cell proliferation.

263 cellent template to study how alterations in intestinal stem cells promote trans-differentiation, cry

264 Surprisingly, of the cells analyzed only the intestinal stem cell protects itself by segregating HNE

265 inal stem cells and support a model in which intestinal stem cell quiescence is maintained by calibra

266 de-induced endothelial cell apoptosis boosts intestinal stem cell radiosensitivity.

267 rs have been shown to play a central role in intestinal stem cell regeneration and, more recently, in

268 ch-wound closure in vitro, increases Lgr5(+) intestinal stem cell regeneration following radiation-in

269 that the activation of TLR4 directly on the intestinal stem cells regulates their ability to prolife

270 he EPHB3 gene that integrates input from the intestinal stem-cell regulator achaete-scute family basi

271 nonical WNT signaling pathway is crucial for intestinal stem cell renewal and aberrant WNT signaling

272 he transcription factor YY1 is essential for intestinal stem cell renewal.

273 e known neutral-drift dynamics that describe intestinal stem cell replacement, we quantify the number

274 Intestinal stem cells require Wnt signaling, but the und

275 Intestinal stem cells reside at the base of the crypt, w

276 cally maintain self-renewal of mouse Lgr5(+) intestinal stem cells, resulting in nearly homogeneous c

277 t mutations of B-catenin (Ctnnb1) within the intestinal stem cell results in widespread expansion of

278 progenitors were well demarcated in LGR5(+) intestinal stem cells, revealing early priming of chroma

279 These aging phenotypes are recapitulated in intestinal stem cell-specific Tsc1 knockout mice.

280 intestine is maintained by actively cycling intestinal stem cells that are regulated by the Paneth c

281 length by superficially similar, multipotent intestinal stem cells that generate new enterocytes and

282 that are rapidly and continually renewed by intestinal stem cells that reside near the base of the c

283 s their growth and promotes proliferation of intestinal stem cells that retain the APC protein; these

284 Since the discovery of LGR5 as a marker of intestinal stem cells, the field has developed explosive

285 paired Wnt signaling and concomitant loss of intestinal stem cells, this phenotype was not reversed u

286 atous polyposis coli (APC) causes Drosophila intestinal stem cells to form adenomas [9].

287 d find that differentiation of mouse colonic intestinal stem cells to intestinal epithelium is not as

288 e (EGFR/MAPK) signalling triggers Drosophila intestinal stem cells to produce enteroblasts (EBs) and

289 ing agent temozolomide caused MSH2-deficient intestinal stem cells to proliferate more rapidly than w

290 Cholinergic blockade reduces Lgr5-positive intestinal stem cell tracing and cell number.

291 ic reversals of the sexual identity of adult intestinal stem cells uncovers the key role this identit

292 ion and consequent cellular proliferation in intestinal stem cells upon initial ingestion into the mu

293 Here we establish the short-term dynamics of intestinal stem cells using the novel approach of contin

294 Because Wnt signaling plays a key role in intestinal stem cells, we analyzed the effects of Wnt si

295 -regulated during the formation of the adult intestinal stem cells, we cloned the Xenopus PRMT1 promo

296 The MSH2-deficient intestinal stem cells were able to colonize the intestin

297 gely intact in Aim2-deficient mice; however, intestinal stem cells were prone to uncontrolled prolife

298 ary sulindac induced apoptosis to remove the intestinal stem cells with nuclear or phosphorylated bet

299 od is critical for epigenetic development of intestinal stem cells, with potential important implicat

300 ductal epithelia, which are connected to the intestinal stem-cell zone.