ライフサイエンスコーパス: intestinal stem cell

1 inal epithelium, and are therefore the small intestinal stem cell.

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

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

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

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

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

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

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

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

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

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

12 in starvation) and assayed both germline and intestinal stem cells.

13 fically, labels "classical" undifferentiated intestinal stem cells.

14 ssion of PUMA and p53 in the crypt cells and intestinal stem cells.

15 ich is required in germline, epithelial, and intestinal stem cells.

16 te from a rare population of putative CD133+ intestinal stem cells.

17 and has been implicated in the regulation of intestinal stem cells.

18 ne stem cells, hematopoietic stem cells, and intestinal stem cells.

19 se Akt and colocalizes with activated Akt in intestinal stem cells.

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

21 olic and proliferative signals in Drosophila intestinal stem cells.

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

23 regulator of postnatal epigenetic changes in intestinal stem cells.

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

25 5 reporter mice, we show that maintenance of intestinal stem cells after damage is severely impaired

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 signaling is required for the maintenance of intestinal stem cells and self-renewal of the intestinal

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

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

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

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

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

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

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

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

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

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

53 PI3K)/protein kinase B (AKT)/p53 axis in the intestinal stem cells as a novel molecular mechanism of

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

55 trands, and this appears to be a property of intestinal stem cells because they are extremely sensiti

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

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

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

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

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

61 dy was to explore the hypothesis that viable intestinal stem cells can be isolated as a side populati

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

63 nthase 2 (Ptgs2) is repositioned next to the intestinal stem cell compartment where local production

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

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

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

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

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

69 diation tissue damage, recent studies showed intestinal stem cell damage is conditionally linked to c

70 After gamma-irradiation, the survival of intestinal stem cells decreased significantly in APOBEC-

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

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

73 mportant gene regulation cascade controlling intestinal stem cell development.

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

75 o not decrease as descendants of multipotent intestinal stem cells differentiate.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 This result demonstrates that intestinal stem cells form an equipotent population in w

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

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

95 clooxygenase-1 (COX-1) and COX-2 protect the intestinal stem cells from IR.

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

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

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

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

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

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

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

103 s to model signals definitively that control intestinal stem cells have been difficult because of a l

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

105 mpact on understanding the regulation of the intestinal stem cell hierarchy during homeostasis and in

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

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

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

109 of PARP-1 in the in vivo damage response of intestinal stem cells in crypts of PARP-1-/- and control

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

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

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

113 sh that PARP-1 acts as a survival factor for intestinal stem cells in vivo and suggest a functional l

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

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

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

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

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

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

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

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

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

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

124 JAK/STAT signaling pathway in the Drosophila intestinal stem cell (ISC) lineage.

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

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

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

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

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

130 ve (Bmi1(+)) lineages, representing putative intestinal stem cell (ISC) populations, were present in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

151 Intestinal stem cells (ISCs) are regulated by the mesenc

152 Intestinal stem cells (ISCs) are the only cells in the a

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

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

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

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

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

158 Intestinal stem cells (ISCs) drive small intestinal epit

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

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

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

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

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

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

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

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

167 Intestinal stem cells (ISCs) in the Drosophila posterior

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

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

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

171 Intestinal stem cells (ISCs) maintain the midgut epithel

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

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

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

175 adult Drosophila midgut contains multipotent intestinal stem cells (ISCs) scattered along its basemen

176 Gut homeostasis is maintained by intestinal stem cells (ISCs) that divide to replenish th

177 is maintained by a population of multipotent intestinal stem cells (ISCs) that resides in epithelial

178 Intestinal stem cells (ISCs) undergo symmetric division

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

180 here, the adult Drosophila midgut, including intestinal stem cells (ISCs), develops from adult midgut

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

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

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

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

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

186 by a population of rapidly cycling (Lgr5(+)) intestinal stem cells (ISCs).

187 hat arise from a population of self-renewing intestinal stem cells (ISCs).

188 rease in the number of crypts, which contain intestinal stem cells (ISCs).

189 y replenished by a distinctive population of intestinal stem cells (ISCs).

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

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

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

193 The adult Drosophila midgut is maintained by intestinal stem cells (ISCs); however, how they are esta

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

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

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

197 Intestinal stem cells, located at the base of the intest

198 se that both these cell types represent true intestinal stem cells maintained in different states (qu

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

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

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

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

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

204 These experiments identify Bmi1 as an intestinal stem cell marker in vivo.

205 The intestinal stem cell marker Lgr5 is identified as a cand

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

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

208 ule-associated kinase DCAMKL-1 is a putative intestinal stem cell marker that is expressed in Apc(Min

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

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

211 e expression of cell lineage markers and the intestinal stem-cell marker, Musashi-1.

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

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

214 rypt-like proliferative zones that expressed intestinal stem cell markers.

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

216 The intestinal stem cell niche provides cues that actively m

217 pmental signaling pathways suggests that the intestinal stem cell niche regulates the activity of the

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

219 66 is highly expressed within the endogenous intestinal stem cell niche.

220 tinal mucosal morphogenesis, we consider the intestinal stem cell niche.

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

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

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

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

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

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

227 cription factors that might recruit Mtgr1 in intestinal stem cells or progenitor cells and found that

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

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

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

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

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

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

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

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

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

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

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

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

240 Intestinal stem cells require Wnt signaling, but the und

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

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

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

244 ng evidence suggests that hyperproliferating intestinal stem cells (SCs) and progenitors drive cancer

245 We investigated the role of PGs in mouse intestinal stem cell survival and proliferation followin

246 Lipopolysaccharide increases intestinal stem cell survival through apobec-1-mediated

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

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

249 any recent advances regarding the biology of intestinal stem cells, the field has been hampered signi

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

251 BMP signaling may control the duplication of intestinal stem cells, thereby preventing crypt fission

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

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

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

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

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

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

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

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

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

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

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

263 lipopolysaccharide before gamma-irradiation, intestinal stem cells were protected by marked increases

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

265 The identification of Drosophila intestinal stem cells with striking similarities to thei

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

267 emonstrate the increased radiosensitivity of intestinal stem cells within the crypts in IL-7R alpha(-

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