ライフサイエンスコーパス: crypt cell

1 specific proliferative effects on intestinal crypt cells.

2 eth cell markers were maximally expressed in crypt cells.

3 d staining along the basolateral membrane of crypt cells.

4 ed iron incorporation into immature duodenal crypt cells.

5 while Klf5 is primarily in the proliferating crypt cells.

6 plaques were formed within a subset of basal crypt cells.

7 alized on the lateral and basal membranes in crypt cells.

8 d 2-3 times higher uptake of ionic iron than crypt cells.

9 mature absorptive rather than proliferative crypt cells.

10 no immunoreactive enzyme was present in the crypt cells.

11 he mRNA encoding isoform II was found in the crypt cells.

12 ng bone marrow and differentiated intestinal crypt cells.

13 cretion in a tissue culture model of colonic crypt cells.

14 contrast, Le(x) antigens were restricted to crypt cells.

15 ogene-induced senescence (OIS) of intestinal crypt cells.

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

17 either renew themselves or become committed crypt cells.

18 ent in villus cells but barely detectable in crypt cells.

19 otein restricted to proliferating intestinal crypt cells.

20 an colon tumor cells and "normal" intestinal crypt cells.

21 ly marks long-term BrdU-retaining intestinal crypt cells.

22 ated an increase in Wnt-activated intestinal crypt cells.

23 that annexin-II binds PG in situ in colonic crypt cells.

24 of 4E-BP1 in IEC-18 nontransformed rat ileal crypt cells.

25 onserved in T84 cells, models for intestinal crypt cells.

26 tracellular cAMP in villus cells, but not in crypt cells.

27 erved in the myenteric plexus and epithelial crypt cells.

28 integrity of the actomyosin cytoskeleton and crypt cell adhesion.

29 label retention by dividing small intestinal crypt cells after a four-week chase.

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

31 The primary coculture system of dental crypt cells also offers a system for the study of osteoc

32 ticipating in electrolyte transport, colonic crypt cells also synthesize and secrete a number of prot

33 NOS mRNA was up-regulated in both villus and crypt cells, although LPS-induced iNOS mRNA was more pro

34 turnover, with an increase in proliferating crypt cells and a decrease in their differentiated villo

35 n method to separate mature enterocytes from crypt cells and analyzed gene expression.

36 d the proliferation of surrounding wild-type crypt cells and drove their differentiation, thereby out

37 tigens in both undifferentiated proliferated crypt cells and in differentiated postmitotic villus-ass

38 is and the expression of PUMA and p53 in the crypt cells and intestinal stem cells.

39 , which reduces the proliferation of colonic crypt cells and potently suppresses intestinal tumour gr

40 h the transferrin receptor (TfR) in duodenal crypt cells and proposed that mutations in HFE attenuate

41 With this input, HFE enables the intestinal crypt cells and reticuloendothelial system to interpret

42 system in 2 dpf larvae, suggesting that the crypt cells and sensory cells in the neuromasts have sim

43 nd shows that tamoxifen induces apoptosis in crypt cells and that suppressing apoptosis alters lineag

44 ppreciably alter radiation damage to jejunal crypt cells and tissue involved in the development of ra

45 esicles (BBMV) were prepared from villus and crypt cells and uptake studies were performed using rapi

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

47 nd EGF-induced migration of small intestinal crypt cells, and that Rho proteins are essential element

48 ncluding blastic lymphocytes), and increased crypt cell apoptosis (more than 2 per 10 crypts).

49 m in the extent of radiation-induced jejunal crypt cell apoptosis, with female mice having higher lev

50 susceptibility to radiation-induced jejunal crypt cell apoptosis.

51 helium for up to 4 months, despite increased crypt cell apoptosis.

52 with epithelial architecture distortion and crypt cell apoptosis.

53 One reports that quiescent crypt cells are Paneth cell precursors.

54 ght to originate in the expansion of colonic crypt cells as a result of aberrant gene expression caus

55 ger colonic crypts and an expansion of Lgr5+ crypt cells at baseline.

56 amic, with proliferation of undifferentiated crypt cells balanced by terminal differentiation and cel

57 Sorting of crypt cells based on staining with anti-beta1 integrin a

58 y normal mucosa, in contrast to targeting of crypt cells by inheritance of an Apc(1638N) allele or ho

59 t was demonstrated that both the surface and crypt cells can perform secretory and absorptive functio

60 lycytidylic acid challenge and expression by crypt cells clearly distinguish Clr-a from the likewise

61 gether with biochemical evidence of NeuGc in crypt cells, correlated exactly with the ability of the

62 n the normal intestine, localizing mainly in crypt cells; d) iNOS inhibitors attenuated PAF-induced i

63 activity in IEC-18 nontransformed intestinal crypt cells determined that PKCalpha suppresses Id1 mRNA

64 r capture microdissection to isolate colonic crypt cells, differentiated surface epithelium, adenomas

65 dine pulse-chase, we find that proliferating crypt cells dilute the (15)N label, consistent with rand

66 ell proliferation, we determined the rate of crypt cell DNA synthesis by detection of 5-bromo-2-deoxy

67 Purified colonic crypt cells exhibiting epigenetic modulation of the tran

68 Endothelial, but not crypt, cells express FGF receptor transcripts, suggestin

69 section was used to isolate mouse intestinal crypt cells following SBR or sham operation.

70 sion specifically within adapting intestinal crypt cells following SBR.

71 sis significantly more often than intestinal crypt cells found in B[c]PhDE-treated Msh2(-/-) or Mlh1(

72 The crypt cell fraction exhibited dramatically higher transf

73 Crypt cells from Gp1 animals formed monolayers as well a

74 V (rhR4) protein protected normal intestinal crypt cells from IR-induced apoptosis by increasing the

75 Importantly, cdk2 activity was unchanged in crypt cells from p21(-/-) mice, which do not develop int

76 Cdk2 activity was increased in crypt cells from p27(Delta51/Delta51) mice, although cyc

77 their differentiation, thereby outcompeting crypt cells from the niche.

78 is list of differentially expressed adapting crypt cell genes with a generalized mouse gene expressio

79 the small intestine and colon by stimulating crypt cell growth and mucosal regeneration in DSS-treate

80 of inflammatory bowel disease by stimulating crypt cell growth, accelerating mucosal regeneration, an

81 cells but produces a marked amplification of crypt cells having a morphology intermediate between Pan

82 n of single Neurog3-labeled mouse intestinal crypt cells, hence deconstructing forward and reverse di

83 us enterotoxin B produces villus atrophy and crypt cell hyperplasia.

84 amine-starved and -sufficient rat intestinal crypt cells (IEC-6).

85 gene alters the proteome of normal-appearing crypt cells in a gene-specific manner, consistent with a

86 e provided a time line of differentiation of crypt cells in development of the olfactory system and d

87 icates a possible functional significance of crypt cells in early life stages of zebrafish.

88 as also maximally expressed in proliferating crypt cells in normal intestine.

89 depth, ornithine decarboxylase activity, and crypt cells in S-phase occurred between enteral intakes

90 equired for the maintenance of proliferating crypt cells in the intestinal epithelium.

91 We find that dividing crypt cells in the small intestines of APC(Min/+) mice e

92 and increase the proliferation of intestinal crypt cells in vitro.

93 nt signaling status, and in mouse intestinal crypt cells in vivo.

94 LF5 (IKLF/BTEB2) is limited to proliferating crypt cells, indicating a growth-promoting role.

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

96 thdrawal in IEC-18 nontransformed intestinal crypt cells, involving rapid disappearance of cyclin D1,

97 ch HFE mutations lead to inappropriately low crypt cell iron, with resultant stabilization of DMT1(IR

98 ay regulate B0AT1 in villus and SN2/SNAT5 in crypt cell is unknown.

99 The migration of crypt cells is accompanied by cellular differentiation t

100 monstrate that FGFBP1, produced by the upper crypt cells, is an essential factor for crypt proliferat

101 Crypt cells isolated from Gp2 animals failed to form the

102 Undifferentiated crypt cells isolated from mouse jejunum showed higher CD

103 ansferrin-bound iron from plasma by duodenal crypt cells, leading to up-regulation of transporters fo

104 Impairment of this process in duodenal crypt cells leads them to be iron poor and to signal the

105 thways were studied using a human intestinal crypt cell line (T84) grown in noncontact coculture with

106 examined directly using the IEC-18 immature crypt cell line as a model system.

107 PKC activation in the IEC-18 intestinal crypt cell line resulted in rapid downregulation of D-ty

108 udy, T84 cell monolayers, a human intestinal crypt cell line, and isolated human PMN were used to exa

109 s C, the tsFHI cells proliferate and display crypt cell markers.

110 the survivin/ABK cascade can explain delayed crypt cell maturation, expansion of proliferative cell p

111 ediated by B0AT1), while it is stimulated in crypt cells (mediated by SN2/SNAT5).

112 Villus height, crypt depth, and crypt cell mitoses were greater in jejunum of transgenic

113 are the result of a stimulus that increases crypt cell mitosis and augments cellular progression alo

114 In contrast, in crypt cells, Na-glutamine co-transport stimulation was r

115 Increased crypt cell numbers come at the expense of Lgr5(+) stem c

116 on of NKCC1 and BKa proteins was enhanced in crypt cells of hyper-aldosterone rats.

117 a(+)-H(+) exchange in the apical membrane of crypt cells of rat distal colon.

118 d chromosomal instability increased in colon crypt cells of the Apcmin/+/Sigirr-/- mice.

119 oliferation, is highly expressed in dividing crypt cells of the gastrointestinal epithelium, and is i

120 is expressed predominantly in the epithelial crypt cells of the gastrointestinal tract and is a membe

121 deoxyuridine incorporated into the nuclei of crypt cells of the ileum.

122 or that is highly expressed in proliferating crypt cells of the intestinal epithelium.

123 ression of hensin in the less differentiated crypt cells of the intestine and the basal cells of the

124 renal proximal convoluted tubular cells, and crypt cells of the small intestine as well as in cerebra

125 aled that LTA4 hydrolase is localized in the crypt cells of the small intestine, white pulp of the sp

126 at recipients showed apoptosis of epithelial crypt cells on day 3 posttransplant as determined by ter

127 The total crypt cell population as well as labeled M phase and S p

128 A nonlinear growth trajectory of the crypt cell population in the first nine days of zebrafis

129 TGF-beta-induced marker of a differentiated crypt cell population.

130 plain the shifts in pattern of proliferative crypt cell populations in early colon tumorigenesis, and

131 Lgr5 and Bmi1 are two molecular markers of crypt-cell populations that replenish all lineages over

132 methylhydrazine had no significant effect on crypt cell production rate nor on crypt area in the dist

133 venously infused EGF significantly increased crypt cell production rate, but the magnitude of the eff

134 E-cadherin or a secondary effect of reduced crypt cell production, another Fabp promoter was used to

135 e killed at 25 weeks and rates of intestinal crypt cell production, crypt size, and crypt fission wer

136 eased in epimorphin-/- mice due to augmented crypt cell proliferation and crypt fission during the ne

137 Decreased crypt cell proliferation and delayed ulcer healing in GM

138 adaptive response characterized by increased crypt cell proliferation and enhanced villus height and

139 of Lgr5(+) stem cells and greater amounts of crypt cell proliferation and expression of Myc (a target

140 In the intestinal epithelium, Notch promotes crypt cell proliferation and inhibits goblet cell differ

141 88-signaling pathway and result in increased crypt cell proliferation and intestinal stem cell number

142 leum, deletion of Gata6 caused a decrease in crypt cell proliferation and numbers of enteroendocrine

143 Markers of crypt cell proliferation are frequently employed in stud

144 irmed the positive action of this hormone on crypt cell proliferation but also demonstrated its key a

145 TbetaR-II:Fc treatment increased crypt cell proliferation but otherwise did not affect un

146 r study shows that Klf5 is a key mediator of crypt cell proliferation in the colon in response to pat

147 nto mice, the protein induced rapid onset of crypt cell proliferation involving beta-catenin stabiliz

148 modulate crypt stem cell number and promote crypt cell proliferation to help maintain gut homeostasi

149 Crypt cell proliferation was assessed by whole-mount mit

150 k between monocyte recruitment and increased crypt cell proliferation was further confirmed using a c

151 Crypt length, crypt cellularity and crypt cell proliferation were assessed in biopsies acqui

152 ement that regulates bacterial colonization, crypt cell proliferation, and epithelial cell regenerati

153 immune responses of nursery pigs, promoting crypt cell proliferation, and reducing the expression of

154 ia (TMCH), which induces colitis and massive crypt cell proliferation, in mice.

155 hydrazine, which are both known to stimulate crypt cell proliferation, on crypt fission in the rat in

156 GATA transcription factors are required for crypt cell proliferation, secretory cell differentiation

157 Homeostatic adult small intestinal crypt cell proliferation, survival, and canonical wingle

158 Excess of IGF-I increased crypt cell proliferation, whereas excess of growth hormo

159 as excess of growth hormone did not increase crypt cell proliferation.

160 ostasis through the modulation of intestinal crypt cell proliferation.

161 pontaneous inflammation or increased colonic crypt cell proliferation.

162 g in both secretory cell differentiation and crypt cell proliferation.

163 f cells per crypt by stimulating the rate of crypt cell proliferation.

164 cute colitis, associated with an increase in crypt cell proliferation.

165 ay have significant and different effects on crypt cell proliferation.

166 PDZ-binding motif protein driving epithelial crypt cells proliferation following damage, suggesting t

167 rly and on basolateral membranes of proximal crypt cells, providing evidence that annexin-II binds PG

168 Crypt cells rapidly absorbed labeled fatty acids, and me

169 Upon irradiation, Math1-deficient crypt cells regenerated and CBCs continued cycling.

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

171 section from either the villus epithelial or crypt cell regions of healthy human small intestinal muc

172 in villus cells, while SN2/SNAT5 levels from crypts cell remained unchanged.

173 hanism underlying its effect on normal colon crypt cells remains poorly understood.

174 nes lacking Gata4 and Cdx2 were deficient in crypt cell replication, whereas combined loss of Hnf4a a

175 sion of cell cycle inhibitors and intestinal crypt cell replication.

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

177 ion and secretion are present in surface and crypt cells, respectively.

178 (NKCC1) is a key component of the intestinal crypt cell secretory apparatus.

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

180 n S100 antibody that specifically recognizes crypt cells showed that S100-positive cells appear in ol

181 Jejunal crypt cell survival was decreased in those mice given si

182 em for the clonal growth of a single colonic crypt cell suspension could facilitate the identificatio

183 oportion (proliferative fraction) of colonic crypt cells that can proliferate; the other is a cell cy

184 ys showed that H7 IAVs bind to chicken colon crypt cells that express SLe(X) but fewer bind to mallar

185 type mice exposed to B[c]PhDE had intestinal crypt cells that underwent apoptosis significantly more

186 ansporters, B0AT1 in villus cells and SN2 in crypts cells that are uniquely altered in the chronicall

187 s of aberrant differentiation of uncommitted crypt cells-these differentiated toward the secretory ce

188 of Clr-a by intestinal epithelial cells and crypt cells throughout the gut.

189 The ability of these progenitor crypt cells to resist apoptosis and ensure restitution d

190 tal dynamics of one of the neuron types, the crypt cells, to determine whether they are differentiate

191 Indeed, Math1-deficient crypt cells tolerated in vivo Paneth cell loss and maint

192 C mutation carriers, indicating that a colon crypt cell under the one-hit state is already abnormal.

193 Jejunal crypt cells undergo apoptosis in response to ionizing ra

194 ecretion has been associated with changes in crypt cell volume, we hypothesized that CFTR-mediated ce

195 BBM, whereas the stimulation of SN2/SNAT5 in crypts cells was reversed secondary to restoration of af

196 Apoptotic positive crypt cells were 15-fold higher in WT-TPN versus TLR4KO-

197 By day 7 numerous apoptotic crypt cells were detected in allografts, but were rarely

198 eptor (MR) function in rat colon surface and crypt cells were examined.

199 y demonstrated that adipsin containing ileum crypt cells were increased in FGSI-treated rats.

200 Surprisingly, distal colonic crypt cells were not as responsive to elevated levels of

201 When isolated crypt cells were stained with the beta1-integrin antibod

202 Crypt cells were then isolated as single cells from norm

203 Villus and crypts cells were isolated from the rabbit intestine usi

204 effect of the HFE-beta2M complex in duodenal crypt cells, where the HFE-beta2M complex appears to fac

205 that this transcript is expressed in colonic crypt cells, whereas Northern blot analysis established

206 xpressed by liver macrophages and intestinal crypt cells, which behave as though they are relatively

207 press SLe(X) but fewer bind to mallard colon crypt cells, which do not express SLe(X); H7 IAVs bind e

208 r, treatment of non-transformed IEC-18 ileal crypt cells with PKC agonists has a biphasic effect on c

209 These defects are observed in normal crypt cells with wild-type levels of beta-catenin and, i