ライフサイエンスコーパス: endocrine cell

1 o (hepatocytes) and in vivo (hepatocytes and endocrine cells).

2 pancreatic cells (including functional islet endocrine cells).

3 novel mutational signature in healthy aging endocrine cells.

4 activating other MAP kinases in neuronal and endocrine cells.

5 , rather than promoted, growth in pancreatic endocrine cells.

6 e pancreas, ST18 expression is restricted to endocrine cells.

7 atively regulates the proliferation of early endocrine cells.

8 ral mucous cells, and a diversity of gastric endocrine cells.

9 fect the specification of hormone-expressing endocrine cells.

10 sing neuronal genes during the maturation of endocrine cells.

11 rbohydrate, lipid and protein sensing in gut endocrine cells.

12 s most radioactivity remained trapped in the endocrine cells.

13 he regulated secretory pathway of neural and endocrine cells.

14 urther develops in vivo to mature pancreatic endocrine cells.

15 e paracrine cholinergic input to surrounding endocrine cells.

16 large islets consisting of several thousand endocrine cells.

17 sting oscillations are common in neurons and endocrine cells.

18 ductal cells, centroacinar cells (CACs) and endocrine cells.

19 mediate cAMP-stimulated exocytosis in other endocrine cells.

20 ined to become the adult midgut is devoid of endocrine cells.

21 trapancreatic duct is the main source of new endocrine cells.

22 ches (termed periphery), produces most islet endocrine cells.

23 on and repression of cytokines in pancreatic endocrine cells.

24 ration and antiapoptosis in nonendocrine and endocrine cells.

25 eatic development and the differentiation of endocrine cells.

26 and wild-type prohormones in CNS neurons and endocrine cells.

27 iposity via interactions with epithelial and endocrine cells.

28 ear whether FoxO1+ Ins(-) cells give rise to endocrine cells.

29 ols cell migration and cell-cell adhesion in endocrine cells.

30 of genes that are specifically expressed in endocrine cells.

31 ed to epithelial and chromogranin A-positive endocrine cells.

32 f differentiated cells, including goblet and endocrine cells.

33 s found in secretory vesicles in neurons and endocrine cells.

34 iate or become reprogrammed into other islet endocrine cells.

35 ions of cellular heterogeneity in pancreatic endocrine cells.

36 notropin (alpha-MSH)], and with somatolactin endocrine cells.

37 sma and for assaying hormone secretions from endocrine cells.

38 G3 is sufficient for formation of pancreatic endocrine cells.

39 ted lineage-specific generation of acinar or endocrine cells.

40 three epithelial tissues: a partial loss of endocrine cells, a disrupted ductal tree and a >90% defi

41 vity and differentiation of gastrointestinal endocrine cells, a relatively quiescent cell population,

42 late blood glucose homeostasis by regulating endocrine cell activity in the pancreatic islets of Lang

43 acing, we demonstrated that CACs do form new endocrine cells after beta-cell ablation or partial panc

44 lines were unable to form mature pancreatic endocrine cells after engraftment of PDX1(+)/NKX6.1(+) p

45 lls efficiently generates glucose-responsive endocrine cells after implantation into mice.

46 gets of NeuroD1 in intestinal and pancreatic endocrine cells, all show similar promoter occupancy by

47 trointestinal (GI) hormones from specialized endocrine cells along the GI tract.

48 natally, an increase in the proliferation of endocrine cells also participates in their expansion.

49 We identified 118 alpha, 105 beta, 6 delta endocrine cells and 47 exocrine cells.

50 ndividual DCVs has been imaged in vitro with endocrine cells and at the neuron soma, growth cones, ne

51 lls, representative of developing pancreatic endocrine cells and beta-cells, respectively, was also d

52 ration and differentiation of epithelial and endocrine cells and cancers.

53 at levels found in postmitotic neuronal and endocrine cells and do not support PACAP-mediated neuros

54 potent by embryonic day 13.5, giving rise to endocrine cells and ductal cells.

55 However, endocrine cells and ducts are largely spared.

56 derm of the early embryo where precursors of endocrine cells and enterocytes of the larval midgut, as

57 hannels are widely expressed in neuronal and endocrine cells and generate slowly activating K+ curren

58 TSG-6 was observed within the islet endocrine cells and in inflammatory infiltrates.

59 sed predominantly on hepatocytes, pancreatic endocrine cells and intestinal cells.

60 le membrane protein expressed in neurons and endocrine cells and involved in the regulation of neurot

61 ulates incretin hormone release from colonic endocrine cells and is implicated in macrophage and adip

62 ed robustly upon differentiation into mature endocrine cells and localized to both alpha and beta cel

63 merging is mediated is poorly understood in endocrine cells and neurons containing small approximate

64 enhances Ca2+-triggered exocytosis from both endocrine cells and neurons, however the relevant target

65 Notch signaling represses differentiation of endocrine cells and promotes proliferation of Nkx6-1(+)P

66 n secretory granules which store hormones in endocrine cells and release them upon cell stimulation.

67 ut does affect the lineage commitment of the endocrine cells and their maturation.

68 Markers of endocrine cells and their progenitors were studied by im

69 om proteins present in secretory granules of endocrine cells, and a number were shared with cells of

70 cts in all pancreatic lineages, although the endocrine cells, and especially the insulin-producing be

71 ure and give rise to hepatocytes, pancreatic endocrine cells, and intestinal epithelial cells when tr

72 levels of endogenous GLP-1 secreted from gut endocrine cells are capable of augmenting glucoregulator

73 erentiation is reduced in Sox2 mutants, some endocrine cells are generated, such as POMC-positive cel

74 Endocrine cells are properly specified in Tshz1-null emb

75 in pancreatic progenitors results in reduced endocrine cell area at birth due to impaired endocrine c

76 In conclusion, although endocrine cells arise from the Sox9(+) ductal domain thr

77 of the developing pancreas (associated with endocrine cells) as early as embryonic day 12.5 (E12.5)

78 ctroscopic features suggestive of pancreatic endocrine cells, as well as assessing the homogeneity of

79 A further objective was to identify endocrine cell biomarkers, targets of diabetic autoimmun

80 e cells nonautonomously regulate the flux of endocrine cell birth as well as proliferative growth of

81 +) pancreatic progenitors (PPs) give rise to endocrine cells both in vitro and in vivo.

82 ptide 1 (GLP-1) is expressed not only in gut endocrine cells, but also in cells in the caudal brainst

83 tion from a ductal progenitor to a committed endocrine cell by repressing a progenitor cell program a

84 s competent to differentiate into ductal and endocrine cells by inducing activators of cell different

85 dicate that CACs are more closely related to endocrine cells by lineage as they share a common progen

86 neurotransmitter secretion from neuronal and endocrine cells by pharmacological and molecular manipul

87 ndicate that fully differentiated pancreatic endocrine cells can be created via stepwise differentiat

88 ting insulin(+) cells, suggesting that islet endocrine cells can intercalate into hyperplastic ducts

89 ntified multifocal aberrant crypt-containing endocrine cell clusters (ACECs) that contain crypt EC ce

90 within islets compared with sub-islet-sized endocrine cell clusters and among pancreatic lobes.

91 for proliferation of beta-cells within small endocrine cell clusters located in the regenerating port

92 y system to pancreas, with formation of many endocrine cell clusters of the type found in normal isle

93 n recently diabetic mice revealed an altered endocrine cell composition that is consistent with a pro

94 est and most diverse population of mammalian endocrine cells, comprise a number of different cell typ

95 Notably, postnatal expansion of the endocrine cell content was extremely poor, and the mutan

96 Very small numbers of non-beta endocrine cells continue to arise from Sox9(+) cells in

97 the gene encoding Foxo1 in mouse intestinal endocrine cells converts them into cells synthesizing an

98 Endocrine cells costaining for insulin and glucagon were

99 We propose that dedifferentiation trumps endocrine cell death in the natural history of beta cell

100 ally, in vitro differentiation of pancreatic endocrine cells derived from human pluripotent stem cell

101 velopment within pancreatic islets, in which endocrine cell-derived VEGF directs the patterning of in

102 tiation diminishes shortly after birth, when endocrine cells detach from the epithelial lining of the

103 novel and conserved role of Arx in mammalian endocrine cell development and provide a potential cause

104 In contrast, neither endocrine cell development nor function was affected in

105 The third step of entero-endocrine cell development takes place at a mid-pupal st

106 etter define the role of Insm1 in pancreatic endocrine cell development we generated mice with an Ins

107 d several transcription factors important in endocrine cell development, including Ngn3, MafA, and Pd

108 on factor involved in duct morphogenesis and endocrine cell development, is downstream Hnf1b.

109 advances in our understanding of pancreatic endocrine cell development, the function of the pancreat

110 expression during late stages of pancreatic endocrine cell development.

111 rt of the secondary transition of pancreatic endocrine cell development.

112 d a reduction, but not a loss, of pancreatic endocrine cell development.

113 ebrafish pancreas matures, hormone-producing endocrine cells differentiate from pancreatic Notch-resp

114 To test whether increased endocrine cell differentiation affected the development

115 ct temporal requirements for Hh signaling in endocrine cell differentiation and describe a dynamic Gl

116 f Pax4 opened new avenues of research in the endocrine cell differentiation and diabetes fields.

117 E16.5, the increased EC population perturbed endocrine cell differentiation and islet cell clustering

118 endocrine cell area at birth due to impaired endocrine cell differentiation and reduced prenatal prol

119 te during epithelial maturation within which endocrine cell differentiation is continually robust and

120 gulate early endoderm patterning and gastric endocrine cell differentiation upstream of the transcrip

121 tiation, with inhibition inducing mucous and endocrine cell differentiation while activation reduced

122 3 (Ngn3) plays a critical role in pancreatic endocrine cell differentiation, although regulation of N

123 ancreatic anlage, a blockage of exocrine and endocrine cell differentiation, and an arrest at the pri

124 Neurog3 is required not only for initiating endocrine cell differentiation, but also for promoting i

125 In pancreatic endocrine cell differentiation, Ngn3 first activates INS

126 r transcription factors required for gastric endocrine cell differentiation, Pdx1, Pax6, and Ngn3; co

127 roper induction of NEUROG3 and initiation of endocrine cell differentiation.

128 play strong inhibitory effects on subsequent endocrine cell differentiation.

129 ranscription factor Ngn3, a key regulator of endocrine cell differentiation.

130 tly different from humans, canine pancreatic endocrine cell distribution is more similar.

131 other major pancreatic cell types including endocrine cells, duct cells and endothelial cells.

132 Mechanisms of the expansion of endocrine cells during embryonic development are not com

133 f, like Pax6, is expressed in all pancreatic endocrine cells during mouse postnatal development and i

134 ferentiation into enterocytes (EC) or entero-endocrine cells (EE).

135 ly, in vivo- but not in vitro-differentiated endocrine cells exhibit close similarity to primary huma

136 t the in vivo maturation period hESC-derived endocrine cells exhibited gene and protein expression pr

137 Pancreatic endocrine cells expand rapidly during embryogenesis by n

138 filing showed that that the Dicer1-deficient endocrine cells expressed neuronal genes before the onse

139 -enriched pattern of Ldb1 was similar to pan-endocrine cell-expressed Islet-1 (Isl1), which was demon

140 ers are closely associated with gonadotropic endocrine cells [expressing luteinizing hormone (LH) and

141 a noncanonical action for Notch2 protein in endocrine cell fate selection, and demonstrate that acqu

142 s express NEUROG3 but do not adopt alternate endocrine cell fates.

143 h, we demonstrated these progenitors produce endocrine cells following inhibition of RA signaling.

144 These new endocrine cells form small clusters known as secondary (

145 of the challenging organs to study, in which endocrine cells form various sizes of islets that are sc

146 ROD1 promoter in vitro and to induce ectopic endocrine cell formation and cell delamination after in

147 Dnmt1 is dispensable for pancreatic duct or endocrine cell formation, but not for acinar cell surviv

148 e RT-PCR, to simultaneously track pancreatic endocrine cell frequencies and phenotypes during a T-cel

149 squamous cells, parietal, chief and gastric endocrine cells from a pre-patterned gastric progenitor

150 We find that islet endocrine cells from older donors display increased leve

151 ress the origination of secondary transition endocrine cells from the ducts.

152 expression, thereby allowing delamination of endocrine cells from the trunk epithelium and revealing

153 rotransmitters may extend beyond controlling endocrine cell function to work as signals modulating va

154 Analysis of endocrine cell gene expression in the absence of neural

155 NEUROG3, is an essential variable in normal endocrine cell genesis.

156 Deletion of Mtor in pancreatic endocrine cells had no significant effect on their embry

157 consequently, differentiation of pancreatic endocrine cells has been restricted to embryonic develop

158 h intercellular communications between these endocrine cells have recently been observed, their roles

159 cagon plays an important role in maintaining endocrine cell homeostasis through feedback mechanisms t

160 nto embryonic fates or adopt alternate islet endocrine cell identities.

161 CTLA-4 antigen was expressed by pituitary endocrine cells in all patients but at different levels.

162 e the differentiation of a limited number of endocrine cells in either organ when activated in Ngn3(+

163 The non-beta endocrine cells in pancreatic islets play an essential c

164 ells to detect neurotransmitter release from endocrine cells in real-time.

165 ffect of microbial metabolites on pancreatic endocrine cells in regulating type 1 diabetes pathophysi

166 is secreted into circulation from the gut L-endocrine cells in response to food intake, thus inducin

167 mach revealed that a significant fraction of endocrine cells in the gastric corpus did not arise from

168 elix (bHLH) protein NeuroD1 is restricted to endocrine cells in the gastrointestinal (GI) tract, wher

169 central nervous system in invertebrates and endocrine cells in the gut or pancreas in vertebrates.

170 In adipocytes, one of the most abundant endocrine cells in the human body, the de novo productio

171 Little is known about less typical endocrine cells in the intestinal mucosa that do not con

172 stasis and is produced by highly specialized endocrine cells in the kidney, known as juxtaglomerular

173 Selective deletion of survivin in pancreatic endocrine cells in the mouse had no discernible effects

174 Notch signaling inhibits differentiation of endocrine cells in the pancreas and intestine.

175 disproportionately inhibit the formation of endocrine cells in the remnant pancreas.

176 detectible NEUROG3 protein and did not form endocrine cells in vitro.

177 progenitors can self-renew and give rise to endocrine cells in vivo, suggesting that they are tissue

178 These endocrine cells include the insulin-producing beta-cells

179 duct cells and longer-term reprogramming to endocrine cells, including insulin(+) beta-cells that ar

180 leads to a dramatic loss of endoderm-derived endocrine cells, including insulin-secreting beta-cells,

181 nt and give rise to duct cells and late-born endocrine cells, including the insulin producing beta-ce

182 ple, T2Rs are found in some gastrointestinal endocrine cells, including those that secrete the peptid

183 gh expression levels of many genes common to endocrine cells, including transcription factors, hormon

184 In vitro tracer uptake in endocrine cells (INS-1 and human islets), but not PANC1

185 dings indicate that in developing pancreatic endocrine cells Insm1 promotes the transition from a duc

186 The decrease in endocrine cells is caused by reduced generation of endoc

187 nt activation of MAP kinases in neuronal and endocrine cells is critical for cell differentiation and

188 (2) the level of VEGF-A production by islet endocrine cells is critical for islet vascularization du

189 that trafficking of steroid hormones out of endocrine cells is not always through a simple diffusion

190 ersion of human pancreatic exocrine cells to endocrine cells is novel and represents a safer and simp

191 al variability, i.e. regional differences in endocrine cell/islet distribution, and marked inter-indi

192 both within the islet and outside the islet endocrine cells, juxtaposed to islet microvessels in T1D

193 exus state to ensure prolonged allocation of endocrine cells late into gestation.

194 internalization studies using the pancreatic endocrine cell line INR1G9 transfected with the human GI

195 N (hNT/N) gene expression in the novel human endocrine cell line, BON, which resembles intestinal N c

196 Therefore, the process of islet endocrine cell lineage allocation is critical to ensure

197 ion factor is critical in the development of endocrine cell lineage.

198 Rathke's pouch is formed and endocrine cell lineages are generated in the anterior/in

199 of distinct populations of hormone-producing endocrine cell lineages in the anterior/intermediate pit

200 ions of Nkx2.2 and Arx in the development of endocrine cell lineages, we generated progenitor cell-sp

201 ing genes that specify the alternative islet endocrine cell lineages.

202 oylates ghrelin when coexpressed in cultured endocrine cell lines with prepro-ghrelin.

203 hat macrophages are essential for preventing endocrine cell loss and diabetes.

204 -cell dedifferentiation, and not necessarily endocrine cell loss, constitutes a major cause of beta-c

205 Endocrine cell mass and proliferation rates were unalter

206 The postnatal expansion of endocrine cell mass was impaired, and consequently Isl-1

207 , these mice display a specific reduction in endocrine cell mass, while their exocrine compartment an

208 enitors and consequently a decrease in islet endocrine cell mass.

209 morphogenesis, which subsequently determines endocrine cell mass.

210 ouse results in the impairment of pancreatic endocrine cell maturation.

211 nd is progressively lost from alpha-cells as endocrine cells mature into adulthood.

212 nd pseudo-plateau bursting patterns found in endocrine cell models that are characterized by a super-

213 s and bihormonal cells that displayed hybrid endocrine cell morphological characteristics.

214 n3 (Ngn3) is a key determinant of pancreatic endocrine cell neogenesis during embryogenesis, many stu

215 t-conducting A fibers that contact pulmonary endocrine cells (neuroepithelial bodies).

216 ed from the differentiating and delaminating endocrine cells nonautonomously regulate the flux of end

217 ring the late larval period, enterocytes and endocrine cells of a transient pupal midgut are selected

218 ers the notion that the seemingly equivalent endocrine cells of each type, as judged by hormone and t

219 nalysis of ECL cells indicated that they are endocrine cells of epithelial origin that do not express

220 on of the recipients and failed to reach the endocrine cells of grafted islets.

221 ponds to sweet compounds and amino acids; in endocrine cells of gut and pancreas T1R3 contributes to

222 ns innervating the islet are also present in endocrine cells of the human islet.

223 a novel distinction between the exocrine and endocrine cells of the pancreas and further identify PKD

224 differentially expressed in the exocrine and endocrine cells of the pancreas.

225 er 2 (KCC2, Slc12a5) is expressed in several endocrine cells of the pancreatic islet, including gluca

226 progenitor cells that differentiate into the endocrine cells of the pituitary gland.

227 gests that ghrelin, a peptide synthesized by endocrine cells of the stomach and a key component of th

228 ing of the mechanisms that govern pancreatic endocrine cell ontogeny may offer strategies for their s

229 This endocrine cell plasticity could have implications for is

230 Expansion of the pancreatic endocrine cell population occurs during both embryonic d

231 delineates a major subgrouping of the islet endocrine cell populations.

232 Pancreatic islets of Langerhans consist of endocrine cells, primarily alpha, beta and delta cells,

233 n contrast, implanted, enriched polyhormonal endocrine cells principally give rise to glucagon cells.

234 We further demonstrate that endocrine cells produced in vitro do not fully eliminate

235 ort the presence of primary cilia on gastric endocrine cells producing gastrin, ghrelin, and somatost

236 er an unexpected Ngn3 expression-independent endocrine cell production pathway, which further bolster

237 , the number of neurogenin 3 (Ngn3)-positive endocrine cell progenitors is significantly reduced.

238 ogenic activity of the stem cells and in the endocrine-cell progenitors differentiating into enteroen

239 linical and biochemical characteristics, and endocrine cell proliferation and apoptosis in 150 baboon

240 lates ERK1/2 phosphorylation, did not affect endocrine cell proliferation by itself, but synergistica

241 ent of ECs and the subsequent stimulation of endocrine cell proliferation during islet development.

242 Endocrine cell proliferation fluctuates dramatically in

243 The emergence of endocrine cells requires E-cadherin downregulation, but

244 Specialized endocrine cells secrete a variety of peptide hormones al

245 Neurons, sensory cells and endocrine cells secrete neurotransmitters and hormones t

246 limentary glucose was reduced and density of endocrine cells secreting glucagon-like peptide-1 increa

247 r cells, centro-acinar cells, and ducts) and endocrine cells serve disparate functions, and have enti

248 Native antral endocrine cells share a surprising degree of transcripti

249 Endocrine cell-specific removal of Ldb1 during mouse dev

250 ption factor that is critical for pancreatic endocrine cell specification and differentiation in the

251 nown about the role of miRNA pathways during endocrine cell specification and maturation during neona

252 ver an unappreciated requirement of Hnf1b in endocrine cell specification and suggest a mechanistic e

253 The current model for endocrine cell specification in the pancreas invokes hig

254 YAP stabilisation and endocrine cell specification rely on Galphai subunits, r

255 endocrine tissue, with the full spectrum of endocrine cell subtypes not yet fully characterized.

256 known about the regeneration of the non-beta endocrine cells such as glucagon-producing alpha-cells a

257 tensities, somewhat unexpected in pancreatic endocrine cells, suggested the presence of a substantial

258 leads to an even greater increase of ectopic endocrine cells, suggesting that Ptf1a also plays a role

259 e significantly decreased in animals lacking endocrine cell survivin, with relative stability of othe

260 reveal an unknown plasticity of human adult endocrine cells that can be modulated.

261 of hES cells to stable, fully differentiated endocrine cells that exhibit physiologically regulated h

262 n with two phenotypically similar subsets of endocrine cells that have different origins and differen

263 cultures of liver hepatocytes and pancreatic endocrine cells that have therapeutic efficacy in animal

264 Intestinal K cells are glucose-responsive endocrine cells that might be engineered to secrete insu

265 mature adipocytes and preadipocytes serve as endocrine cells that secrete a number of soluble molecul

266 f many electrically excitable cells, such as endocrine cells that secrete hormones and some types of

267 Ariyachet et al. (2016) reprogrammed gastric endocrine cells to generate a renewable source of insuli

268 pathway acts both in neurons and in gonadal endocrine cells to regulate oxygen preference.

269 bility of acinar cells to change fate and of endocrine cells to reorganize in association with duct s

270 ncreases alpha cell generation, the earliest endocrine cell type to be formed in the developing pancr

271 rine progenitors, regardless of the specific endocrine cell-type chosen.

272 required for the differentiation of selected endocrine cell types and acts as the major activator of

273 lt human nonendocrine pancreatic tissue into endocrine cell types by exposure to bone morphogenetic p

274 The specific arrangement of endocrine cell types in islets suggests a coupling betwe

275 lized and differentiate into the appropriate endocrine cell types in response to physiological stress

276 sed in most beta-cells and a subset of other endocrine cell types in the pancreas.

277 subsets of all six terminally differentiated endocrine cell types of the pituitary gland.

278 astic decrease in the differentiation of all endocrine cell types owing to defects in the delaminatio

279 There are four endocrine cell types within the adult islet, including t

280 ZBTB20 is highly expressed by all the mature endocrine cell types, and to some less extent by somatol

281 c islets of Langerhans contain five distinct endocrine cell types, each producing a characteristic ho

282 Many terminally differentiated endocrine cell types, however, remain enriched for LDB1,

283 th its function after e12.5, late-developing endocrine cell types, such as beta, delta and PP cells,

284 ise to the full array of mature exocrine and endocrine cell types.

285 Human pancreatic islets consist of multiple endocrine cell types.

286 d to the transdifferentiation into the other endocrine cells types, indicating that this factor still

287 of the adult pancreas no longer give rise to endocrine cells under both normal conditions and in resp

288 In the mammalian pancreas, endocrine cells undergo lineage allocation upon emergenc

289 tic endoderm that differentiates into mature endocrine cells upon engraftment in mice.

290 pancreatic endoderm cells using CD142 and of endocrine cells using CD200 and CD318.

291 nditional deletion of survivin in pancreatic endocrine cells using mice with a Pax-6-Cre transgene pr

292 islets of Langerhans remodeling and relative endocrine-cell volume in baboons.

293 out development, whereas the total number of endocrine cells was unchanged.

294 ne progenitor cells from the differentiating endocrine cells, we developed a mouse model (Ngn3-Timer)

295 or optimal vesicle exocytosis in neurons and endocrine cells where it functions to prime the exocytic

296 of food (fat) are sensed by antral cilia on endocrine cells, which modulates gastrin secretion and g

297 GPBAR1) is expressed by enteric neurons and endocrine cells, which regulate motility and secretion.

298 When expressed in endocrine cells, wild-type and mutant proteins were foun

299 iphatic amines, are reported in exocrine and endocrine cells, with insulin-producing beta cells showi

300 Regeneration of missing endocrine cells would be a significant improvement over