ライフサイエンスコーパス: liver cell

1 ly, asymptomatic stage as hypnozoites inside liver cells.

2 d the receptor responsible for its uptake in liver cells.

3 -mediated delivery of bioactive molecules to liver cells.

4 proliferative activity in multiple types of liver cells.

5 as first found to maintain energy balance in liver cells.

6 eration by studying intact mice and cultured liver cells.

7 rbation is a collective reaction of resident liver cells.

8 onses, inflammation, or recruitment of other liver cells.

9 ausing increased levels of glycogen in human liver cells.

10 dent interferon responses in non-parenchymal liver cells.

11 enome-wide in embryonic stem cells and fetal liver cells.

12 SLC13A5 affects lipid accumulation in human liver cells.

13 to maintain chromatin architecture in mouse liver cells.

14 an liver and repopulation with derived human liver cells.

15 long-term viability of isolated and diseased liver cells.

16 ereby increasing glucose production in human liver cells.

17 ficient mice in the presence of scurfy fetal liver cells.

18 ulation of genetic and epigenetic changes in liver cells.

19 pharmacology in both Huh-7 and primary human liver cells.

20 based nanoparticle (KSI) that targets CAR on liver cells.

21 of miRNAs implicated in insulin signaling in liver cells.

22 wild-type Fah protein in approximately 1/250 liver cells.

23 man primary adipocytes, skeletal muscle, and liver cells.

24 AdipoR1 protein synthesis in both muscle and liver cells.

25 C50 value of 8 +/- 3 nM and on mRNA level in liver cells.

26 e ER-Golgi intermediate compartment of human liver cells.

27 ariable expression of CLDN proteins in human liver cells.

28 ositive regulator of Akt activation in human liver cells.

29 ranslation in rhesus macaque kidney or human liver cells.

30 response was further confirmed in zebrafish liver cells.

31 volvement of a factor secreted by responding liver cells.

32 sistance to Fas-mediated apoptosis in normal liver cells.

33 s and increased fat accumulation in cultured liver cells.

34 ate the fibrogenic actions of nonparenchymal liver cells.

35 gramming capacity compared to differentiated liver cells.

36 ice, and decreased glucose production in rat liver cells.

37 athies by exploring their functions in fetal liver cells.

38 eded to study viral replication in quiescent liver cells.

39 del for understanding virus interaction with liver cells.

40 ting apoptosis and reducing proliferation of liver cells.

41 primary human hepatocytes and nonparenchymal liver cells.

42 vels are generally associated with damage to liver cells.

43 nctional and expression analyses of isolated liver cells.

44 ed-F8 (BDD-F8) at the albumin (Alb) locus in liver cells.

45 hibited free radical formation in muscle and liver cells.

46 injury and reduced BA-triggered apoptosis in liver cells.

47 bility of tracer-based metabolism in primary liver cells.

48 epithelial, urinary bladder epithelial, and liver cells.

49 nd its effects on chromosomes and genomes of liver cells.

50 lular carcinoma cells as compared to healthy liver cells.

51 ne, displaying the highest toxicity in HepG2 liver cells.

52 importing citrate from the circulation into liver cells.

53 mes without killing erythrocytes, neurons or liver cells.

54 different species of malaria parasite invade liver cells.

55 likely due to more active ATRA metabolism in liver cells.

56 ockdown of ANLN blocked cytokinesis in H2.35 liver cells.

57 en the three-dimensional liver bud and fetal liver cells.

58 envelope glycoprotein-mediated infection of liver cells.

59 In mouse liver cells, 89% of sites that bound FXR were bound by o

60 gh deposition of excess triglycerides within liver cells, a hallmark of NAFLD, is associated with a l

61 onstrated that supernatant from HCV-infected liver cells activated human monocytes/macrophages with M

62 In H4IIE rat liver cells, ANC decreased glucose production and enhanc

63 are transferred from the plasma through the liver cell and into the bile.

64 anism that is distinct from that observed in liver cells and adipocytes.

65 Saturated fatty acids are toxic to liver cells and are believed to play a central role in t

66 nd GLP-1, which become available to resident liver cells and are strongly associated with the severit

67 Hepatitis B is a DNA virus that infects liver cells and can cause both acute and chronic disease

68 Liver cells and fibrosis were studied by histologic, bio

69 ed Lamina-associated domains (LADs) in mouse liver cells and found that boundaries of LADs are enrich

70 is caused by intrinsic damage to the native liver cells and from the abnormal microenvironment in wh

71 ignificantly reduced invasiveness in chicken liver cells and impaired survival in chicken macrophages

72 ivity in Leghorn male hepatoma (LMH) chicken liver cells and in chickens.

73 tes viral RNA accumulation in cultured human liver cells and in the livers of infected chimpanzees.

74 c conjugation for efficient uptake by target liver cells and indicate that GalNAc-conjugated PNAs hav

75 nd molecular mechanisms of miR-223 action in liver cells and liver diseases remain unclear.

76 t is associated with transdifferentiation of liver cells and may play an important role in hepatic re

77 SLU7 knockdown in human liver cells and mouse liver resulted in profound changes

78 ith small interfering RNAs (siRNAs) in H2.35 liver cells and performed image analyses of cells underg

79 owledge of the interactions between the host liver cells and the invading metastases that has implica

80 t cells, the nucleus of Hoechst stained live liver cells and the mitochondria of MitoTracker Red labe

81 ression of HAI-1 and -2 transcripts in fetal liver cells and this induction could be antagonized by a

82 In an analysis of zebrafish and human liver cells and tissues, we found GPER1 to be a hepatic

83 huttle signals from outside to the inside of liver cells and/or vice versa.

84 f ISG15 production both in vitro (Huh7-S10-3 liver cells) and in vivo (liver tissues from HEV-infecte

85 ification experiment in statin-treated HepG2 liver cells, and 280 unique N-glycosylated sites were qu

86 tional properties were investigated in human liver cells, and compound activity and target engagement

87 rent transcription factors were expressed in liver cells, and markers of pluripotency were examined,

88 n between obesity and MAM formation in mouse liver cells, and obesity-related cellular changes that a

89 hepatectomy (PH) to initiate growth, protect liver cells, and sustain functions of the remnant liver.

90 epatectomy (PH), to initiate growth, protect liver cells, and sustain remnant liver functions.

91 erative activity to change within individual liver cells, and that coordinate proliferative activity

92 with AAT significantly decreased Jo2-induced liver cell apoptosis and prolonged survival of mice.

93 10 expression was positively correlated with liver cell apoptosis in humans and mice.

94 ic application of CXCL10 led to TLR4-induced liver cell apoptosis in vivo.

95 , which was strongly associated with reduced liver cell apoptosis.

96 cence or homeostasis, evidence suggests that liver cells are capable of interconverting between cellu

97 By contrast, transformed liver cells are not protected against TNF due to metabol

98 effects regulated by FXR in mouse and human liver cells are regulated by the FXRalpha2 isoform via s

99 liferative activity among different types of liver cells, are not well understood.

100 in hemophilic mice, BDD-F8 was expressed in liver cells as functional human FVIII, leading to increa

101 d sensor system which uses RLC-18 cells (rat liver cells) as the detection layer for the detection of

102 C cells and ATRA-PLLA did not inhibit normal liver cells, as expected because ATRA selectively inhibi

103 transgene-expressing cells represented 4% of liver cells at E11.5 when other markers were expressed,

104 We labeled Sox9(+) mouse liver cells at low density with a multicolor fluorescent

105 The analyses of liver cells based on the transcriptome of rat PMFs, comp

106 rcinoma (HCC), a cancer that is derived from liver cells bearing a unique gene expression profile.

107 obligatory developmental phase in the host's liver cells before they are able to infect erythrocytes

108 Knockdown of ANLN in liver cells blocks cytokinesis and inhibits development

109 ver-changing anabolic/catabolic state of the liver cell, but the wiring of this process is still larg

110 seven host proteins were screened in chicken liver cells by a truncated avian HEV capsid protein (ap2

111 nt IF strategy, first separating dissociated liver cells by gradient centrifugation into two portions

112 iR-23b), miR-146b, and miR-183 expression in liver cells by increasing the level of DEAD-box helicase

113 Various mediators produced by other liver cells can regulate Kupffer cell activation, which

114 Lack of STAT5 in fetal liver cells caused rapid differentiation and loss of rep

115 that Trem2 expression in the nonparenchymal liver cells closely correlates with resistance to liver

116 high concentration of EVE may induce EMT in liver cells confirming previous published evidences obta

117 we review how interactions between different liver cells culminate in fibrosis development in NASH, f

118 nsduced only CD105-positive cells in primary liver cell cultures.

119 interventions that alter lipid metabolism in liver cell cultures.

120 ely resulting from systemic inflammation and liver cell damage.

121 ces autophagy, which attenuates APAP-induced liver cell death by removing damaged mitochondria.

122 Liver cell death has an essential role in nonalcoholic s

123 ituation characterized by sudden and massive liver cell death in the absence of preexisting liver dis

124 ted with reduction in cytokines, chemokines, liver cell death, and brain water.

125 etermine if RIP3 is involved in APAP-induced liver cell death.

126 es in vitro and improve our understanding of liver cell dedifferentiation in pathologic conditions.

127 e first that directly compare multiple human liver cells, define a model for enhanced maintenance of

128 when Runx1 is conditionally deleted in fetal liver cells, demonstrating that the requirement for Runx

129 Fetal liver cells derived from low-density-lipoprotein recepto

130 immune recognition of rAAV in primary human liver cells did not induce a type I interferon response,

131 s reveal that YAP/TAZ activity levels govern liver cell differentiation and proliferation in a contex

132 strate that a subset of nonparenchymal mouse liver cells displays high levels of ALDH activity, allow

133 nalyzed the changes in nuclear morphology of liver cells due to hepatitis C virus (HCV) infection usi

134 mic features and gene expression patterns in liver cells during hepatocarcinogenesis in mice with hom

135 on targeted to candidate enhancers active in liver cells, enriched for the binding sites of the FOXA1

136 ion, which in turn confers cytoprotection to liver cells exposed to chemical insults.

137 Human HepG2 liver cells expressing Cd47 were less frequently contact

138 re validated biomechanically by showing that liver cells expressing HCV proteins possessed enhanced c

139 patocytes have long been considered the only liver cells expressing SR-B1; however, in this study we

140 ic pathology in mice transplanted with fetal liver cells expressing translocated in liposarcoma (TLS)

141 recombinant cytoplasmic exonuclease Xrn1 and liver cell extracts show that miR-122-mediated protectio

142 known chemical reactivity and metabolism in liver cell extracts, 15 candidate metabolites were ident

143 r cells, because Vav-iCre Ripk1(fl/fl) fetal liver cells failed to reconstitute hematopoiesis in leth

144 role for Hippo/YAP signaling in controlling liver cell fate and reveal an unprecedented level of phe

145 arly pancreas development causes pancreas-to-liver cell fate conversion.

146 FEB and a primary mediator of its effects on liver cell fate.

147 epatocytes in adult liver (adult HCs), fetal liver cells (FLCs), induced hepatic stem cells (iHepSCs)

148 ulture system, wherein primary human healthy liver cells form long-term expanding organoids that reta

149 Liver cell fractionation showed that macrophages and act

150 Fetal liver cells from Cited2 null embryos give rise to reduce

151 Immunopurified E19 liver cells from DPPIV+ rats were transplanted via splen

152 Fetal liver cells from Dusp16tp/tp embryos efficiently reconst

153 the dosage of stimulus gradually increases, liver cells from obese mice will reach the state of satu

154 cells had different costimulatory profiles; liver cells from patients with chronic HBV infection had

155 s, with higher levels of PD-1, compared with liver cells from patients with chronic HCV infection.

156 In independent experiments, using mice with liver cells grafted from different sources, an E1E2 vari

157 Both parenchymal and non-parenchymal liver cells grown in ALTCs exhibited markedly different

158 PL transcripts in MSM hepatocytes whereas B6 liver cells had significantly more FLIPR mRNA.

159 tis B and hepatitis D viruses to enter human liver cells has been identified as a protein that transp

160 bles hepatitis C virus (HCV) to infect human liver cells has not been well understood because of the

161 Adult liver cells have been considered restricted regarding th

162 Both hepatocytes and non-parenchymal liver cells have detectable Bmp6 mRNA.

163 embryonic day (E)8.5 endoderm, E14.5 Dlk1(+) liver cells (hepatoblasts), and adult liver by employing

164 ation, being able to differentiate to mature liver cells (hepatocytes, cholangiocytes) and mature pan

165 fraction (SVF) cells to vascularize a human liver cell (HepG2) implant.

166 lite, N-desethylamiodarone (NDEA), in single liver cells (HepG2 and HepaRG cells).

167 flammatory cytokine expressed by human fetal liver cells (HFLCs) after infection with cell culture-de

168 mouse model with autologous human immune and liver cells, human liver and blood samples and cell cult

169 r lipid and amino acid metabolism; 3) induce liver cell immune responses to adapt to the high tempera

170 d mosquitoes, adding them to confluent human liver cells in 384-well plates, and measuring luciferase

171 (FFAs) are known to induce lipoapoptosis in liver cells in a c-Jun-NH2-terminal kinase (JNK)-depende

172 sugars to other cells (e.g., intestinal and liver cells in animals, photosynthetic cells in plants),

173 intercellular crosstalk and reprogramming of liver cells in health and disease.

174 human fetal thymic tissue and CD34(+) fetal liver cells in nonobese diabetic (NOD)/severe combined i

175 tic reconstitution with Mafb-deficient fetal liver cells in recipient LDL receptor-deficient hyperlip

176 est an important role of the non-parenchymal liver cells in regulating iron-homeostasis by acting as

177 cholestasis, as well as in human and murine liver cells in response to bile acid loading.

178 detected no cytotoxicity of Gd-lip in human liver cells including cancer HepG2, progenitor (non-diff

179 ecipitation binding sites in human islet and liver cells, including at MTNR1B, where fine mapping imp

180 se isoforms regulated metabolic functions in liver cells, including carbon metabolism and lipogenesis

181 F increases glucose metabolism in muscle and liver cells independent of insulin.

182 ecrotic liver injury and found that necrotic liver cells induced eosinophil recruitment.

183 diated depletion of SRSF3, but not SRSF4, in liver cells inhibited accumulation of both mRNA expresse

184 y, cirrhosis develops after a long period of liver-cell injury that leads to the deposition of collag

185 ent study, we transplanted necdin-null fetal liver cells into lethally irradiated recipients.

186 ng and specific drug delivery to parenchymal liver cells is a promising strategy to treat various liv

187 and TLR7-mediated signaling was assessed in liver cells isolated from these mice.

188 y, we performed transcriptional profiling of liver cells isolated from zebrafish larvae at the earlie

189 ments, SLC7A11 was highly expressed in human liver cells; its expression is positively correlated wit

190 suppress glucose production was abolished in liver cells lacking Stat3 or IL-13 receptor alpha1 (Il-1

191 tivity and transcription of Hamp in cultured liver cells; levels of Hamp were reduced after administr

192 In a human liver cell line (HepG2) and in a validated hepatic 3D mo

193 loci by silencing candidate genes in a human liver cell line (HuH7) using small-interfering RNA and t

194 ChIP-seq for H3K27ac on HepG2 cells, a human liver cell line commonly used for pharmacokinetic, metab

195 plicated in dyslipidemia and the human HepG2 liver cell line to demonstrate unique functions of this

196 a cell line) and HL-7701 cells (human normal liver cell line) by a confocal imaging technique.

197 ver cancer theranostics, on the surface of a liver cell line.

198 identify an unexplored pathway that controls liver cell lineage commitment and whose dysregulation ma

199 re we report that the Hippo pathway controls liver cell lineage specification and proliferation separ

200 d with human parenchymal and non-parenchymal liver cell lines (HepG2 and LX2 cells, respectively), hu

201 (HepG2, HLE, HLF, and Huh7) and immortalized liver cell lines (THLE-2 and THLE-3) were incubated with

202 top identified gene were measured in 9 human liver cell lines and compared with expression profiles o

203 receptors (RARs) in mouse liver and in human liver cell lines has also been shown.

204 ive intracellular detection of Fe(3+) in two liver cell lines i.e., HepG2 cells (human hepatocellular

205 whether of primary liver tissue origin, from liver cell lines, or derived from stem cells, adequately

206 PA (HPA) indeed induces lipotoxic effects in liver cells, low-level PA (LPA) increases mitochondrial

207 lish and sustain a therapeutically effective liver cell mass in patients, a lesson learned from clini

208 Knockdown of phosphatase 1G in a human liver cell model resulted in decreased apolipoprotein E

209 V-1 cells also represented CITCO activity in liver cell models was not hitherto investigated.

210 roliferation, lobular cholestasis, and acute liver cell necrosis, together with central vein thrombos

211 ciency of LPCs, compared with differentiated liver cells, occurred independently of proliferation rat

212 Liver cells of the mice had a strong oxidative stress re

213 erentiation stage of freshly isolated, mouse liver cells on the reprogramming efficiency.

214 etion or knockdown approaches in alpha mouse liver cells or primary hepatocytes, respectively, we inv

215 f exogenous gene expression than the healthy liver cells (P<0.01).

216 Genome-wide gene expression analyses in liver cells performed in this study have revealed a stro

217 Therefore, we investigated whether liver cell plasticity could contribute to IHBD regenerat

218 We conclude that liver cell plasticity is competent for regeneration of I

219 duced by HEV replication in Huh7-S10-3 human liver cells plays an immunomodulatory role by negatively

220 issue-specific ablation of Bmp6 in different liver cell populations and evaluated their iron phenotyp

221 Upon tissue loss, both liver cell populations need to be regenerated.

222 Bmp6 messenger RNA expression from isolated liver cell populations.

223 Adult liver cells possess a remarkable plasticity to assume ne

224 Despite minimal turnover, liver cells possess immense regenerative capacity.

225 Intriguingly, we observed that MSM liver cells predominantly express the FLIPL variant, in

226 ation by its association with AMPK regulates liver cell proliferation and fatty acid oxidation, most

227 scovered that TCS was capable of stimulating liver cell proliferation and fibrotic responses, accompa

228 in and MK2206 was more effective in reducing liver cell proliferation and inducing cell death than ei

229 ncing a key pathway involved in regenerating liver cell proliferation and survival.

230 receptor superfamily, is a strong inducer of liver cell proliferation in rats and mice.

231 biliary epithelial cells, thereby regulating liver cell proliferation, differentiation, and malignant

232 t Med1 alone is necessary and sufficient for liver cell proliferation.

233 d communications between CCA cells and other liver cells provide a potential novel target for the man

234 In cultured liver cells, pterosin A inhibited inducer-enhanced PEPCK

235 We observed that the liver cell putative enhancers in the ruminant evolutiona

236 ient HCV RNA replication efficiency in mouse liver cells remains elusive.

237 Little has been known, however, about how liver cells respond to SFTSV and how the response is reg

238 Treatment of hepatic stellate cells (liver cells responsible for fibrosis) with nM concentrat

239 A variety of insults to liver cells result in a consistent pattern of rapid-onse

240 n and differentiation of single parasites in liver cells, resulting in the formation and release of t

241 Knockdown of FoxK1 and FoxK2 in liver cells results in upregulation of genes related to

242 bryonic lethality, and Srsf2-deficient fetal liver cells showed significantly enhanced apoptosis and

243 Liver cell-specific ribosome profiling uncovered a robus

244 ntent, whereas TM6SF2 overexpression reduced liver cell steatosis.

245 luated for their ability to deliver siRNA to liver cell subpopulations.

246 In the endoplasmic reticulum of liver cells, such enzymes metabolize ~75% of the pharmac

247 aled deamidation of cy-2-glu in prostate and liver cells, suggesting release of glucosamine.

248 topoietic abnormalities in Klotho(-/-) fetal liver cells, suggesting that the effects of klotho in he

249 these compounds against human colorectal and liver cells (TB assay) was observed.

250 ve replication inside their mammalian host's liver cells that depends on the parasite's ability to ob

251 transplanted with NP23 bone marrow or fetal liver cells that had been transduced with a Bcor sgRNA d

252 Liver cell therapies using induced pluripotent stem cell

253 ressed in future studies aimed at developing liver cell therapies with lab-made hepatocytes.

254 es, supporting the feasibility of autologous liver cell therapies.

255 s that can potentially be used in autologous liver cell therapies.

256 antages as an alternative to hepatocytes for liver cell therapy.

257 standing roadblock on the path to autologous liver cell therapy.

258 cast doubt on the potential of iPSC-Heps for liver cell therapy.

259 n will help optimize clinical strategies for liver cell therapy.

260 of promoters of gluconeogenic genes in human liver cells, thereby enhancing gluconeogenesis.

261 ound its connections to energy regulation in liver cells to be tight and complex.

262 hepatic stellate cells (HSCs), are the first liver cells to encounter gut-derived and systemic antige

263 st that Kupffer cells orchestrate with other liver cells to relay inflammatory signals and to maintai

264 es highlight the heightened vulnerability of liver cells to subtle changes in nononcogenic RTK levels

265 s led to controversies about the capacity of liver cells to switch their fate.

266 uricases were stably transfected into HepG2 liver cells to test one hypothesis that uricase pseudoge

267 dy therefore does not necessarily predispose liver cells to transformation but might promote genetic

268 factor (Gdown1) in the maintenance of normal liver cell transcription through constraints on cell cyc

269 r interfering with oncogenic signals driving liver cell transformation and tumor progression, thus pr

270 rom 20 hepatoblastomas (HBs), 1 transitional liver cell tumor (TCLT), 1 hepatocellular carcinoma, and

271 r gene expression and regulation in a common liver cell type such as HepG2, advocating that antibioti

272 rganoids that comprise different parenchymal liver cell types and have structural features of the liv

273 crocirculation along with changes in various liver cell types are among the earliest changes.

274 Including multiple human liver cell types can mimic cell-cell interactions in spe

275 It is unclear whether other liver cell types can regenerate hepatocytes.

276 e 3-dimensional interactions among different liver cell types during organogenesis or disease develop

277 ng BECs or LPCs as the origin of ICCs, other liver cell types have not been considered.

278 he complex interactions between the distinct liver cell types involved in the repair process.

279 The presentation of antigens by different liver cell types results in incomplete activation of CD8

280 erging evidence suggests that other resident liver cell types such as progenitors, liver sinusoidal e

281 ibution of Gal, GalR1, and GalR2 in specific liver cell types was assessed by laser-capture microdiss

282 roapoptotic functions of CXCL10 on different liver cell types were evaluated in detail in vitro.

283 conditions; and (iv) in skeletal muscle and liver cells, uptake per mitochondrion varies in magnitud

284 in induced inhibition of the Na-/K-ATPase in liver cells using a magnetic resonance (MR) compatible b

285 rting polypeptide 1A2 (OATP1A2) from chicken liver cells was identified to interact with ap237, a tru

286 ST18 expression in liver cells was induced by inflammatory cues, including

287 Furthermore, undesired uptake into liver cells was suppressed by using l-deoxygalactosyl mo

288 genes between the mouse tumor and non-tumor liver cells, we identified changes similar to those dete

289 to irradiated C57BL/6J mice, and spleen and liver cells were analyzed by flow cytometry.

290 Bone marrow cells and, alternatively, fetal liver cells were cultured in media containing M-CSF for

291 When murine fetal liver cells were transduced with either of the human acu

292 In further experiments, liver cells were treated with curcumin after exposure to

293 75-fold higher, compared with unsorted fetal liver cells, when 3 reprogramming factors were transduce

294 A large amount of enzyme also appeared in liver cells, where it reduced heparan sulfate and beta-h

295 rine erythroleukemia cells, as well as fetal liver cells, whereas an increase in PIAS3 levels inhibit

296 express the FLIPL variant, in contrast to B6 liver cells, which have higher levels of cFLIPR.

297 ences between the wild and aquacultured fish liver cells, which mainly indicated that the level of gl

298 H2.35 liver cells with shRNA knockdown of ANLN formed tumors m

299 cles were investigated in vitro in zebrafish liver cells (ZFL) cells and in zebrafish embryos and nov

300 uding human keratinocytes (HaCaT), zebrafish liver cells (ZFL), and zebrafish embryos were also used