ライフサイエンスコーパス: liver cell

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

2 ereby increasing glucose production in human liver cells.

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

4 ulation of genetic and epigenetic changes in liver cells.

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

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

7 of miRNAs implicated in insulin signaling in liver cells.

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

9 AdipoR1 protein synthesis in both muscle and liver cells.

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

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

12 ariable expression of CLDN proteins in human liver cells.

13 ositive regulator of Akt activation in human liver cells.

14 ranslation in rhesus macaque kidney or human liver cells.

15 volvement of a factor secreted by responding liver cells.

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

17 s and increased fat accumulation in cultured liver cells.

18 ate the fibrogenic actions of nonparenchymal liver cells.

19 importing citrate from the circulation into liver cells.

20 gramming capacity compared to differentiated liver cells.

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

22 athies by exploring their functions in fetal liver cells.

23 eded to study viral replication in quiescent liver cells.

24 different species of malaria parasite invade liver cells.

25 del for understanding virus interaction with liver cells.

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

27 ting apoptosis and reducing proliferation of liver cells.

28 primary human hepatocytes and nonparenchymal liver cells.

29 vels are generally associated with damage to liver cells.

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

31 nctional and expression analyses of isolated liver cells.

32 tivation in non-bone-marrow-derived resident liver cells.

33 l biosynthetic pathway in pancreatic but not liver cells.

34 lly transduced murine CD47 (Cd47) into human liver cells.

35 -1 production in murine adipose, muscle, and liver cells.

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

37 hibitor of cytochrome P450 7A1, and toxic in liver cells.

38 ll found to be replication competent in Huh7 liver cells.

39 ing its normal antiproliferative activity in liver cells.

40 because they contain human immune system and liver cells.

41 of Hh ligands and activated Hh signaling in liver cells.

42 bone marrow (BM)-derived and non-BM-derived liver cells.

43 tivate Gal4 LXRbeta fusion proteins in huh-7 liver cells.

44 envelope glycoprotein-mediated infection of liver cells.

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

46 -mediated delivery of bioactive molecules to liver cells.

47 proliferative activity in multiple types of liver cells.

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

49 eration by studying intact mice and cultured liver cells.

50 mes without killing erythrocytes, neurons or liver cells.

51 rbation is a collective reaction of resident liver cells.

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

53 ausing increased levels of glycogen in human liver cells.

54 dent interferon responses in non-parenchymal liver cells.

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

56 SLC13A5 affects lipid accumulation in human liver cells.

57 to maintain chromatin architecture in mouse liver cells.

58 an liver and repopulation with derived human liver cells.

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

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 formance on five test sets of in vitro human liver cell and in vivo animal toxicity experiments.

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

65 thesized that CypA is released from necrotic liver cells and acts as a DAMP to mediate acetaminophen-

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

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

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

69 the profibrogenic effects in both endogenous liver cells and BM-derived cells.

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

71 In nontransformed liver cells and cultured primary liver cells, loss of p5

72 Liver cells and fibrosis were studied by histologic, bio

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

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

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

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

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

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

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

80 n on promoting survival and proliferation of liver cells and on regulating leukocyte recruitment and

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

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

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

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

85 exclusively in this subpopulation of normal liver cells and was highly enriched relative to other ce

86 HCV replication in cultured hepatoma Huh7.5 liver cells and whether RBV resistance develops in HCV p

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

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

89 hage-specific markers CD 11b, F4/80 in fetal liver cells, and bone marrow-derived macrophages were de

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

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

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

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

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

95 10 expression was positively correlated with liver cell apoptosis in humans and mice.

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

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

98 ion of T cells and macrophages, and promoted liver cell apoptosis.

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

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

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

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

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

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

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

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

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

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

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

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

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 logic models of immediate-early signaling in liver cells by training a literature-based prior knowled

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

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

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

117 cell cytolytic activity against HAV-infected liver cells, compared with the shorter TIM-1 protein wit

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

119 of antigen-donor cells, different subsets of liver cells could cross-present a hepatocyte-associated

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

121 antiviral cytokines and pathways in primary liver cell cultures.

122 interventions that alter lipid metabolism in liver cell cultures.

123 ely resulting from systemic inflammation and liver cell damage.

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

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

126 Hepatosteatosis and liver cell death occur when humans are deprived of choli

127 Cholestasis leads to liver cell death, fibrosis, cirrhosis, and eventually li

128 f the albumin promoter (AFC8), which induces liver cell death, in Balb/C Rag2(-/-) gammaC-null mice.

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

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

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

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

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

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

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

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

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

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

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

140 Human HepG2 liver cells expressing Cd47 were less frequently contact

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

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

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

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

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

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

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

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

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

150 Liver cell fractionation showed that macrophages and act

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

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

153 Fetal liver cells from Dusp16tp/tp embryos efficiently reconst

154 uding MIC1-1C3, to isolate subpopulations of liver cells from normal adult mice or those undergoing a

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

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

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

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

159 This led to liver cell growth arrest involving cyclin-dependent kina

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

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

162 ched vesicles, although direct evidence from liver cells has been lacking.

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

164 Adult liver cells have been considered restricted regarding th

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

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

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

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

169 llowing HCV infection of primary human fetal liver cell (HFLC) cultures from 18 different donors.

170 nstrate that primary cultures of human fetal liver cells (HFLC) reliably support infection with labor

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

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

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

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

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

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

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

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

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

180 and function of A1AT in subsequently derived liver cells in vitro and in vivo.

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

182 contribution of NOX1 and NOX2 in endogenous liver cells, including hepatic stellate cells (HSCs), an

183 rtant role in hepatic fibrosis in endogenous liver cells, including HSCs, whereas NOX2 has a lesser r

184 Antigen cross-presentation by liver cells induced efficient CD8+ T-cell proliferation

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

186 gene expression profiling of human HepG2-A16 liver cells infected with Plasmodium falciparum sporozoi

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

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

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

190 patitis C virus (HCV) replication in primary liver cells is less robust than that in hepatoma cell li

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

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

193 Here, using four-way liver cell isolation and parallel comparison of candidat

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

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

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

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

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

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

200 Using an insulin-sensitive liver cell line, we show that localization of Egr1 to ch

201 n in response to osmotic swelling in a model liver cell line.

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

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

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

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

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

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

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

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

210 transformed liver cells and cultured primary liver cells, loss of p53 (but not p21) resulted in chrom

211 x scaffolds and in an HDM tailored for adult liver cells, lost stem cell markers and differentiated t

212 thermore, we observe that in PU.1(-/-) fetal liver cells, low levels of the IE GATA-1 isoform is expr

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

214 iRNAs was required for efficient recovery of liver cell mass.

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

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

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

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

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

220 c inhibition of fatty acid oxidation renders liver cells partially resistant to ER stress-induced UPR

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

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

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

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

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

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

227 Bmp6 messenger RNA expression from isolated liver cell populations.

228 Adult liver cells possess a remarkable plasticity to assume ne

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

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

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

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

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

234 iver contributes to hepatocyte apoptosis and liver cell proliferation culminating in the development

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

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

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

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

239 In liver cells, raptor phosphorylation is essential for bot

240 Previously we showed that the ~2% of fetal liver cells reactive with an anti-CD3epsilon monoclonal

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

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

243 Little is known about host liver cell response to sporozoite invasion, or whether i

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

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

246 Liver cell-specific ribosome profiling uncovered a robus

247 ntent, whereas TM6SF2 overexpression reduced liver cell steatosis.

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

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

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

251 epatotoxic compounds based on in vitro human liver cell tests.

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

253 They are also the principal fetal liver cells that express CXCL12, a factor required for H

254 Liver cell therapies using induced pluripotent stem cell

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

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

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

258 sibility of isolating viable hepatocytes for liver cell therapy from the plentiful source of morgue c

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

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

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

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

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

264 surface of lipid droplets (LDs) in infected liver cells through a process dependent on host diacylgl

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

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

267 In vitro exposure of liver cells to high concentrations of free fatty acids (

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

286 Using primary human liver cells, we identified a novel mechanism of rAAV rec

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

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

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

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

291 75-fold higher, compared with unsorted fetal liver cells, when 3 reprogramming factors were transduce

292 capsulated cassette 1a permeated Clone 9 rat liver cells, where it localized in the mitochondria and

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

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

295 ates the profibrogenic effects in endogenous liver cells, whereas NOX2 mediates the profibrogenic eff

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