ライフサイエンスコーパス: hepatocyte

1 intracellular accumulation of albumin in the hepatocyte.

2 eads to toxic bile acid (BA) accumulation in hepatocytes.

3 Receptor BI (SR-BI), respectively, to infect hepatocytes.

4 sm is used following repopulation with human hepatocytes.

5 ne expression differ from those of adult rat hepatocytes.

6 eneration occurs through self-replication of hepatocytes.

7 2), the principle calcium release channel in hepatocytes.

8 human hepatic HepaRG cell line, and primary hepatocytes.

9 te HCV infection in human hepatoma cells and hepatocytes.

10 lfed Ags into MHC I:peptide complexes within hepatocytes.

11 total cellular iron removal, particularly in hepatocytes.

12 ptor-expressing CHO-IR cells and primary rat hepatocytes.

13 or in liver to the induction of autophagy in hepatocytes.

14 esidual glucose production by G6pc-deficient hepatocytes.

15 e oxygen species in mouse livers and primary hepatocytes.

16 nals regulating the differentiation of human hepatocytes.

17 gnificant emergence of cholangiocyte-derived hepatocytes.

18 te adipose tissue, brown adipose tissue, and hepatocytes.

19 t views that HJV is a coreceptor for BMP6 in hepatocytes.

20 ranslocation of Nrf2 in 100% of HCV infected hepatocytes.

21 profile in steatotic hepatocytes versus lean hepatocytes.

22 cells could represent a source of expandable hepatocytes.

23 developing intestinal enterocytes and liver hepatocytes.

24 tivates hepcidin both in vitro and in murine hepatocytes.

25 es, erythrocyte precursors, macrophages, and hepatocytes.

26 lation of p38(MAPK) and MK2 in primary mouse hepatocytes.

27 th without compromising the health of normal hepatocytes.

28 lanation to how ethanol induces lipophagy in hepatocytes.

29 y response, fibrosis, and apoptotic death of hepatocytes.

30 edicted an IC50 of 1-1.2 mum for SB203580 in hepatocytes.

31 cates from the nucleus into the cytoplasm of hepatocytes.

32 n to allow pro-regenerative proliferation of hepatocytes.

33 s through conferring apoptosis resistance to hepatocytes.

34 RBP4 is produced mainly by hepatocytes.

35 of human HCC cells as well as healthy human hepatocytes.

36 n part, HCV's limited ability to enter mouse hepatocytes.

37 g the release of adenosine triphosphate from hepatocytes.

38 y interacts with and deubiquitinates ASK1 in hepatocytes.

39 expression, and reduce glucose production in hepatocytes.

40 Akt/FoxO1 pathway in HCV protein-expressing hepatocytes.

41 ession with efficiencies comparable to human hepatocytes.

42 tients that selectively destroyed transduced hepatocytes.

43 teatosis, with large lipid droplets in their hepatocytes.

44 n Receptor (ASGR)-mediated uptake into liver hepatocytes.

45 ot cytotoxic and maintained the viability of hepatocytes above 80%.

46 In regenerating liver, hepatocytes accumulate lipids before the major wave of p

47 In liver steatosis (i.e. fatty liver), hepatocytes accumulate many large neutral lipid storage

48 t conditioned medium from HCV-infected human hepatocytes activates fibrosis-related markers in hepati

49 rried through the exosomes from HCV-infected hepatocytes activates HSC by modulating the SOCS-STAT3 a

50 In livers of control mice and primary rat hepatocytes, activation of FXR with obeticholic acid inc

51 ire <24 h to find, locate, and kill infected hepatocytes, active migration of Ag-specific CD8(+) T ce

52 dothelial, smooth muscle cells, macrophages, hepatocytes, adipocytes, skeletal muscle, and finally, t

53 Early cell cycle initiation in hepatocytes after GSK3 inhibition was because of rapid i

54 In vitro, M2-polarized macrophages protected hepatocytes against apoptosis.

55 resulted in almost exclusive transduction of hepatocytes allowing analysis of hepatocyte-specific tra

56 In human hepatocytes, an RNA interference-mediated knockdown of O

57 development, including parallel formation of hepatocyte and cholangiocyte anatomical structures.

58 However, how relative levels of hepatocyte and cholangiocyte gene expression are determi

59 networks control the differentiation of the hepatocyte and cholangiocyte lineages from embryonic liv

60 notype of global Bmp6 knockout mice, whereas hepatocyte and macrophage Bmp6 conditional knockout mice

61 alized eukaryotic cells such as in mammalian hepatocytes and B-cells.

62 anscriptional network dynamics of developing hepatocytes and balances both cholangiocyte populations

63 epaRG, can be directed to differentiate into hepatocytes and biliary epithelia.

64 Here, we genetically deleted Srebf-2 from hepatocytes and confirmed that SREBP-2 regulates all gen

65 t B lymphocytes and instead primarily target hepatocytes and dendritic cells.

66 Using primary rat hepatocytes and human hepatoma cells, we found that trea

67 SPA70 inhibits hPXR in human hepatocytes and humanized mouse models and enhances the

68 inhibited the catalytic activity of MNADK in hepatocytes and in livers in mice with methotrexate inje

69 ed liver injury, diminished proliferation of hepatocytes and leukocytes, and attenuated overall infla

70 signaling in human hepatoma cells and murine hepatocytes and may contribute to the ability of LPS to

71 E1 expression and proliferation of surviving hepatocytes and nonparenchymal cells, including CD45(+)

72 noviruses is caused mostly by replication in hepatocytes and not by the abortive infection of Kupffer

73 he hepatopancreatic duct cells connect liver hepatocytes and pancreatic acinar cells to the intestine

74 ficiency of AAVs intracellular processing in hepatocytes and thus the outcome of liver-directed gene

75 llular defenses, HCV is able to replicate in hepatocytes and to establish a chronic infection that co

76 otein receptors (ASGPR) to enhance uptake to hepatocytes and to increase potency.

77 the periphery (including that in pericentral hepatocytes) and glutamine catabolism in (periportal) he

78 ic anti-inflammatory effects on macrophages, hepatocytes, and adipocytes, which is distinct from the

79 rains, inhibits development of P. berghei in hepatocytes, and at doses up to 100 mg/kg also inhibits

80 sed by different malaria parasites to infect hepatocytes, and establish a functional link between a s

81 udy the interactions among HCV, HCV-infected hepatocytes, and HCV-specific CD8 T cells.

82 d CAR proteins in Huh-7 cells, mouse primary hepatocytes, and mouse livers, coimmunoprecipitation and

83 ilizes cytosolic lipases for LD breakdown in hepatocytes, and perturbation of this pathway could be a

84 was performed on isolated steatotic primary hepatocytes, and T-cell markers were assessed in hepatic

85 y of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic l

86 at 18 months of age preceded by spontaneous hepatocyte apoptosis and liver inflammation within the f

87 Concomitant hepatocyte apoptosis and regeneration is a hallmark of c

88 Accumulated levels of hepatocyte apoptosis determine and predict subsequent he

89 showed that chronic alcohol exposure induced hepatocyte apoptosis in association with increased hepat

90 Hepatocyte apoptosis in nonalcoholic steatohepatitis (NA

91 Understanding the regulation of hepatocyte apoptosis is therefore important to identify

92 nisms: First, it prevents DNA-damage-induced hepatocyte apoptosis through suppression of p53 and enha

93 s that correlated with increased DEN-induced hepatocyte apoptosis.

94 ent pathway of sterile liver injury in which hepatocytes are both the targets of damage and the princ

95 nstrate that cholesterol and FA synthesis in hepatocytes are coupled and that flux through the choles

96 ylation, and ROS accumulation in surrounding hepatocytes are present.

97 tic stellate-cell activation by HCV-infected hepatocytes are underexplored.

98 Hepatocyte area (HA) and lobule radius (LR) were also me

99 Molecular studies have identified adult hepatocytes as the cell of origin.

100 pressing cells and were able to recapitulate hepatocyte ASO uptake and activity in cells engineered t

101 In addition, hepatocyte ATX ablation and the consequent deregulation

102 However, hepatocyte autonomous JAK2 signaling regulates liver lip

103 In primary hepatocytes, autophagy was inhibited by 3MA or autophagy

104 vs. 2.0 +/- 0.8; P = 0.014) and presence of hepatocyte ballooning (60.9% vs. 73.4%; P = 0.045).

105 portal inflammation (taurolithocholate), and hepatocyte ballooning (taurocholate).

106 test and histological study revealed minimal hepatocyte, biliary epithelium and vascular endothelium

107 KT cell homeostasis in a manner dependent on hepatocyte CD1d.

108 IL6 blockade significantly inhibited hepatocyte cell cycle progression while promoting a hype

109 e to robustly quantify parasite infection of hepatocyte cell lines by flow cytometry.

110 However, cells with hepatocyte characteristics can be produced from induced

111 et al. establish a self-assembling, primary hepatocyte co-culture system that can be infected with p

112 ncreased FGF21 gene transcription in primary hepatocyte cultures.

113 o induce Hamp in response to Bmp6 in primary hepatocyte cultures.

114 inusoidal congestion, and extensive midzonal hepatocyte death in control mice, which were strongly mi

115 Here, we use a model of selective hepatocyte death to investigate sterile liver injury.

116 tic sinusoids of infected mice, resulting in hepatocyte death, inflammation, and progressive liver fi

117 terized by dysregulated immune responses and hepatocyte death.

118 of human BM-derived MSCs, globule-containing hepatocytes declined and donor-derived cells expressed h

119 e also discuss the potential applications of hepatocytes derived from human pluripotent stem cells an

120 Primary cultures of hepatocytes derived from wild-type or hepatocyte-specifi

121 In ischemic liver injury, hepatocyte-derived Gal-9 is both diagnostic and cytoprot

122 the presence of DGLA, which was involved in hepatocyte DGLA uptake.

123 mice lacking beta-arrestin 1 selectively in hepatocytes did not show any changes in glucose homeosta

124 yte specific microRNA 122 (MIR122) regulates hepatocyte differentiation and metabolism.

125 nhibitor NUMB in HepaRG resulted in enhanced hepatocyte differentiation and proliferation whereas ove

126 ncover regulatory pathways with new roles in hepatocyte differentiation by identifying cellular proce

127 ion of the gene encoding HSP90beta represses hepatocyte differentiation during the formation of hepat

128 or intrahepatic cross-presentation, confirms hepatocytes directly contribute to cross-presentation of

129 TA4, a master transcription factor driver of hepatocyte epithelial lineage fate.

130 he persistence of hepatitis B virus (HBV) in hepatocytes, even in the presence of available antiviral

131 es a novel pathway in which HCV infection in hepatocytes exacerbates Tfr cell responses to subvert an

132 and obese mice, as well as EVs released from hepatocytes exposed to ethanol.

133 We further observed that these HCV-infected hepatocytes express transforming growth factor beta, whi

134 More than a third of LAP+ fetal hepatocytes expressed ductal markers.

135 ting polypeptide (hNTCP), on macaque primary hepatocytes facilitates HBV infection in vitro, where al

136 ytokeratin 19(+) cells but fewer features of hepatocyte fate characterized progenitor cell activation

137 secretion and in adipocytes, monocytes, and hepatocytes for insulin action-associated loci.

138 d a short half-life in the presence of mouse hepatocyte fractions.

139 Damaged hepatocytes from ASH mice are a key EV source with a spe

140 Contrarily, hepatocytes from cynomolgus macaques, rhesus macaques, a

141 6Pase transcript levels are downregulated in hepatocytes from GCN5L1 liver specific knockout mice and

142 regulatory element-binding protein 1/CD36 in hepatocytes from high fat-fed mice.

143 cyte differentiation during the formation of hepatocytes from iPSCs.

144 and a novel therapeutic target for restoring hepatocyte function.

145 ression of cholangiocyte genes and represses hepatocyte genes in undifferentiated progenitor cells in

146 infected ones because more of the permissive hepatocytes get infected.

147 ntaining exosomes released from HCV-infected hepatocytes given that blockade of exosome-associated TG

148 We previously identified KLF6 as mediator of hepatocyte glucose and lipid homeostasis.

149 ernal high-fat diet on glucose tolerance and hepatocyte glucose metabolism in female offspring.

150 lipid lysophosphatidic acid (LPA) regulates hepatocyte glucose production by antagonizing glucagon-i

151 s FoxO1, gluconeogenic enzyme expression and hepatocyte glucose production.

152 Hepatocyte growth factor (HGF) induces cell migration an

153 ated that these endothelial cells supply the hepatocyte growth factor (HGF) required for the chemotac

154 Expression of the MET ligand, hepatocyte growth factor (HGF), by tissues innervated by

155 osine kinases could be MET, the receptor for hepatocyte growth factor (HGF).

156 gested that patients with high expression of hepatocyte growth factor or unmethylated O(6)-methylguan

157 wth arrest specific protein 6, oncostatin M, hepatocyte growth factor receptor etc.

158 interleukin 18 and IP-10 but lower levels of hepatocyte growth factor than those without such abnorma

159 ayed a 55-fold increase in the expression of hepatocyte growth factor, known to be involved in myogen

160 fficacy with expression levels of MET ligand hepatocyte growth factor, O(6)-methylguanine-DNA methylt

161 fensin 1 and E-cadherin, and upregulation of hepatocyte growth factor-regulated tyrosine kinase subst

162 n as the top positive correlated gene, while hepatocyte growth factor-regulated tyrosine kinase subst

163 The growth and motility factor Hepatocyte Growth Factor/Scatter Factor (HGF/SF) and its

164 plasma angiogenesis factors (angiopoietin 2; hepatocyte growth factor; platelet-derived growth factor

165 CAR in metabolically competent human primary hepatocytes (HPH) and HepaRG cells.

166 noma (HepG2) cell line or immortalized human hepatocytes (IHH) and activation of its downstream signa

167 and in vitro and was up-regulated in zone 3 hepatocytes in human alcoholic steatosis.

168 ution of Sox9(+) hepatic progenitor cells to hepatocytes in the liver.

169 1 and OCLN facilitates HCV uptake into mouse hepatocytes in vitro and in vivo In efforts to refine th

170 Ultradian rhythms in mouse hepatocytes in vivo have been published, and we validate

171 After viral delivery of Cre recombinase to hepatocytes in vivo, GsD is expressed and allows CNO-dep

172 boxylated derivative, 5(6)-carboxy-DCFH2, to hepatocytes in vivo.

173 delivery of therapeutically active siRNAs to hepatocytes in vivo.

174 f syndecan-1, the major cell-surface HSPG of hepatocytes, in AILI.

175 role of parenchymal cells, as shown here for hepatocytes, in tissue-specific regulation of CD1d-restr

176 Expression of XBP1 by hepatocytes increased immediately after PH (priming phas

177 In hepatocytes incubated in the presence of insulin, treatm

178 quantified in Huh7.5 cells or primary human hepatocytes infected with the Japanese fulminant hepatit

179 en species and contribute to alcohol-induced hepatocyte injury.

180 ial TRL after SFA, and lower LDL binding and hepatocyte internalization, provide mechanisms for the g

181 ump (BSEP/ABCB11) transports bile salts from hepatocytes into bile canaliculi.

182 morphogenetic protein 6 (BMP6) signaling in hepatocytes is a central transcriptional regulator of th

183 optosis signal-regulating kinase 1 (ASK1) in hepatocytes is a key process in the progression of nonal

184 Chronic loss of hepatocytes is associated with regenerative efforts char

185 at prior convertase cleavage of protein C in hepatocytes is critical for its thrombin activation.

186 Furthermore, we found that STAT3 in hepatocytes is dispensable for HCC formation when mammal

187 efficient liver repopulation by transplanted hepatocytes is low in livers of old animals.

188 late gestation (embryonic day 19) fetal rat hepatocytes is mitogen-independent and that mechanisms r

189 these enzymes function in TLR4 responses of hepatocytes is unknown.

190 independent endogenous glucose production in hepatocytes isolated from a liver-specific GSD Ia mouse

191 e displayed by MHC I is however defective in hepatocytes lacking collectrin, an intracellular chapero

192 ed glucose production or PEPCK expression in hepatocytes lacking STAT3.

193 Fasting elicits transcriptional programs in hepatocytes leading to glucose and ketone production.

194 e induced pluripotent stem cells (iPSCs) and hepatocyte-like cells (HLCs) for genome-wide mapping of

195 Currently, hepatocyte-like cells differentiated from stem cells sti

196 Here, we have used hepatocyte-like cells generated from homozygous familial

197 importance of benchmarking stem cell-derived hepatocyte-like cells to their terminally differentiated

198 id not form, their soluble factors induced a hepatocyte-like phenotype in HE-iPSCs, resulting in the

199 wn inhibits hepatitis-C virus replication in hepatocytes, likely because translated viral proteins ar

200 homeostasis, and hematopoiesis (enterocytes, hepatocytes, macrophages, hematopoietic cells, and in th

201 e mesoderm-derived paracrine signals promote hepatocyte maturation in liver organoids, but organoid s

202 s in a cycle of AA-enrichment in pericentral hepatocytes, membrane release of AA, and generation of p

203 neage-tracing studies have shown that mature hepatocytes (MHs) convert to an immature state during ch

204 thione reduction renders nematodes and human hepatocytes more resistant against oxidative stress.

205 foci, immune cell infiltration, and altered hepatocyte morphology.

206 To distinguish the role of hepatocyte NAD levels from any systemic effects of NR, w

207 The hepatocyte nuclear factor (HNF) family regulates complex

208 Variants in HNF1A encoding hepatocyte nuclear factor 1alpha (HNF-1A) are associated

209 The transcription factor hepatocyte nuclear factor 1beta (HNF1beta) is ubiquitous

210 Hepatocyte nuclear factor 4 (HNF4) is the most ancient f

211 e network, which was down-regulated in mouse hepatocyte nuclear factor 4A knockout mice; were early-s

212 ass represented 29% of all HCCs; expressed a hepatocyte nuclear factor 4A-driven gene network, which

213 Here, we evaluated the potential role of hepatocyte nuclear factor-1beta (HNF-1beta) in regulatin

214 The transcription factor hepatocyte nuclear factor-1beta (HNF-1beta) is essential

215 Reduced hepatocyte nuclear factor-4alpha was associated with act

216 gly, we found that elimination of Srebf-2 in hepatocytes of mice also markedly reduced SREBP-1c and t

217 ducible expression of oncogenic Kras(V12) in hepatocytes of transgenic zebrafish resulted in accelera

218 we found impaired mitochondrial function in hepatocytes of Zdhhc13-deficient mice and Zdhhc13-knockd

219 he poor proliferative capacity of aged donor hepatocytes or the regenerative impairment of the recipi

220 script (pri-MIR122, to overexpress MIR122 in hepatocytes) or vector (control).

221 he HCV core-expressing cell surface of human hepatocyte origin and activation of phospho-SMAD1/5 and

222 different quaternary structures in infected hepatocytes, participate in and regulate HBV virion asse

223 terbalanced with a decrease in the number of hepatocytes per lobule (p = 0.029).

224 Expression of hNTCP in mouse, rat, and dog hepatocytes permits HDV infection but does not allow est

225 enetic alterations), to dedifferentiate into hepatocyte precursor cells (which then become HCC cells

226 eover, acellular liver scaffolds seeded with hepatocytes produced functional bioengineered livers for

227 enerative efforts characterized by continual hepatocyte proliferation and often has adverse consequen

228 lineage traced with concurrent inhibition of hepatocyte proliferation by beta1-integrin knockdown or

229 ere we use two independent systems to impair hepatocyte proliferation during liver injury to evaluate

230 To study its involvement in hepatocyte proliferation, we specifically inhibited its

231 ng cell nuclear antigen were used to measure hepatocytes proliferation.

232 pletion of Ahr, Med1, or Ctcf in Mir122(-/-) hepatocytes reduced Cyp1a2 expression.

233 s, yet the mechanisms of parasite entry into hepatocytes remain poorly understood.

234 esults show that expressing hNTCP on macaque hepatocytes renders them susceptible to HBV infection, t

235 Raven et al. (2017) now shows that blocking hepatocyte replication is essential for the hepatic diff

236 es) and glutamine catabolism in (periportal) hepatocytes represents the high-affinity ammonia-detoxif

237 ngineered liver scaffolds with human primary hepatocytes reseeded under dynamic conditions were maint

238 Because the lipases that catabolize LDs in hepatocytes reside on the sER, LDs can now be catabolize

239 ontribute in replacement of 40% and 13% host hepatocytes, respectively.

240 ing to increased lipid droplets formation in hepatocytes resulting in a downstream effect contributin

241 tation that formation of AFB1-DNA adducts in hepatocytes seeds a population of mutations, mainly G:C-

242 ent with increased apoptosis, HOIP-deficient hepatocytes showed enhanced caspase activation and endog

243 Here, we show that, in mice, liver mass, hepatocyte size, and protein levels follow a daily rhyth

244 clic AMP-responsive element binding protein, hepatocyte specific (CREBH), is a liver-enriched, endopl

245 n of cAMP-responsive element binding protein-hepatocyte specific and peroxisome proliferator-activate

246 The hepatocyte specific microRNA 122 (MIR122) regulates hepa

247 tennary N-acetyl galactosamine = GalNAc) for hepatocyte-specific asialoglycoprotein receptors (ASGPR)

248 However, hepatocyte-specific beta-arrestin 2 deficiency did not a

249 Using mouse models, we show that hepatocyte-specific deletion of c-Fos protects against d

250 We show that the hepatocyte-specific deletion of Stat3, genetic ablation

251 Mice with hepatocyte-specific disruption of Hif1alpha developed le

252 Hepatocyte-specific double-knockout Smad1(fl/fl);Smad5(f

253 res of hepatocytes derived from wild-type or hepatocyte-specific furin, PC5/6, or complete PACE4 knoc

254 e were crossed with Albcre mice to produce a hepatocyte-specific ILK deletion (ILK(lox/lox)Albcre).

255 Similar findings were made in mice with hepatocyte-specific loss of CD1d, confirming a critical

256 Mice with hepatocyte-specific loss of MTP exhibit defects in the f

257 Importantly, hepatocyte-specific overexpression of beta-arrestin 2 gr

258 sduction of hepatocytes allowing analysis of hepatocyte-specific transcription factor activity.

259 Hepatocyte-specific, conditional genetic deletion and/or

260 d gamma-glutamyltranspeptidase), whereas the hepatocyte specification marker HNF4alpha was suppressed

261 e has high contrasting properties, liver and hepatocyte specificity and strong liver persistence.

262 eneration reveals local clonal expansions of hepatocyte stem/progenitors at injured sites that are li

263 vates oncogenic Nrf2 signaling that promotes hepatocyte survival and oncogenesis by inducing Mdm2-med

264 Furthermore, hepatocyte-targeted liposomes were developed to deliver

265 tide conjugated to N-acetylgalactosamine for hepatocyte targeting and endosomal escape, and cholester

266 labeled trivalent conjugate showed selective hepatocyte targeting with no detectable distribution in

267 d activation of the p38(MAPK)/MK2 pathway in hepatocytes that was calibrated to quantitative data on

268 ticoid receptor and PPARgamma and transduces hepatocytes, these data indicate a potential role for Vp

269 mous program to activate STAT3 signalling in hepatocytes through IL-6 produced in the liver microenvi

270 In cultured human hepatocytes, Tm6sf2 overexpression reduced apolipoprotei

271 that chronic alcohol feeding sensitizes rat hepatocytes to Ca(2+) -mobilizing hormones resulting in

272 ered to chicken and double-crested cormorant hepatocytes to determine effects on 7-ethoxyresorufin-O-

273 e propose ZIP14 mediates zinc transport into hepatocytes to inhibit protein-tyrosine phosphatase 1B (

274 r injury to evaluate the contribution of non-hepatocytes to parenchymal regeneration.

275 1a1, Slc10a1, Slco2b1, Slco1b2, Slco1a4) and hepatocyte-to-blood transporter induction (Abcc4, Abcc3)

276 fic genes, thereby allowing the execution of hepatocyte transdifferentiation; moreover, they highligh

277 expression leads to reversible premalignant hepatocyte transformation and enhanced DEN-carcinogenesi

278 ncreased 45.4-fold, consistent with blood-to-hepatocyte transporter repression (Slco1a1, Slc10a1, Slc

279 complex pattern than observed in surrounding hepatocytes; tumor HRMS were a composite of the 10-wk sp

280 hway activation in macrophages compared with hepatocytes, underscoring the importance of cell type-sp

281 ingly differential gene profile in steatotic hepatocytes versus lean hepatocytes.

282 und that Nox4 mediated LPS-TLR4 signaling in hepatocytes via NF-kB and AP-1 pathways.

283 generating family member 3 alpha (hREG3A) in hepatocytes, via the albumin gene promoter.

284 provide new insights into the regulation of hepatocyte viability in NASH.

285 als, the long-term regenerative potential of hepatocytes was unimpaired, and growth of aggressive exp

286 ies of hepatoma cell lines and primary human hepatocytes, we found that infection with HCV leads to a

287 Furthermore, using cultured primary hepatocytes, we found that lipogenesis was increased by

288 Primary hepatocytes were analyzed for insulin signaling, reactiv

289 o, effects of ConA-conditioned HSC medium on hepatocytes were determined.

290 Fetal hepatocytes were isolated using a monoclonal antibody ag

291 Because juvenile and senescent donor hepatocytes were likewise functional, host-derived facto

292 ter expressed at the canalicular membrane of hepatocytes, where it mediates phosphatidylcholine (PC)

293 animals reconstituted with haplotype-matched hepatocytes, whereas viremia remained stable in mice rec

294 , restraining TNFR1-independent apoptosis in hepatocytes which, in its absence, is causative of TNFR1

295 cterized by accumulation of triglycerides in hepatocytes, which leads to hepatocellular carcinoma.

296 induced by immune-mediated lysis of infected hepatocytes will be critical for the future design of cu

297 Mdr2(-/-) mice contain hepatocytes with a notable persistent DNA damage respons

298 Treatment of primary hepatocytes with exogenous LPA blunted glucagon-induced

299 Complementation of mouse hepatocytes with hNTCP confers susceptibility to HDV but

300 ed Huh7 and Huh7.5.1 cells and primary human hepatocytes with Japanese fulminant hepatitis-1 (JFH1) H