ライフサイエンスコーパス: primary hepatocyte

1 A and protein expression of SLC13A5 in human primary hepatocytes.

2 is markedly up-regulated relative to normal primary hepatocytes.

3 cholate-rich diet for 5 days and in cultured primary hepatocytes.

4 hich exhibit metabolic properties similar to primary hepatocytes.

5 -sensitive factor (NSF), both in vivo and in primary hepatocytes.

6 of miR-185 in human HCC cells compared with primary hepatocytes.

7 -derived molecules (PAMPs) in mice and human primary hepatocytes.

8 imary hepatocytes but not in the Agpat2(-/-) primary hepatocytes.

9 pcidin expression in hepatic HepG2 cells and primary hepatocytes.

10 ocytes, similar to what is observed in human primary hepatocytes.

11 ds C16:0 and C18:1 failed to increase HGP in primary hepatocytes.

12 the glucose and fatty acid metabolism in the primary hepatocytes.

13 (ser473) in both hepatic tissue and isolated primary hepatocytes.

14 PBA in HCC cells, and to a lesser extent in primary hepatocytes.

15 nhances proliferation of in vitro cultivated primary hepatocytes.

16 genesis by decreasing SREBP-1c expression in primary hepatocytes.

17 the absence of either Furin or PC7 in mouse primary hepatocytes.

18 3 cells stably expressing IRS2 as well as in primary hepatocytes.

19 and cell death in hepatoma cells, but not in primary hepatocytes.

20 PEPCK) but not serpinB1 expression in mouse primary hepatocytes.

21 n mouse and human liver sections, as well as primary hepatocytes.

22 markedly, an observation confirmed in mouse primary hepatocytes.

23 tion of ERK1/2 and AKT by TCA and S1P in rat primary hepatocytes.

24 nhibited glucagon-induced gluconeogenesis in primary hepatocytes.

25 n, gluconeogenic gene expression, and HGP in primary hepatocytes.

26 sion of gluconeogenic genes in the liver and primary hepatocytes.

27 es; estrogen promoted proliferation of human primary hepatocytes.

28 lated IL1Rn and down-regulated IL15Ralpha in primary hepatocytes.

29 id synthesis but not sterol synthesis in rat primary hepatocytes.

30 nscript increases in hepatoma cell lines and primary hepatocytes.

31 Akt-phosphorylation are decreased in BKS-db primary hepatocytes.

32 e expression consistent with the findings in primary hepatocytes.

33 s inhibition by TSA were replicated in human primary hepatocytes.

34 degradation and cytotoxicity by palmitate in primary hepatocytes.

35 in LH mice fed a high-fat diet as well as in primary hepatocytes.

36 d STAT5-null mouse embryonic fibroblasts and primary hepatocytes.

37 y in the human hepatic HepaRG cell line, and primary hepatocytes.

38 reactive oxygen species in mouse livers and primary hepatocytes.

39 creatic hormones on AMPK activation in mouse primary hepatocytes.

40 +) mouse livers at 12 days and in all Cre(+) primary hepatocytes.

41 a level indistinguishable from ACC-deficient primary hepatocytes.

42 during PB-induced CYP2B6 expression in human primary hepatocytes.

43 heterodimeric BMP2/6 were blunted in Hfe KO primary hepatocytes.

44 ressed both HNF4alpha and CES1 expression in primary hepatocytes.

45 rated that HRI regulates Fgf21 expression in primary hepatocytes.

46 ll lines, in human hepatocytes, and in mouse primary hepatocytes.

47 inhibited TNF-alpha/ZVAD-induced necrosis in primary hepatocytes.

48 entacapone when incubated at 50 muM with rat primary hepatocytes.

49 In nontumorigenic cells and primary hepatocytes, AEG-1/RXR colocalizes in the nucleu

50 Sixteen devices with rat primary hepatocytes and 12 with human HepG2/C3A cells we

51 it an 8-fold reduction of heparan sulfate in primary hepatocytes and a 5-fold reduction of heparan su

52 xamethasone increased Angptl4 mRNA levels in primary hepatocytes and adipocytes (2-3-fold) and in the

53 iglyceride accumulation in Hepa1-6 cells and primary hepatocytes and also attenuated oleic acid-elici

54 G0S2 inhibited fatty acid oxidation in mouse primary hepatocytes and caused sustained steatosis in li

55 Furthermore, primary hepatocytes and cholangiocytes isolated from Yap

56 KT signaling in an ex vivo model of cultured primary hepatocytes and determined how this HBx activity

57 In human primary hepatocytes and hCAR-KO HepaRG cells, PB-induced

58 Med1 in vivo in mouse liver and in cultured primary hepatocytes and HEK293 and HeLa cells.

59 The effects of ethanol on primary hepatocytes and hepatic cell lines were also stu

60 gen sulfotransferase (SULT1E1) gene in human primary hepatocytes and hepatocellular carcinoma Huh7 ce

61 ulation and tunicamycin-induced ER stress in primary hepatocytes and hepatocyte cell lines.

62 esenchymal transition and migration, we used primary hepatocytes and hepatoma and macrophage cell lin

63 omyelin synthesis but reduced secretion from primary hepatocytes and hepatoma cells.

64 Incubation of primary hepatocytes and Huh7 cells with palmitate or lys

65 ates the regulation of IRAK-1 degradation in primary hepatocytes and in HEK cells overexpressing the

66 lucotoxicity in a hepatoma cell line then in primary hepatocytes and in the liver of diabetic mice.

67 nd produced high levels of triphosphate 6 in primary hepatocytes and in the livers of rats, dogs, and

68 Analysis of the EL processing in primary hepatocytes and in vivo revealed that it is most

69 Metformin treatment of primary hepatocytes and intact murine liver requires AMP

70 PEPCK enzymatic activity is half that of primary hepatocytes and is localized exclusively to the

71 nfirm our findings, we knocked down CideB in primary hepatocytes and isolated ER and cytosol to exami

72 Primary hepatocytes and Kupffer cells were isolated and

73 oorly understood, we addressed this issue in primary hepatocytes and livers of hepatocyte-specific c-

74 n at its therapeutic concentrations in human primary hepatocytes and LS174T human colon cancer cells.

75 d gain- and loss-of-function models in mouse primary hepatocytes and measured hepatocyte insulin resp

76 rget genes were increased in ethanol-treated primary hepatocytes and mouse liver.

77 cked down using an adenoviral shRNA in mouse primary hepatocytes and myotubes.

78 RVFV infection in mammalian cells, including primary hepatocytes and neurons.

79 hosphodiesterase (ns2-H126R) was assessed in primary hepatocytes and primary central nervous system (

80 thways that are regulated by HBx in cultured primary hepatocytes and provide potential mechanisms for

81 amp mRNA in Smad1(fl/fl);Smad5(fl/fl);Cre(+) primary hepatocytes and SMAD1/SMAD5 knockdown Hep3B cell

82 icillin-clavulanate or flucloxacillin and in primary hepatocytes and stem cell-derived organoids from

83 We report that HBx activates AKT in primary hepatocytes and that the activation of AKT decre

84 nduced Lpcat2/4 and Smpd3 gene expression in primary hepatocytes and the induction was diminished by

85 altered insulin signaling in mouse and human primary hepatocytes and treatment of CypD knockout mice

86 ion is associated with de-differentiation of primary hepatocytes and with the appearance of markers i

87 to development of NAFLD using mouse models, primary hepatocytes, and human cell lines.

88 of S. mansoni-infected hamsters, Huh7 cells, primary hepatocytes, and human liver biopsies.

89 es were evaluated in ASGR binding assays, in primary hepatocytes, and in mice.

90 d tunicamycin (TM)-treated HuH7 cells, mouse primary hepatocytes, and in the plasma of TM-treated C57

91 lization of ERalpha in vivo was confirmed in primary hepatocytes, and it resulted in female infertili

92 icin can enhance lipid accumulation in human primary hepatocytes, and knockdown of SLC13A5 expression

93 ly tagged CAR proteins in Huh-7 cells, mouse primary hepatocytes, and mouse livers, coimmunoprecipita

94 that replicate function and proliferation of primary hepatocytes, and reduces liver fibrosis.

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

96 BCA1-dependent cholesterol efflux from mouse primary hepatocytes, and this effect was shown to be res

97 In primary hepatocytes, ANGPTL3 was processed into a shorte

98 Moreover, primary hepatocytes are the current gold standard for in

99 Using chromatin immunoprecipitation in human primary hepatocytes as well as electrophoretic mobility

100 duction and gluconeogenic gene expression in primary hepatocytes at concentrations found in the porta

101 tal AAV capsids was found to transduce human primary hepatocytes at high efficiency in vitro and in v

102 In primary hepatocytes, autophagy was inhibited by 3MA or a

103 tivation was suppressed by insulin in the WT primary hepatocytes but not in the Agpat2(-/-) primary h

104 vent infection of Huh-7.5 hepatoma cells and primary hepatocytes by cell-culture-derived HCV (HCVcc).

105 In cultured primary hepatocytes, C/EBPbeta stimulates the program of

106 Similarly, in primary hepatocytes, CA-FoxO1 suppressed SREBP1-c expres

107 n studies, adenoviral expression of SOCS3 in primary hepatocytes caused a 50% decrease in 8-br-cAMP-d

108 e show that pharmacologic HDAC inhibition in primary hepatocytes causes histone hyperacetylation but

109 e, Winer et al. establish a self-assembling, primary hepatocyte co-culture system that can be infecte

110 ction for over 30 days in a self-assembling, primary hepatocyte co-culture system.

111 gnificant increase in FAO in SIRT4 knockdown primary hepatocytes compared with control, and this effe

112 on profile and functional characteristics of primary hepatocytes compared with unsorted HLCs.

113 ased secretion of apolipoproteins and TAG in primary hepatocytes, compared with control cells.

114 els of reactive oxygen species in livers and primary hepatocytes, compared with control mice.

115 Studies in human primary hepatocytes confirmed that IL-6 markedly induced

116 gical activation or inhibition of A(2b)AR in primary hepatocytes confirmed the regulation of SREBP-1

117 E4LDLR(-/-) primary hepatocytes cultured in high glucose accumulated

118 day hepatotoxicity assessment in which human primary hepatocytes cultured in the bioreactor were trea

119 s in mice and decreased hydrolysis of TAG in primary hepatocyte cultures and in vitro assays.

120 liver-specific ACSL and FATP isoform in rat primary hepatocyte cultures and subsequently analyzed re

121 UP1 directly decreased glucose production in primary hepatocyte cultures by inhibiting the expression

122 atrix for enhanced albumin synthesis rate of primary hepatocyte cultures for a period of 10 d as comp

123 sis revealed that utilization of Adipogel in primary hepatocyte cultures increased serine, glycine, t

124 O-deethylase (EROD) activity was assessed in primary hepatocyte cultures prepared from chicken (Gallu

125 Using primary hepatocyte cultures to screen for endogenous sig

126 Incubating primary hepatocyte cultures with recombinant FGF-19 supp

127 interaction on the CYP2B6 promoter in human primary hepatocyte cultures.

128 l toxins-induced microvesicular steatosis in primary hepatocyte cultures.

129 e in limiting the spread of HCV infection in primary hepatocyte cultures.

130 eas neutralization of LCN13 increased HGP in primary hepatocyte cultures.

131 esponse, as well as visualizing infection of primary hepatocyte cultures.

132 suppress hepatic glucose production (HGP) in primary hepatocyte cultures.

133 nsulin increased FGF21 gene transcription in primary hepatocyte cultures.

134 failed to induce Hamp in response to Bmp6 in primary hepatocyte cultures.

135 However, the scarcity and variability of primary hepatocytes currently limits their utility.

136 In addition, in mouse and human primary hepatocytes, deficiency of both BMPR2 and ActR2a

137 Primary hepatocytes deficient in STIM1 exhibited elevate

138 Cultures of primary hepatocytes deficient in Tak1 exhibited spontane

139 pressed during fasting in mouse liver and in primary hepatocytes dependent on PGC-1alpha.

140 Primary hepatocytes derived from livers with advanced ci

141 from iPFK2-overexpressing adipocytes, mouse primary hepatocytes displayed metabolic and inflammatory

142 Rgs16 transcription in liver and in cultured primary hepatocytes during gluconeogenesis.

143 ion of P. cynomolgi-infected M. fascicularis primary hepatocytes during which hypnozoites persist and

144 In our use of mouse primary hepatocytes, E(2) suppressed HGP and gluconeogen

145 hesize that modulation of miR-221 targets in primary hepatocytes enhances proliferation, providing no

146 Necrotic human primary hepatocytes exposed to acetaminophen, but not he

147 do not express CPS1, whereas cultured human primary hepatocytes express abundant levels.

148 We report that primary hepatocytes express REST and most of the reprogr

149 Reducing GRK2 levels in murine primary hepatocytes facilitates glucagon-induced glucose

150 transporting polypeptide (hNTCP), on macaque primary hepatocytes facilitates HBV infection in vitro,

151 association was evaluated in cultured human primary hepatocytes from 44 donors.

152 th overexpression or knockdown of AEG-1, and primary hepatocytes from AEG-1 transgenic (Alb/AEG-1) an

153 ytes, an effect that was further enhanced in primary hepatocytes from Agpat2(-/-) mice.

154 Primary hepatocytes from APOM Tg mice generated larger n

155 Studies in primary hepatocytes from c/ebpbeta(-/-) mice confirmed t

156 and mitochondrial mass were also reduced in primary hepatocytes from CCl4-treated KO mice.

157 Similarly, primary hepatocytes from donor livers preconditioned wit

158 Ad5.FX transduction was abrogated in primary hepatocytes from Ext1(HEP) mice.

159 Glucose output of primary hepatocytes from HDAC6KO mice was diminished.

160 In primary hepatocytes from healthy animals, metformin and

161 etion reduced both TG content and LD size in primary hepatocytes from mice harboring floxed alleles o

162 Analysis of primary hepatocytes from mice lacking furin, PC5, PACE4,

163 c JFH1 replicon in embryonic fibroblasts and primary hepatocytes from mice with disruptions in genes

164 Primary hepatocytes from mice, rats, dogs, pigs, rhesus

165 xpressing fatty acid transporters as well as primary hepatocytes from mouse and human livers were inc

166 esidual BCKDC activity in cultured cells and primary hepatocytes from patients and a mouse model of m

167 altered in a model of alcoholic fatty liver, primary hepatocytes from rats fed a 6-week EtOH-containi

168 Primary hepatocytes from rhesus macaques are also permis

169 Accordingly, primary hepatocytes from SIRT4 knockout (KO) mice exhibi

170 portantly, glycolytic flux was diminished in primary hepatocytes from Sirt5(-/-) compared to WT mice.

171 The presence of the preS1-receptor in primary hepatocytes from some non-HBV-susceptible specie

172 ible human hepatoma cell line and studies of primary hepatocytes from Tupaia belangeri have provided

173 Furthermore, both A302 and control primary hepatocytes from which Irs2 was deleted showed m

174 To this end, primary hepatocytes from wild type (WT) and PLTP knock-o

175 This effect was retained in isolated primary hepatocytes from wild-type (WT) mice, but not Gc

176 nd to be higher in the isolated and cultured primary hepatocytes from ZF rats than that from ZL rats.

177 uring liver fibrosis; however, its effect on primary hepatocyte function is unknown.

178 Specific knockdown of IRF-1 in human primary hepatocytes gave similar results.

179 organ with strong regenerative capacity, yet primary hepatocytes have a low amplification potential i

180 ble B7 molecules in supernatants of isolated primary hepatocytes, hepatic sinusoidal endothelial cell

181 In both hepatic mitochondria and isolated primary hepatocytes, heterozygosity of MTP caused an app

182 this study, we have developed a unique human primary hepatocyte (HPH)-leukemia cell coculture model;

183 195 on hCAR in metabolically competent human primary hepatocytes (HPH) and HepaRG cells.

184 ug Matrix (DM) and open TG-GATEs (TG), human primary hepatocytes (HPH) from TG, and mouse liver/HepG2

185 er failure is impeded by a shortage of human primary hepatocytes (HPH), along with current differenti

186 induce CYP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).

187 vivo genetic evidence that syndecan-1 is the primary hepatocyte HSPG receptor mediating the clearance

188 d that E2 repressed BSEP expression in human primary hepatocytes, Huh 7 cells, and in vivo in mice.

189 Human primary hepatocytes, Huh7 hepatoma cells with silenced P

190 lpha signaling pathways were examined in rat primary hepatocytes, human hepatocellular carcinoma cell

191 and DCA were able to inhibit LCFA uptake by primary hepatocytes in a FATP5-dependent manner.

192 sed mTORC2 signaling in liver in vivo and in primary hepatocytes in an AMPK-dependent manner.

193 JNK1 in both hepatoma H4IIE cells and mouse primary hepatocytes in both dose-dependent and time-depe

194 ique configuration was mimicked by embedding primary hepatocytes in collagen gel and overlaying the m

195 terferons are predominantly induced in human primary hepatocytes in response to HBV infection, throug

196 fect on the glycolytic metabolism in healthy primary hepatocytes in vitro and the liver of healthy mi

197 Administration of genotoxic agents to primary hepatocytes in vitro confirmed that DNA damage w

198 n by pancreatic microislets and viability of primary hepatocytes in vitro, as well as normal tissue h

199 ld be immediately successful at transfecting primary hepatocytes in vivo.

200 ALR depletion from primary hepatocytes increased oxidative stress, miR-540

201 cells, and up-regulated in fibrosis, whereas primary hepatocytes induced CCL20 upon experimental inju

202 Consistently, SCD1 inhibition in primary hepatocytes induced FGF21 expression, which was

203 tation followed by sequencing (eCLIP-seq) in primary hepatocytes induced with glucagon.

204 In mouse primary hepatocytes, inhibition of alpha6beta4 integrin

205 nostimuli in mouse embryonic fibroblasts and primary hepatocytes isolated from Clock-deficient mice i

206 insulin action were assessed in vitro using primary hepatocytes isolated from HET and wildtype (WT)

207 Primary hepatocytes isolated from hLrp1(-/-) mice also a

208 In contrast, HDL secretion from primary hepatocytes isolated from hLrp1(-/-) mice was si

209 However, primary hepatocytes isolated from ksr2(-/-) mice show no

210 nd lipid metabolism assays were conducted in primary hepatocytes isolated from mice transduced with c

211 were MyD88-dependent, and were attenuated in primary hepatocytes isolated from Nox4-deficient mice.

212 Primary hepatocytes isolated from these mice were used t

213 co-2 cell layer, and then metabolized by the primary hepatocyte layer.

214 as KLF6 overexpression in HCC cell lines and primary hepatocytes led to reduced MDM2 levels and incre

215 In vitro in mitogen-stimulated primary hepatocytes, MKlp2 accumulated in the nucleus du

216 The carp primary hepatocyte model serves as a useful system for s

217 restricted to the centrilobular area, and in primary hepatocytes, mTORC1 inhibition by hypoxia is ind

218 In isolated mouse livers and primary hepatocytes, NIK also promoted glucagon action a

219 ier, biotransformation of THC was reduced in primary hepatocytes obtained from FABP1-knockout (FABP1-

220 erexpressing CypD enhanced insulin action in primary hepatocytes of diabetic mice.

221 Together with complementary studies using primary hepatocytes of different species, we hypothesize

222 strate that EFV stimulates the activation in primary hepatocytes of key cell stress regulators: inosi

223 Further, anti-miR-34a treatment in primary hepatocytes of obese mice restored FGF19-activat

224 CD36, was greatly decreased in the liver and primary hepatocytes of TAK1(/) mice.

225 In vitro culture of primary hepatocytes on collagen matrix of tunable rigidi

226 Primary hepatocytes on fibronectin are protected from re

227 ects of expression of these factors by mouse primary hepatocytes on HCV replication.

228 Loss of SRA in primary hepatocytes or a hepatocyte cell line upregulate

229 Electron microscopy (EM) of primary hepatocytes or hepatocyte-derived cell lines sup

230 In primary hepatocytes, p16-deficiency was associated with

231 Surface staining of human donor and RM primary hepatocytes (PH) ex vivo revealed the majority o

232 Furthermore, in both cultured MSCs and primary hepatocytes, polyploidization was associated wit

233 Yap deletion in primary hepatocytes potentiates the gluconeogenic gene r

234 We show that mouse primary hepatocytes prefer glycerol to pyruvate/lactate

235 Primary hepatocytes prepared from S1P(2) knock out (S1P(

236 Here, using primary hepatocytes, primary liver macrophages, dominant

237 ts of metformin on hepatic glucose output in primary hepatocytes; rather, their data suggest that the

238 In primary hepatocytes, recombinant LCN13 directly suppress

239 However, fully functional primary hepatocytes remain difficult to expand in vitro,

240 eased into the culture media of HCV-infected primary hepatocytes repeatedly passage to naive hepatocy

241 sis of engineered liver scaffolds with human primary hepatocytes reseeded under dynamic conditions we

242 own approaches in alpha mouse liver cells or primary hepatocytes, respectively, we investigated the r

243 cells or genetic knock-out of Tip30 in mouse primary hepatocytes results in the trapping of EGF-EGFR

244 as most predictive among those examined: rat primary hepatocyte (RPH) cytolethality/volume of distrib

245 data from several sources: rat liver and rat primary hepatocytes (RPH) from Drug Matrix (DM) and open

246 Previous work with HepG2 cells and primary hepatocytes showed that carboxyl ester lipase (C

247 Studies in primary hepatocytes showed that DGAT1 deficiency protect

248 (-), CD8(+) T cells with sporozoite-infected primary hepatocytes significantly inhibited liver-stage

249 HCV nonstructural component NS5A in Huh7 or primary hepatocytes stimulated PEPCK gene expression and

250 Here we show that hepatoma cells and primary hepatocytes strongly up-regulate hepcidin when e

251 and functional activities typical of mature primary hepatocytes, such as LDL storage and uptake, ICG

252 cient mice suppress P450 expression in human primary hepatocytes, suggest that this mouse model may p

253 /4 and down-regulated Slc10a1 and Slco1a1 in primary hepatocytes, suggesting an association between t

254 Normally differentiated human primary hepatocytes supported productive replication of

255 posed of cryopreserved, micropatterned human primary hepatocytes surrounded by supportive stromal cel

256 ignificantly, when tested in humanized mouse primary hepatocytes, TA inhibits hLRH-1 sumoylation and

257 We report a culture system of primary hepatocytes that support productive replication

258 ed either low or high fat diets, in isolated primary hepatocytes the absence of ACSL1 diminished the

259 In primary hepatocytes these IFN-independent require MAVS a

260 centrations suppressed glucose production in primary hepatocytes through AMPK; activation of the cAMP

261 x stiffness activated mechanotransduction in primary hepatocytes through focal adhesion kinase.

262 Silencing Klf10 also sensitized primary hepatocytes to apoptosis along with increased ca

263 Here we used cultured primary hepatocytes to elucidate biochemical and cellula

264 lyzed human hepatoma (HepG2) cells and mouse primary hepatocytes to study transcriptional control of

265 ffects of exposure of carp (Cyprinus carpio) primary hepatocytes to the human PXR agonist rifampicin

266 mming of human endoderm-derived cells (i.e., primary hepatocytes) to pluripotency.

267 Moreover, fat-laden primary hepatocytes treated with alphaVEGFR2 stored sign

268 d macrophages suppresses UPR target genes in primary hepatocytes treated with ER stress inducers.

269 Primary hepatocytes treated with KD3010 but not GW501516

270 and the suppression of glucose production in primary hepatocytes treated with metformin.

271 We measured rates of fatty acid oxidation in primary hepatocytes using radiolabeled palmitate and in

272 ion, were constitutively impaired in FL-N/35 primary hepatocytes via deregulation of TNFalpha/SOCS3.

273 Optimal transfection of primary hepatocytes was achieved on as few as 250cellspe

274 The mobility of glucagon receptor in primary hepatocytes was reduced by galectin-9 binding, a

275 rnative to using donor livers as a source of primary hepatocytes, we explored the possibility of gene

276 Furthermore, using cultured primary hepatocytes, we found that lipogenesis was incre

277 riptionally altered in HCC cells compared to primary hepatocytes, we investigated the implication of

278 Using RNA-seq in primary hepatocytes, we show that these cytokines regula

279 Primary hepatocytes were analyzed for insulin signaling,

280 Serum, liver tissues, and primary hepatocytes were collected from 1-week-old to 20

281 Primary hepatocytes were harvested from mouse liver and

282 H4IIE hepatoma cells and rat primary hepatocytes were incubated with oxyrase to induc

283 Primary hepatocytes were isolated from 4 Holstein calves

284 epatoma cells, but human- and tupaia-derived primary hepatocytes were resistant to hepatitis D viruse

285 In vivo, Cd47-positive human primary hepatocytes were selectively retained following

286 Primary hepatocytes were treated with IL-33 to assess th

287 ers of PPARbeta/delta-null mice and in mouse primary hepatocytes when this receptor was knocked down

288 etion of SH2B1 impaired insulin signaling in primary hepatocytes, whereas SH2B1 overexpression stimul

289 or miR-107 decreased luciferase activity in primary hepatocytes, whereas transfection with antisense

290 n and enhanced ethanol-induced cell death in primary hepatocytes, which suggests that FoxO3a is a key

291 min failed to suppress glucose production in primary hepatocytes with constitutively activated PKA an

292 thway are examined via TR4 knockout mice and primary hepatocytes with either knockdown or overexpress

293 Treatment of primary hepatocytes with exogenous LPA blunted glucagon-

294 Treating primary hepatocytes with glucagon resulted in a 4-fold i

295 ommon mechanism is involved we treated human primary hepatocytes with IL-6, the major mediator of the

296 Treatment of mice and human primary hepatocytes with most Toll-like receptor ligands

297 Stimulation of mouse primary hepatocytes with NGF or pro-NGF increased LDLR e

298 Treatment of both HepG2 cells and primary hepatocytes with subcytotoxic concentrations of

299 ects of insulin in autophagy-deficient mouse primary hepatocytes would be attenuated.

300 mation were observed among zebrafish models (primary hepatocytes, ZFL and ZELH-zfER cell lines).