ライフサイエンスコーパス: primary hepatocyte

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

2 hich exhibit metabolic properties similar to primary hepatocytes.

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

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

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

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

7 pcidin expression in hepatic HepG2 cells and primary hepatocytes.

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

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

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

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

12 nhances proliferation of in vitro cultivated primary hepatocytes.

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

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

15 3 cells stably expressing IRS2 as well as in primary hepatocytes.

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

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

18 markedly, an observation confirmed in mouse primary hepatocytes.

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

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

21 nhibited glucagon-induced gluconeogenesis in primary hepatocytes.

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

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

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

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

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

27 e expression consistent with the findings in primary hepatocytes.

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

29 degradation and cytotoxicity by palmitate in primary hepatocytes.

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

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

32 g TNF-induced proliferation and apoptosis in primary hepatocytes.

33 on to induce both apoptosis and autophagy in primary hepatocytes.

34 G2 hepatocarcinoma cells as well as in mouse primary hepatocytes.

35 either rat hepatoma cells or apoE(-/-) mouse primary hepatocytes.

36 hat sequesters CAR in the cytoplasm of mouse primary hepatocytes.

37 n sequestering CAR in the cytoplasm of mouse primary hepatocytes.

38 nous CYP2b10 gene by PB and TCPOBOP in mouse primary hepatocytes.

39 a level indistinguishable from ACC-deficient primary hepatocytes.

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

41 ressed both HNF4alpha and CES1 expression in primary hepatocytes.

42 rated that HRI regulates Fgf21 expression in primary hepatocytes.

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

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

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

46 reactive oxygen species in mouse livers and primary hepatocytes.

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

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

49 ific for macrophages, as in transduced mouse primary hepatocytes: 1) ApoE2 was secreted as efficientl

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

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

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

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

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

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

56 Paradoxically, in previous studies in primary hepatocytes and cell lines, hepcidin response to

57 Furthermore, primary hepatocytes and cholangiocytes isolated from Yap

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

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

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

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

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

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

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

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

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

67 glycogen synthase activity by bile acids in primary hepatocytes and in the intact liver was investig

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

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

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

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

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

73 Primary hepatocytes and Kupffer cells were isolated and

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

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

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

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

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

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

80 o analyze angiogenesis in 3D cultures of rat primary hepatocytes and rat/human microvascular endothel

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

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

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

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

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

86 pression in hepatocytes (Hep3B cell line and primary hepatocytes) and coronary artery smooth muscle c

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

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

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

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

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

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

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

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

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

96 In primary hepatocytes, ANGPTL3 was processed into a shorte

97 The culture of primary hepatocytes as spheroids creates an efficient th

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

99 sphorylation and glycogen synthesis in mouse primary hepatocytes as well as in human hepatocarcinoma

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 Fresh primary hepatocytes constitute a sufficient system for t

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

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

120 NF-kappaB activation in both HepG2 cells and primary hepatocytes cultured in vitro.

121 Primary hepatocytes cultured without matrix dedifferenti

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

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

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

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

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

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

128 Using primary hepatocyte cultures to screen for endogenous sig

129 Incubating primary hepatocyte cultures with recombinant FGF-19 supp

130 nsulin increased FGF21 gene transcription in primary hepatocyte cultures.

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

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

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

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

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

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

137 nzyme activities and expression in liver and primary hepatocyte cultures.

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

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

140 Primary hepatocytes deficient in STIM1 exhibited elevate

141 Cultures of primary hepatocytes deficient in Tak1 exhibited spontane

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

143 Primary hepatocytes derived from livers with advanced ci

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

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

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

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

148 However, in primary hepatocytes, even in the absence of IFNgamma, we

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

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

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

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

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

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

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

156 Primary hepatocytes from APOM Tg mice generated larger n

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

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

159 Similarly, primary hepatocytes from donor livers preconditioned wit

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

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

162 In primary hepatocytes from healthy animals, metformin and

163 Hepcidin induction by BMP6 was examined in primary hepatocytes from Hfe KO mice; data were compared

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

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

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

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

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

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

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

171 Primary hepatocytes from rhesus macaques are also permis

172 Primary hepatocytes from several different species rapid

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

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

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

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

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

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

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

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

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

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

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

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

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

186 195 on hCAR in metabolically competent human primary hepatocytes (HPH) and HepaRG cells.

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

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

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

190 Human primary hepatocytes, Huh7 hepatoma cells with silenced P

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

192 and DCA were able to inhibit LCFA uptake by primary hepatocytes in a FATP5-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 n hepatoblastoma cell line (HepG2) cells and primary hepatocytes in vitro, and casein injection in ap

198 the liver can induce phenotypic functions in primary hepatocytes in vitro; however, the molecular med

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

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

201 In mouse primary hepatocytes, inhibition of alpha6beta4 integrin

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

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

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

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

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

207 In this study, we used primary hepatocytes isolated from Met-KO and control (Cr

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

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

210 Primary hepatocytes isolated from these mice were used t

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

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

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

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

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

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

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

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

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

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

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

222 Primary hepatocytes on fibronectin are protected from re

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

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

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

226 Yap deletion in primary hepatocytes potentiates the gluconeogenic gene r

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

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

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

230 In primary hepatocytes, recombinant LCN13 directly suppress

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

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

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

234 Previously, using primary hepatocytes residing in early G1 phase, we demon

235 We now report that freshly isolated murine primary hepatocytes responded to holotransferrin but not

236 Inhibition of p38 kinase activity in primary hepatocytes results in approximately 5-10-fold r

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

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

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

240 Our results from isolated primary hepatocytes show that SDF-1alpha and SDF-1beta i

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

242 Studies in primary hepatocytes showed that DGAT1 deficiency protect

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

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

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

246 ne expression signature established in mouse primary hepatocytes successfully discriminated distinct

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

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

249 /4 and down-regulated Slc10a1 and Slco1a1 in primary hepatocytes, suggesting an association between t

250 Normally differentiated human primary hepatocytes supported productive replication of

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

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

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

254 enhanced DCA + MEK1/2 inhibitor toxicity in primary hepatocytes that was dependent on expression of

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

256 Similar to results in primary hepatocytes, the inhibition of the proteasome wi

257 In primary hepatocytes these IFN-independent require MAVS a

258 is capable of inhibiting gluconeogenesis in primary hepatocytes through a signaling pathway distinct

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

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

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

262 We further show that a prolonged exposure of primary hepatocytes to oleate elevated the protein level

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

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

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

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

267 Primary hepatocytes treated with KD3010 but not GW501516

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

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

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

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

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

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

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

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

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

277 In isolated primary hepatocytes, we studied the effect of HNP-1 and

278 Primary hepatocytes were analyzed for insulin signaling,

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

280 a model metabolomic study in which cultured primary hepatocytes were given [(14)C]glucose and organi

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 resistant to 2-AG-induced ROS i

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

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

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

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

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

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

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

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

292 Treatment of primary hepatocytes with exogenous LPA blunted glucagon-

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

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

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

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

297 r results show that a prolonged treatment of primary hepatocytes with oleate blunted insulin suppress

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).