ライフサイエンスコーパス: hepatocyte

1 hed from 0% (HB1) to 14.3% (HB5) of infected hepatocytes.

2 ependently at distinct steps of lipophagy in hepatocytes.

3 B-induced CYP2B6 expression in human primary hepatocytes.

4 did not differ between WT and CD36-deficient hepatocytes.

5 transferase 2 (NAT2), are expressed in human hepatocytes.

6 metformin's control of glucose metabolism in hepatocytes.

7 imeric BMP2/6 were blunted in Hfe KO primary hepatocytes.

8 droplet formation in E4bp4-LKO primary mouse hepatocytes.

9 e metabolism is tightly regulated in healthy hepatocytes.

10 NPs, this LNP does not preferentially target hepatocytes.

11 ed to knock down antigen expression in mouse hepatocytes.

12 sive accumulation of lipid droplets (LDs) in hepatocytes.

13 lls, endothelial cells, B cells, T cells and hepatocytes.

14 h expanded tropism for both murine and human hepatocytes.

15 172 and suppression of glucose production in hepatocytes.

16 greater induction of CXCL1 and IL-8 in human hepatocytes.

17 acks hydroxylated prolines in ChREBP-deleted hepatocytes.

18 nly in mononuclear cells but also notably in hepatocytes.

19 only a few on endothelial cells and none on hepatocytes.

20 rifapentine) were compared in primary human hepatocytes.

21 levels, and growth of normal and neoplastic hepatocytes.

22 n of glucose-6-P and glycogen in primary rat hepatocytes.

23 crophages and increased clearance of damaged hepatocytes.

24 dback inhibits TFEB nuclear translocation in hepatocytes.

25 its ligand NPY was secreted by peritumorous hepatocytes.

26 d its orthodox pathway in pericentral normal hepatocytes.

27 ular DNA (cccDNA), is long lived in infected hepatocytes.

28 n line with the strong expression of GCGR on hepatocytes.

29 t that adropin suppresses gluconeogenesis in hepatocytes.

30 ty lipoprotein) cholesterol and steatosis in hepatocytes.

31 s related receptors are expressed in chicken hepatocytes.

32 t PPARalpha mediated these effects of JNK in hepatocytes.

33 ced protein 1 (MCPIP1) can reduce HBV RNA in hepatocytes.

34 xed circular DNA delivered by the virions to hepatocytes.

35 e designed for receptor-mediated delivery to hepatocytes.

36 out; and 7) activates hPXR in primary human hepatocytes.

37 cells, whereas VDR expression is very low in hepatocytes.

38 g vaccines effectively targeted parasites in hepatocytes.

39 straints on cell cycle re-entry of quiescent hepatocytes.

40 impaired alanine-dependent GNG in AnxA6(-/-) hepatocytes.

41 nt, especially macrophages in clearing dying hepatocytes.

42 hormones on AMPK activation in mouse primary hepatocytes.

43 and upstream of endocrine FGF21 expressed by hepatocytes.

44 tocytes and by compensatory proliferation of hepatocytes across liver zones.

45 ocytes but concentrated in a small subset of hepatocytes acting like stem cells, located around the c

46 Mechanistically, Shp deletion in hepatocytes activated NF-kappaB and impaired Pparg activ

47 Primary mouse hepatocytes administrated with recombinant mouse resisti

48 tion of complementary metabolic functions in hepatocytes along a portocentral axis is called liver zo

49 d using adult primary human islets and adult hepatocyte and cholangiocyte organoids.

50 Transcriptomic analysis of cultured hepatocyte and HCC cells found that cyclin D1 knockdown

51 minichromosome in the nucleus of an infected hepatocyte and serves as the template for the transcript

52 have revealed a degree of plasticity between hepatocytes and biliary cells.

53 ne synthetase (GS)(-) hepatocytes into GS(+) hepatocytes and by compensatory proliferation of hepatoc

54 miR-181c promoted apoptosis of HCV-infected hepatocytes and can be inhibited by overexpression of AT

55 hat ATM expression is higher in HCV-infected hepatocytes and chronic HCV-infected liver biopsy specim

56 s in mice, we manipulated Hippo signaling in hepatocytes and examined its effects in nonparenchymal c

57 ine aminotransferase II activity in cultured hepatocytes and forebrain cortical slices.

58 dies were performed in primary rat and human hepatocytes and HepG2 cells.

59 a transmembrane protein expressed mainly in hepatocytes and in developing erythroid cells and is an

60 e (ACC) and increased lipid content in human hepatocytes and in the liver of treated mice by inducing

61 Metformin treatment of primary hepatocytes and intact murine liver requires AMPK regula

62 hance infection efficiency in keratinocytes, hepatocytes and neuronal cells.

63 In primary, cultured hepatocytes and precision-cut liver slices we demonstrat

64 clavulanate or flucloxacillin and in primary hepatocytes and stem cell-derived organoids from multipl

65 cts that stimulate immune-mediated damage of hepatocytes and the biliary tree.

66 4, Rspo1, and Rspo3 were highly expressed in hepatocytes and their expressions were sensitive to ener

67 In hepatocytes and tumor cells, YAP/TEA domain transcriptio

68 Targeting mito-DAMP release from hepatocytes and/or modulating the phagocytic function of

69 d genetic disruption of GPR55 in mice, human hepatocytes, and human hepatic stellate cells.

70 rexin is expressed and secreted from chicken hepatocytes, and that orexin induced hepatic lipogenesis

71 6 protein to inhibit its activation, keeping hepatocyte apoptosis in check.

72 tory factor (IRF3) initiates alcohol-induced hepatocyte apoptosis, which fuels a robust secondary inf

73 Hepatocytes are a major target of yellow fever virus (YF

74 w hepatitis B virions released from infected hepatocytes are the result of an intricate maturation pr

75 PCSK9 is predominantly expressed in hepatocytes as a critical regulator of lipid metabolism,

76 periportally restricted, toward pericentral hepatocytes, as was visualized using a fluorescently lab

77 from liver with DAA leaving <2% HCV-infected hepatocytes at Day 7.

78 Inflamed human hepatocytes attracted neutrophils more effectively than

79 ings delineate mechanisms by which decreased hepatocyte autophagy promotes IL-1beta/TNF-induced necro

80 tance, low AGER1 levels were associated with hepatocyte ballooning degeneration and ductular reaction

81 luding macrosteatosis, lobular inflammation, hepatocyte ballooning degeneration and periportal/perisi

82 The STAM mice developed steatosis, hepatocyte ballooning, and inflammation, which were sign

83 by the additional emergence of inflammation, hepatocyte ballooning, and liver fibrosis.

84 rophils more effectively than inflamed mouse hepatocytes because of the greater induction of CXCL1 an

85 vel system provides a powerful tool to study hepatocyte biology, disease mechanisms, genetic variatio

86 mpairs Plasmodium berghei development inside hepatocytes, both in vitro and in vivo.

87 his ability is not equally distributed among hepatocytes but concentrated in a small subset of hepato

88 f GPRC6A by conditionally deleting Gprc6a in hepatocytes by cross breeding Alb-Cre and Gprc6a(flox/fl

89 direct activation of the phagocytic NOX2 in hepatocytes by p52Shc binding and activating the p47(pho

90 AMPs is controlled by efferocytosis of dying hepatocytes by phagocytic resident liver macrophages and

91 deletion in the liver induces cyclin D1 and hepatocyte cell cycle progression; concurrent cyclin D1

92 The hepatocyte cell line depicted closer proximity to the em

93 s glucose 6-phosphate (G6P) in mouse and rat hepatocytes challenged with high glucose or gluconeogeni

94 s reveal previously unsuspected roles of the hepatocyte clock in the physiological coordination of nu

95 nstrates the hierarchy of the cell-intrinsic hepatocyte clock mechanism and the feeding environment.

96 following a circadian pattern and regulated hepatocyte clock-genes by neutrophil elastase (NE) secre

97 tion on the CYP2B6 promoter in human primary hepatocyte cultures.

98 cold-stressed and damage-prone CC1-deficient hepatocyte cultures.

99 ity, reactive metabolite (RM) formation, and hepatocyte cytolethality, along with physicochemical pro

100 lipid accumulation, which results in reduced hepatocyte damage and fibrosis.

101 n-dependent drug-induced cellular damage and hepatocyte death.

102 The proportion of infected hepatocytes decreased with antiviral exposure from 96.4%

103 encing studies of HEV-infected primary human hepatocytes demonstrated a temporally structured transcr

104 Consequently, hepatocyte derivation, as measured by expression of spec

105 on microscopy (EM) of primary hepatocytes or hepatocyte-derived cell lines supports the existence of

106 This effect was independent of hepatocyte-derived hepcidin or systemic iron levels.

107 Hepatocyte-derived NPY promoted HCC progression by Y5R a

108 Mice with increased polyploid hepatocytes develop fewer liver tumors following chronic

109 cts as a major regulator of HNF4alpha during hepatocyte development, pointing to a target in the trea

110 However, their targeted deletion in adult hepatocytes did not noticeably impair liver regeneration

111 In vivo, liver cancer cells but not hepatocytes display cell surface Cnx.

112 Additionally, we discovered that hepatocytes displayed malfunctioning beta-oxidation, ref

113 We found that modest proliferation of hepatocytes distributed throughout the lobule maintains

114 Under a chronic "ketogenic environment," the hepatocyte diverted more acetyl-CoA away from lipogenesi

115 Loss of both mitoferrins in hepatocytes dramatically reduced regeneration in the adu

116 YR61) as a chemokine that is up-regulated by hepatocytes during liver injury but is expressed at sign

117 We first developed a CD-AOF medium for hepatocytes, ECs, and stage-matched MCs, i.e., septum tr

118 mimicking the organogenic interactions among hepatocytes, endothelial cells (ECs), and mesenchymal ce

119 with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion,

120 Mice lacking PCBP1 in hepatocytes exhibited defects in liver iron homeostasis

121 PCBP1-deleted hepatocytes exhibited increased labile iron and producti

122 f oxidation and glucose metabolism in bovine hepatocytes exposed to increasing concentrations of chol

123 angiocytes expressed GalR1, whereas HSCs and hepatocytes expressed GalR2.

124 Despite no difference in hepatocyte expression, K14-Rac1V12(-/+) mice demonstrate

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

126 Hepatocyte, fibrotic lesion, and bile duct (cancer) were

127 rt-term induction of MYC and beta-catenin in hepatocytes, followed by RNA-sequencing profiling, allow

128 that YAP/TAZ are practically dispensable in hepatocytes for liver development and regeneration.

129 In mice, genetically invalidated in hepatocytes for the chromatin remodeler Arid1a, and for

130 ted p53 stabilization, successfully restored hepatocyte formation from hESCS.

131 n of telomerase and silencing of p53 rescued hepatocyte formation in telomerase mutants.

132 rate that DCLK1-overexpressing primary human hepatocytes formed spheroids in suspension cultures.

133 r capture microdissection, we isolated >1100 hepatocytes from 5 HIV/HBV coinfected persons with incre

134 mary human hepatocytes in culture, including hepatocytes from AAT deficient patients.

135 d metabolic gene expression in primary mouse hepatocytes from E4bp4(flox/flox) but not E4bp4 liver-sp

136 lear inclusions (NI) are a common finding in hepatocytes from patients with liver disease especially

137 gets in human liver tissue and primary human hepatocytes from the Gene Expression Omnibus.

138 clear estrogen receptor 2b (esr2b) increased hepatocyte gene expression and blocked the effects of E2

139 Analyses of tough decoy abundance in hepatocyte genomic DNA and input plasmid pools identifie

140 Hepatitis C virus (HCV) infection promotes hepatocyte growth and progress to hepatocellular carcino

141 and potentially therapeutic applications in hepatocyte growth biology, hepatocellular carcinoma, and

142 Hepatocyte growth factor (HGF) is a multifunctional prot

143 ascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) with the aim of disruptin

144 owth factor (epithelial growth factor (EGF), hepatocyte growth factor (HGF)) and the activation of th

145 Co-occurrence of aberrant hepatocyte growth factor (HGF)/MET proto-oncogene recept

146 The human hepatocyte growth factor receptor (c-MET) signaling path

147 have transformed the human insulin (hIR) and hepatocyte growth factor receptor (hMET) into glutamate

148 Crosstalk between the oncogenic RTK hepatocyte growth factor receptor (MET), epidermal growt

149 f both normal and cancer cells, and MET, the hepatocyte growth factor receptor, are potential targets

150 Beclin 1 promoted endosomal recruitment of hepatocyte growth factor tyrosine kinase substrate (HRS)

151 Lungs were evaluated for HGF (hepatocyte growth factor), a protein involved in alveola

152 The ability of hepatocyte growth factor, the ligand for MET, to promote

153 the 3'UTR of a short isoform of HGF encoding hepatocyte growth factor.

154 istance of PDAC cells induced by CAF-derived hepatocyte growth factor.

155 We therefore conclude that polyploid hepatocytes have extensive regenerative capacity in situ

156 ), and Il2ry (-/-) mice engrafted with human hepatocytes (hFRG mice) and rhesus macaques using a high

157 LPS also increased NLRP3 response in human hepatocytes, however, overexpression of PAFR restored th

158 YP2B6 by phenobarbital (PB) in human primary hepatocytes (HPHs).

159 Validation studies in primary human hepatocytes identified CDKN2C as an important host facto

160 Senescent beta-catenin-depleted hepatocytes in aged mice create an inflammatory microenv

161 ied mRNA encoding human AAT in primary human hepatocytes in culture, including hepatocytes from AAT d

162 rotection, highlighting the critical role of hepatocytes in fueling the cGAS-IRF3 response to alcohol

163 populated DCLK1-overexpressing primary human hepatocytes in humanized FRG mouse livers demonstrated a

164 s the principal mechanism for generating new hepatocytes in liver homeostasis and regeneration.

165 ISCs) but find limited roles for pericentral hepatocytes in liver parenchyma homeostasis.

166 to localize and quantify clonal expansion of hepatocytes in normal and injured liver.

167 We found that YAP/TAZ were activated in hepatocytes in response to carbon tetrachloride toxic in

168 by which nitric oxide, which is produced in hepatocytes in response to inflammation, triggers the ub

169 ur transcriptomic analysis demonstrates that hepatocytes in SACC-PHHs maintain a mature hepatic pheno

170 usly unrecognized mechanism for replenishing hepatocytes in the inflammatory liver and, if unchecked,

171 fumarylacetoacetate hydrolase (FAH)-positive hepatocytes in the liver, and rescued weight loss in mic

172 ntly produced by other cell types, including hepatocytes in various liver pathologies, such as autoim

173 dministration of genotoxic agents to primary hepatocytes in vitro confirmed that DNA damage was indee

174 genesis in vivo, as well as in primary mouse hepatocytes in vitro.

175 adeno-associated virus-mediated approach in hepatocytes in vivo reversed AGER1 downregulation, lower

176 Inhibition of AGEs or RAGE deletion in hepatocytes in vivo reversed these effects.

177 sis (chronic damage), as well as necrosis of hepatocytes in zone 3 of the Rappaport acinus (acute dam

178 ed in human (10.6-fold) and mouse (4.6-fold) hepatocytes incubated with 10 muM 12-D(3)NVP vs NVP.

179 at interferon alpha (IFN-alpha) treatment of hepatocytes induced a prolonged suppression of human and

180 ollowed by sequencing (eCLIP-seq) in primary hepatocytes induced with glucagon.

181 evere YF has long been attributed to massive hepatocyte infection and destruction that results in a d

182 ges of treatment, it comes at the expense of hepatocyte injury and is suboptimal because of lower exp

183 P metabolites is a key determinant for early hepatocytes injury, the recruitment of cells of innate i

184 uss pathways through which stressed and dead hepatocytes instigate the profibrogenic crosstalk with H

185 vein-juxtaposed glutamine synthetase (GS)(-) hepatocytes into GS(+) hepatocytes and by compensatory p

186 homeostatic and reparative potential of all hepatocytes, irrespective of their lobular location or p

187 ional differences between portal and central hepatocytes is missing thus far.

188 Although hepatocyte junctions were intact, KO/KD livers had signi

189 and 3D human cell-based co-culture of human hepatocytes, KCs (Kupffer cells), LECs (Liver Endothelia

190 Human stem cell-derived hepatocyte-like cells (HLCs) offer an attractive platfor

191 ocytes (PHHs), pluripotent stem cell-derived hepatocyte-like cells (HLCs), and hepatoma cells exhibit

192 e unpaired 3 (upd3) in Drosophila oenocytes (hepatocyte-like cells) is the primary non-autonomous mec

193 temic lipid homeostasis by activating TOR in hepatocyte-like cells.

194 uscle-derived Pvf1 signals to the Drosophila hepatocyte-like cells/oenocytes to suppress lipid synthe

195 Thus, infection of cell types other than hepatocytes likely contributes to the consumptive coagul

196 In mice with NASH, LPS serum levels and LPS hepatocyte localization were increased compared with con

197 NASH patients had higher serum LPS and hepatocytes LPS localization than controls, which was co

198 SH, focusing on triggers and consequences of hepatocyte-macrophage-hepatic stellate cell (HSC) crosst

199 ptor (ESR) signaling enhanced liver size and hepatocyte marker expression.

200 ibited significantly increased expression of hepatocyte markers with no impact on liver progenitors,

201 tributed throughout the lobule maintains the hepatocyte mass and that most hepatocytes proliferate to

202 r and establish a critical crosstalk between hepatocyte metabolism and HSC senescence that promotes t

203 Strategies to increase numbers of polypoid hepatocytes might be effective in preventing liver cance

204 liver repopulation, implicating the targeted hepatocyte miRNAs as regulators of this process.

205 Hepatocyte NF 4alpha (Hnf4a) is a major regulator of ren

206 It also involves dynamic expression of hepatocyte nuclear factor (Hnf)4alpha, Yes-associated pr

207 acious first-line treatment in patients with hepatocyte nuclear factor 1alpha (HNF1A) diabetes, but S

208 s constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha) to induce

209 a constitutive androstane receptor (CAR) and hepatocyte nuclear factor 4 alpha (HNF4alpha).

210 Hepatocyte nuclear factor 4alpha (HNF4alpha) is a master

211 Hepatocyte nuclear factor-1beta (HNF-1beta) is a tissue-

212 te-specific gene expression, liver size, and hepatocyte number.

213 Despite an equivalent rate of mitosis in hepatocytes of differing ploidies, we found no lagging c

214 elated highly across the cryopreserved human hepatocytes of rapid, intermediate, and slow acetylator

215 Ablation of cGAS in hepatocytes only phenocopied this hepatoprotection, high

216 Electron microscopy (EM) of primary hepatocytes or hepatocyte-derived cell lines supports th

217 er vaccines that target parasite invasion of hepatocytes or the invasion of and egress from erythrocy

218 types of organoids, including kidney, colon, hepatocyte, ovarian, and breast.

219 In primary hepatocytes, p16-deficiency was associated with elevated

220 ood restriction, VSG corrected the effect of hepatocyte p53 ablation to lower energy expenditure, res

221 These data reveal an important new role for hepatocyte p53 in the regulation of energy expenditure a

222 sessed in terms of their distribution around hepatocytes [pericellular elastosis (PCE)] and within br

223 first contact between HBV and primary human hepatocytes (PHH) in vitro and in vivo.

224 mains challenging, as cultured primary human hepatocytes (PHHs), pluripotent stem cell-derived hepato

225 is-like mechanism and in the process eat the hepatocyte piece by piece.

226 Mice with knockdown of ANLN had hepatocyte ploidy above physiologic levels and developed

227 plantation, providing direct evidence of the hepatocyte ploidy conveyor model.

228 the liver disrupts the normal development of hepatocyte polarity, specification of cell-cell junction

229 licular defects, which resulted from loss of hepatocyte polarity.

230 Increased hepatocyte polyploidy was not associated with altered re

231 maintains the hepatocyte mass and that most hepatocytes proliferate to regenerate it, with diploidy

232 Here, we demonstrate that loss of hepatocyte proliferation is not only an outcome but also

233 Hepatocyte proliferation is the principal mechanism for

234 o study the outcome of CDK1 loss and blocked hepatocyte proliferation on lipid metabolism and the con

235 function stimulate DNA damage responses and hepatocyte proliferation, thereby promoting hepatocarcin

236 function stimulate DNA damage responses and hepatocyte proliferation, thereby promoting hepatocarcin

237 We further demonstrate that FBP1-deficient hepatocytes promote HSC activation by releasing HMGB1; b

238 Indeed, JNK1/2 deficiency in hepatocytes protects against the development of steatosi

239 ormation, impacts on phase II metabolism and hepatocyte protein expression should be considered when

240 ing mass spectrometry proteomics, changes in hepatocyte protein expression, including an increase in

241 tic lipogenesis, in which fructolysis within hepatocytes provides a signal to promote the expression

242 YAP-expressing hepatocytes rapidly and potently activate the expression

243 to proliferate is broadly distributed among hepatocytes rather than limited to a rare stem cell-like

244 ng that Pol II redistribution may facilitate hepatocyte re-entry into the cell cycle.

245 pable of eliminating developing parasites in hepatocytes, resulting in protective immunity.

246 ced by nonhepatocytic cells, and the loss of hepatocyte REV-ERBs remodels the rhythmic transcriptomes

247 fasting conditions and by AMPK deficiency in hepatocytes, revealing metabolic inflexibility and empha

248 In the absence of p53, Gdown1-deficient hepatocytes show a severe dysregulation of cell cycle pr

249 Shp deletion in murine hepatocytes (Shp (Hep-/-)) resulted in massive infiltrat

250 Here, we showed that hepatocytes, sinusoidal endothelial, stellate, and liver

251 nockdown markedly increased liver weight and hepatocyte size in L-G6pc(-/-) mice.

252 g was used to rule out repopulation from non-hepatocyte sources.

253 Mice with a tamoxifen-inducible, hepatocyte-specific Atg5 knockout were similarly sensiti

254 Liver regeneration is impaired in mice with hepatocyte-specific deficiencies in microRNA (miRNA) pro

255 Moreover, hepatocyte-specific deletion of Reverbalpha drives only

256 d at significantly lower levels in mice with hepatocyte-specific deletion of YAP or TAZ.

257 D, and Shc inhibition by LV in older mice or hepatocyte-specific deletion resulted in significantly i

258 Hepatocyte-specific Fbp1 deletion results in steatosis,

259 ng liver development significantly decreased hepatocyte-specific gene expression, liver size, and hep

260 Hepatocyte-specific glypican-3 transgenic mice have decr

261 Hepatocyte-specific HuR knockout reduces the expression

262 patoprotection against AILI was abolished in hepatocyte-specific IL-6 receptor knockout mice.

263 We show here that hepatocyte-specific loss of the gluconeogenic enzyme fru

264 The metabolic deficits induced by hepatocyte-specific p53 ablation were corrected, in part

265 gery was performed in high-fat diet-fed male hepatocyte-specific p53 wild-type and knockout littermat

266 s, our studies identify an important role of hepatocyte-specific peroxisomal import in mediating non-

267 h models of HBV infection, mice that express hepatocyte-specific small hairpin RNAs or that were give

268 diet-fed hepatitis C virus NS5A Tg mice with hepatocyte-specific TBC1D15 deficiency or expression of

269 In contrast, hepatocyte-specific YAP and YAP/TAZ knockouts exhibit li

270 ed hepatotoxicant treatment on functional 3D hepatocyte spheroids tethered directly on polystyrene mu

271 Some studies suggest existence of a hepatocyte subset with such unique capabilities.

272 indicates that Rspo1/Rspo3-LGR4 signaling in hepatocytes suppresses cholesterol synthesis via the AMP

273 After phlebotomy, mice with hepatocyte-targeted Ncoa4 knockdown exhibited anemia and

274 t RNA nanoparticle harboring three copies of hepatocyte targeting-ligands, one copy of miR122, and 24

275 well as the receptor-mediated endocytosis by hepatocyte targeting-ligands.

276 to copolymerize these prodrug monomers with hepatocyte-targeting GalNAc monomers.

277 nsient increase in p21 in a subpopulation of hepatocytes that persists in adult mice.

278 rom activated ILC1s promoted the survival of hepatocytes through upregulation of Bcl-xL.

279 l hepatectomy is enabled by proliferation of hepatocytes throughout the liver, rather than by a peric

280 nderlying DILI vulnerability at the level of hepatocytes, thus facilitating future mechanistic studie

281 ink changes in the lipidome of proliferating hepatocytes to altered metabolic pathways including lipo

282 Silencing Klf10 also sensitized primary hepatocytes to apoptosis along with increased caspase 3

283 n-1-hepatic nuclear factor 4alpha circuit in hepatocytes to downregulate ApoM.

284 We imaged dividing hepatocytes to estimate the frequency of mitotic errors

285 coactivator with PDZ-binding motif (TAZ) in hepatocytes to facilitate cell-cell interactions that st

286 sing MCJ expression enhances the capacity of hepatocytes to mediate beta-oxidation of fatty acids and

287 We performed live-cell microscopy of hepatocytes to monitor the dynamic interactions between

288 phenotypes in Jag1(+/-) mice without ectopic hepatocyte-to-cholangiocyte transdifferentiation or long

289 TA-mediated ablation of AXIN2(+) pericentral hepatocytes transiently disrupts this zone, which is ree

290 PRMT1V2, was stabilized in fasted liver and hepatocytes treated with glucagon, in a PGC1alpha-depend

291 d a transgenic mouse overexpressing Sulf2 in hepatocytes under the control of the transthyretin promo

292 Multicolored polyploid hepatocytes undergo ploidy reduction and subsequent re-p

293 ficient infection of primary human and swine hepatocytes using the developed protocol could be observ

294 early activated the gluconeogenic program in hepatocytes via interactions with PGC1alpha, a key trans

295 ure the metabolic signature of proliferating hepatocytes, we applied state-of-the-art systems biology

296 -7 hepatocellular carcinoma and AML12 normal hepatocytes were incubated with [(2)H(7)]glucose.

297 Primary hepatocytes were isolated from 4 Holstein calves and mai

298 enzyme, glutamine synthetase, in pericentral hepatocytes, where it converts potentially toxic ammonia

299 In addition, hepatocytes with c-Jun activation show cell activation a

300 Challenge of hepatocytes with metformin-induced metabolic stress stre