ライフサイエンスコーパス: hepatocyte proliferation

1 miR-221 overexpression accelerates hepatocyte proliferation.

2 calization with GPC3 increased at the end of hepatocyte proliferation.

3 by histologic assessment and measurement of hepatocyte proliferation.

4 key regeneration-linked processes including hepatocyte proliferation.

5 y-) mice had the greatest liver recovery and hepatocyte proliferation.

6 , showing delayed regeneration and decreased hepatocyte proliferation.

7 ation plays an important role in suppressing hepatocyte proliferation.

8 fibronectin is not essential for subsequent hepatocyte proliferation.

9 ke of zinc during liver regeneration and for hepatocyte proliferation.

10 sed phosphorylation of c-Met, which promoted hepatocyte proliferation.

11 rmal signaling downstream of IL-6 and normal hepatocyte proliferation.

12 levation determines the extent of subsequent hepatocyte proliferation.

13 s, VEGFR2-Id1 activation in LSECs stimulates hepatocyte proliferation.

14 This treatment significantly inhibited hepatocyte proliferation.

15 5 led to diminished p15(INK4B) and increased hepatocyte proliferation.

16 tration ([Ca(2+)](ER)) homeostasis to affect hepatocyte proliferation.

17 iptional regulator of FoxM1 and compensatory hepatocyte proliferation.

18 is specifically related to liver growth and hepatocyte proliferation.

19 Here we investigated the role of GPC3 in hepatocyte proliferation.

20 ote or diminish hepatic steatosis, influence hepatocyte proliferation.

21 ols, with no effect on liver regeneration or hepatocyte proliferation.

22 modulating lipid homeostasis and regulating hepatocyte proliferation.

23 spase activation, injury, and alterations in hepatocyte proliferation.

24 obiotic and endobiotic metabolism as well as hepatocyte proliferation.

25 ntiate to myofibroblasts and did not support hepatocyte proliferation.

26 mixture resulted in moderate suppression of hepatocyte proliferation.

27 ression and Stat3 activation, and suppressed hepatocyte proliferation.

28 proteins (cyclin D, cyclin E, and Stat3) and hepatocyte proliferation.

29 e in liver size within days but only minimal hepatocyte proliferation.

30 ween beta-catenin/TCF signaling activity and hepatocyte proliferation.

31 orts liver regeneration through promotion of hepatocyte proliferation.

32 egeneration only during inhibition of innate hepatocyte proliferation.

33 ver growth, activation of Cdk2, and enhanced hepatocyte proliferation.

34 eration and molecular events associated with hepatocyte proliferation.

35 holipid formation, DNA hypermethylation, and hepatocyte proliferation.

36 ies indicate that JNK1 is more important for hepatocyte proliferation.

37 of transcription factors, DNA synthesis, and hepatocyte proliferation.

38 wth factor (TGF)-beta, a potent inhibitor of hepatocyte proliferation.

39 lins A, E, and B1, as well as suppression of hepatocyte proliferation.

40 liver tumors also implicates this pathway in hepatocyte proliferation.

41 (cip1), and SOCS1) in liver regeneration and hepatocyte proliferation.

42 lly reduced TCPOBOP-induced hepatomegaly and hepatocyte proliferation.

43 erokine which regulates liver metabolism and hepatocyte proliferation.

44 plays a dual role in modulating the rate of hepatocyte proliferation.

45 by targeting CCN1-inhibitable EGFR-dependent hepatocyte proliferation.

46 jury in the context of hepatotoxin-inhibited hepatocyte proliferation.

47 rentiation and maturation, but also enhanced hepatocyte proliferation.

48 ocked the stimulating effect of platelets on hepatocyte proliferation.

49 hereas insulin triggered EGFR activation and hepatocyte proliferation.

50 PHx, LSP1 increased after the termination of hepatocyte proliferation.

51 ostasis and for linking mtDNA expansion with hepatocyte proliferation.

52 SP1 expression plasmid also led to decreased hepatocyte proliferation.

53 howed a marked reduction in regeneration and hepatocyte proliferation.

54 n gamma by natural killer T cells, promoting hepatocyte proliferation.

55 RT mice, which showed increased survival and hepatocyte proliferation.

56 y leads to severe liver necrosis and reduced hepatocyte proliferation.

57 vel type of serotonin receptor implicated in hepatocyte proliferation.

58 usly decreased cyclin-D1 expression to block hepatocyte proliferation.

59 In vitro treatment with IFN-gamma inhibited hepatocyte proliferation.

60 d signaling pathways related to these benign hepatocyte proliferations.

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

62 ation prior to day 3 post-PHx but attenuates hepatocyte proliferation 3 days after PHx.

63 etion of Epac1 and/or Epac2 led to increased hepatocyte proliferation 36 h post surgery, and the tran

64 on protein (Mcl-1) expression, and increased hepatocyte proliferation after APAP treatment in their l

65 enhanced hepatocyte necrosis and suppressed hepatocyte proliferation after BDL.

66 Ad-Nor-1(small hairpin RNA) reduced the hepatocyte proliferation after hepatectomy.

67 hesized the existence of mechanisms to limit hepatocyte proliferation after injury to maintain metabo

68 stration of an endogenous mechanism to limit hepatocyte proliferation after injury.

69 r function by restraining the first round of hepatocyte proliferation after partial hepatectomy by pr

70 in the regenerating liver markedly inhibited hepatocyte proliferation after partial hepatectomy, conf

71 of quiescent hepatocytes and is required for hepatocyte proliferation after partial hepatectomy.

72 ncy caused an approximately 20-hour delay in hepatocyte proliferation after partial hepatectomy.

73 lack of correlation between IL-6 levels and hepatocyte proliferation after PH, and the accelerated s

74 both intrahepatic platelet accumulation and hepatocyte proliferation after PHx, indicating that fibr

75 e-activated receptor-4 did not contribute to hepatocyte proliferation after PHx, indicating that thro

76 patocyte integrin alphavbeta8 would increase hepatocyte proliferation and accelerate liver regenerati

77 te integrin alphavbeta8 results in increased hepatocyte proliferation and accelerated liver regenerat

78 Deletion of Tob1 increases hepatocyte proliferation and accelerates restoration of

79 Cell death was compensated by hepatocyte proliferation and alanine amino transferase l

80 rs) or miR-21 caused a 50% reduction in both hepatocyte proliferation and anchorage-independent growt

81 We demonstrate that TNF-induced hepatocyte proliferation and apoptosis are both governed

82 n insulin and FFA was studied with regard to hepatocyte proliferation and apoptosis in isolated rat a

83 ver, the mechanisms by which fibrates induce hepatocyte proliferation and cholestasis are still not f

84 f PPARalpha, in modulating WY-14,643-induced hepatocyte proliferation and cholestasis.

85 ced tumorigenesis, associated with increased hepatocyte proliferation and compromised genome integrit

86 These results reveal an unexpected route for hepatocyte proliferation and define a murine model of he

87 tein (YAP) have been shown to play a role in hepatocyte proliferation and development of HCC in anima

88 and hepatic ECM-signaling for regulation of hepatocyte proliferation and differentiation.

89 ew the molecular pathways involved in benign hepatocyte proliferation and discuss how this basic know

90 aNrf2-transgenic mice as a result of delayed hepatocyte proliferation and enhanced apoptosis of these

91 This study investigates the role of GPC3 in hepatocyte proliferation and hepatomegaly induced by the

92 e receptor (CAR) agonist that induces robust hepatocyte proliferation and hepatomegaly without any li

93 ound to be strongly associated with enhanced hepatocyte proliferation and increased cyclin D1 express

94 mice and found that they exhibited decreased hepatocyte proliferation and increased PCD during liver

95 is the mechanism whereby FGF19 can increase hepatocyte proliferation and induce hepatocellular carci

96 p2 contributes to both normal and pathologic hepatocyte proliferation and is linked to tumor aggressi

97 ime, and introduces Epac1/2 as regulators of hepatocyte proliferation and lipid accumulation in the r

98 function as an endogenous regulator of adult hepatocyte proliferation and liver homeostasis.

99 Erlotinib also decreased hepatocyte proliferation and liver injury.

100 We also examined BEC and hepatocyte proliferation and liver marker gene expressio

101 e-targeted overexpression of GPC3 suppresses hepatocyte proliferation and liver regeneration after pa

102 nic littermates but had a suppressed rate of hepatocyte proliferation and liver regeneration after pa

103 ell death in vitro and substantially reduced hepatocyte proliferation and liver regeneration after PH

104 hepatocyte overexpression of GPC3 suppresses hepatocyte proliferation and liver regeneration and alte

105 Nogo-B expression in hepatocytes facilitates hepatocyte proliferation and liver regeneration.

106 study was to determine the role of Nogo-B in hepatocyte proliferation and liver regeneration.

107 and activation of NF-kappaB are required for hepatocyte proliferation and liver regeneration.

108 r receptor (EGFR) is a critical regulator of hepatocyte proliferation and liver regeneration.

109 licated in tissue repair, is dispensable for hepatocyte proliferation and liver regrowth after injury

110 Increased hepatocyte proliferation and liver tumor formation have

111 cyte alphavbeta8, after partial hepatectomy, hepatocyte proliferation and liver-to-body weight ratio

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

113 suggest that YAP promotes cholangiocyte and hepatocyte proliferation and prevents parenchymal damage

114 a potentially druggable target that enhances hepatocyte proliferation and promotes liver regeneration

115 ha in adult hepatocytes results in increased hepatocyte proliferation and promotion of DEN-induced he

116 in the blood early after PH, stimulate both hepatocyte proliferation and protection, in part through

117 , increased neutrophil infiltration, reduced hepatocyte proliferation and reduced ductular reaction 7

118 SB225002 treatment increased hepatocyte proliferation and regeneration in a manner id

119 Hepatocyte proliferation and regeneration was accelerate

120 ore, heterochronic parabiosis increased aged hepatocyte proliferation and restored the cEBP-alpha com

121 ovel roles for E2F and ZFP161 in PB-mediated hepatocyte proliferation and suggest that PB-mediated su

122 critical role in promoting cholangiocyte and hepatocyte proliferation and survival during embryonic l

123 imulates and enhances growth factor-mediated hepatocyte proliferation and survival following partial

124 SRF is essential for hepatocyte proliferation and survival, liver function, a

125 the ability of CDK4/6 inhibition to inhibit hepatocyte proliferation and the effect of RB status on

126 Core protein induces hepatocyte proliferation and the expression of inflammat

127 rticularly beta2SP, plays a critical role in hepatocyte proliferation and transitional phenotype and

128 tion of insulin and FFAs, however, abolished hepatocyte proliferation and triggered CD95-dependent ap

129 ough activation of Sestrin2, which regulates hepatocyte proliferation and tumor development in mice w

130 s have highlighted its role in inhibition of hepatocyte proliferation and tumor suppression.

131 Cs provide hepatocyte growth factor, promote hepatocyte proliferation, and are necessary for normal l

132 Ctgf loss attenuated inflammation, hepatocyte proliferation, and collagen synthesis, wherea

133 g, increased HGF-induced but not EGF-induced hepatocyte proliferation, and tended to reduce TGF-beta1

134 negative regulator of liver regeneration and hepatocyte proliferation, and that this regulation may i

135 hat GPC3 plays a negative regulatory role in hepatocyte proliferation, and this effect may involve CD

136 DEN-induced HCC with increased inflammation, hepatocyte proliferation, and tumor burden.

137 r damage, recruitment of inflammatory cells, hepatocyte proliferation, and ultimately to spontaneous

138 in the liver and monitored their effects on hepatocyte proliferation, apoptosis, gene expression pro

139 odel of chronic inflammation associated with hepatocyte proliferation, apoptosis, oxidative stress, a

140 he mechanisms by which liver injury triggers hepatocyte proliferation are incompletely understood.

141 re associated with accelerated initiation of hepatocyte proliferation, as assessed by hepatocyte brom

142 rly development led to liver enlargement and hepatocyte proliferation, associated with elevated Erk p

143 - or PCNA-positive cells at the time of peak hepatocyte proliferation at 40 hours, which coincided wi

144 y increases in EGFR and Met allow for normal hepatocyte proliferation at 48 hours in KO, which, howev

145 ours after PH, concomitant with reduction of hepatocyte proliferation at the same time point.

146 RT mice showed increased mortality, impaired hepatocyte proliferation, BA accumulation, and profuse l

147 Liver histology, hepatocyte proliferation, BA concentrations (plasma, bil

148 In conclusion, in addition to regulating hepatocyte proliferation, beta-catenin may also control

149 tive regulator of beta-catenin signaling and hepatocyte proliferation, both in vitro and in vivo.

150 t liver injury or ConA-induced impairment of hepatocyte proliferation but did increase the numbers of

151 Lack of Nogo-B delayed hepatocyte proliferation but did not affect the liver-to

152 ariants that have lost the ability to induce hepatocyte proliferation but that still are effective in

153 aneous survivors revealed not only increased hepatocyte proliferation, but also a strong down-regulat

154 ranscription factor is a master regulator of hepatocyte proliferation, but its role in inflammatory c

155 nd transcription analyses revealed increased hepatocyte proliferation, but not apoptosis, in the enla

156 In vitro exposure to IL-4 did not affect hepatocyte proliferation, but surprisingly, genetic abla

157 enin both play a crucial role in stimulating hepatocyte proliferation, but whether these 2 pathways c

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

159 Moreover, cooperative stimulation of hepatocyte proliferation by combined TNF and TGF-alpha t

160 and SnoN during liver regeneration may favor hepatocyte proliferation by inhibiting TGF-beta signals.

161 At later times, SOCS2 enhances hepatocyte proliferation by modulating a decrease in ser

162 Bid regulates hepatocyte proliferation by positively affecting [Ca(2+)

163 ntiation, has been recently shown to inhibit hepatocyte proliferation by way of unknown mechanisms.

164 nding clones may be associated with enhanced hepatocyte proliferation capacity.

165 2) in the LSECs impairs the initial burst of hepatocyte proliferation (days 1-3 after partial hepatec

166 tocyte cultures, GPC3 reaches a plateau when hepatocyte proliferation decreases.

167 In the liver, HuR plays a crucial role in hepatocyte proliferation, differentiation, and transform

168 pid and bile acid (BA) metabolism and induce hepatocyte proliferation downstream of Wnt/beta-catenin

169 this increased cellular stress, insufficient hepatocyte proliferation due to G1 /S-phase cell cycle a

170 aling is involved in regulating zonation and hepatocyte proliferation during homeostasis.

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

172 However, Bid also promotes hepatocyte proliferation during liver regeneration and c

173 ur findings reveal that miR-21 enables rapid hepatocyte proliferation during liver regeneration by ac

174 However, whether miRNAs regulate hepatocyte proliferation during liver regeneration is un

175 or the first time a role of NF-Y activity on hepatocyte proliferation during liver regeneration.

176 show that miRNAs are critical regulators of hepatocyte proliferation during liver regeneration.

177 nin is critical for the proper regulation of hepatocyte proliferation during liver regeneration; howe

178 d whether increased levels of HNF6 stimulate hepatocyte proliferation during mouse liver regeneration

179 Deletion of Cul4A in the liver impairs hepatocyte proliferation during regeneration after carbo

180 We investigated the effects of estrogen on hepatocyte proliferation during zebrafish development, l

181 Hepatocyte proliferation early after liver resection is

182 Patients with AH show impaired hepatocyte proliferation, expansion of inefficient ductu

183 A mice develop normally but exhibit aberrant hepatocyte proliferation following liver partial hepatec

184 Hepatocyte proliferation following partial hepatectomy a

185 -6) a key cytokine required for induction of hepatocyte proliferation following PH.

186 jected to PH, Wls-LKO showed prolongation of hepatocyte proliferation for up to 4 days compared with

187 pFXR-KO mice was unaffected, a delay in peak hepatocyte proliferation from day 2 to day 3 after PHX w

188 Partial hepatectomy triggers hepatocyte proliferation, hepatic matrix remodeling, and

189 ted serum levels of AST) but negatively with hepatocyte proliferation (hepatocyte PCNA and Ki-67 posi

190 ed CAR activation, resulting in uncontrolled hepatocyte proliferation, hepatomegaly and rapid lethali

191 and TRAIL and expression of a suppressor of hepatocyte proliferation, Hnf4alpha.

192 to wild-type (WT) mice resulted in increased hepatocyte proliferation; however, no mitogenic response

193 normal liver regeneration, and Tob1 controls hepatocyte proliferation in a dose-dependent fashion.

194 the idea of critical efficacy and including hepatocyte proliferation in a viral kinetic model, we ca

195 itro, we show that SOCS3 deficiency enhances hepatocyte proliferation in association with enhanced ST

196 fibroblast accumulation, RF ablation induced hepatocyte proliferation in both the ablated lobe and an

197 Decreased hepatocyte proliferation in copeb morphants is accompani

198 d to reduce TGF-beta1-induced suppression of hepatocyte proliferation in cultured hepatocytes.

199 Mechanistically, hepatocyte proliferation in DEN-treated P2y(2)r (-/-) mi

200 lso block liver repair through inhibition of hepatocyte proliferation in HCV-infected patients, playi

201 c cannabinoid 1 receptors (CB1Rs) to promote hepatocyte proliferation in liver regeneration by induci

202 Deletion of p21 led to continuous hepatocyte proliferation in mice with severe injury allo

203 eta-catenin is involved in the regulation of hepatocyte proliferation in multiple contexts, including

204 ation after PH, and the accelerated start of hepatocyte proliferation in Myd88 null mice despite abro

205 by which eosinophil-derived IL-4 stimulates hepatocyte proliferation in regenerating liver.

206 t to determine whether eNOS is essential for hepatocyte proliferation in response to partial hepatect

207 to regeneration-promoting cells that support hepatocyte proliferation in the diseased liver.

208 ss of persistent transgene expression due to hepatocyte proliferation in the growing liver.

209 decreased hepatic PI3K activity and reduced hepatocyte proliferation in the transgenics compared wit

210 IL-22 likewise connected to augmented hepatocyte proliferation in this experimental setting.

211 BrdU and ki67 staining confirmed extensive hepatocyte proliferation in this model.

212 o confer both FGFR4 activation and increased hepatocyte proliferation in vivo to FGF21.

213 We show that IFN-gamma blocks hepatocyte proliferation in vivo, and that in combinatio

214 e, to determine how these findings relate to hepatocyte proliferation in vivo, mice were exposed to c

215 ury, a process that coincided with increased hepatocyte proliferation in vivo.

216 miR-221 in the mouse liver also accelerates hepatocyte proliferation in vivo.

217 in contrast to FGF19, FGF21 does not induce hepatocyte proliferation in vivo.

218 TR exacerbated liver pathology and inhibited hepatocyte proliferation in vivo.

219 e mechanistically how AhR activity modulates hepatocyte proliferation in vivo.

220 type mice; there were no differences seen in hepatocyte proliferation in wild-type mice versus knocko

221 results highlight a key role of p38alpha in hepatocyte proliferation, in the development of hepatome

222 y and liver size, with evidence of decreased hepatocyte proliferation, increased p21 and reduced prol

223 vates a transcriptional program that induces hepatocyte proliferation independently of inflammatory s

224 Inhibition of AMPK by compound C decreased hepatocyte proliferation induced by Med1 and also by the

225 regulation of liver size and termination of hepatocyte proliferation induced by the xenobiotic mitog

226 al cells appear and expand in the liver when hepatocyte proliferation is compromised.

227 be a source of regenerating hepatocytes when hepatocyte proliferation is compromised.

228 The damage response that occurs when hepatocyte proliferation is impaired is thought to be me

229 In severe liver injury, hepatocyte proliferation is impaired-a feature of human

230 tor/oval cells appear in injured livers when hepatocyte proliferation is impaired.

231 enitor/oval cell (OC) activation occurs when hepatocyte proliferation is inhibited and is tightly ass

232 in the form of ductular reactions (DRs) when hepatocyte proliferation is inhibited during severe live

233 epatocytes, oval cells proliferate only when hepatocyte proliferation is inhibited.

234 However, how this pathway is turned off when hepatocyte proliferation is no longer required is unknow

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

236 We show that TNF-induced hepatocyte proliferation is regulated by an inducible, c

237 Hepatocyte proliferation is required for liver regenerat

238 Hepatocyte proliferation is the principal mechanism for

239 ether these 2 pathways cooperate in inducing hepatocyte proliferation is unclear.

240 r, its role in normal liver regeneration and hepatocyte proliferation is unknown.

241 D contributes to liver damage and consequent hepatocyte proliferation known to favour tumorigenesis.

242 Despite suppression of hepatocyte proliferation lasting into day 3 after PHx, l

243 rophils, and similar pathways operant during hepatocyte proliferation/liver regeneration to formulate

244 hepatic necrosis with mild inflammation and hepatocyte proliferation, lymphoid depletion, and inters

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

246 Interestingly, GC-1 does not induce hepatocyte proliferation or Wnt/beta-catenin signaling i

247 r IL-6 or c-met significantly reduced global hepatocyte proliferation (P < .05 for both), with the fo

248 his, we found decreased GPC3-CD81 binding at hepatocyte proliferation peak, increased CD81-Hhex bindi

249 or expression in the liver, liver histology, hepatocyte proliferation, plasma bile acid concentration

250 t eNOS is a critical mediator of EGF-induced hepatocyte proliferation, potentially via its influence

251 Fak deletion enhances hepatocyte proliferation prior to day 3 post-PHx but att

252 tes, and its potential role in EGFR-mediated hepatocyte proliferation, remains unexplored.

253 suppressor PML coincided with an increase in hepatocyte proliferation, resulting in development of mu

254 ating metabolic liver zonation and promoting hepatocyte proliferation, resulting in hepatomegaly.

255 hed p53 activation and elevated compensatory hepatocyte proliferation, resulting in increased HCC.

256 fetal development in the rodent, a burst of hepatocyte proliferation results in a tripling of liver

257 ress, fibrosis, and compensatory increase in hepatocyte proliferation secondary to platelet-derived g

258 There was an accompanying decrease in basal hepatocyte proliferation showed by Ki-67 staining.

259 /My-) mice had enhanced liver recovery, with hepatocyte proliferation similar to CXCR2(Hep-/My-) mice

260 However, both independently increased hepatocyte proliferation, suggesting that additional mec

261 atenin/TCF signaling does not correlate with hepatocyte proliferation, suggesting that this regulatio

262 l of combined liver injury and inhibition of hepatocyte proliferation that causes physiologically sig

263 The increases in hepatic levels of zinc and hepatocyte proliferation that occurred following partial

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

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

266 uced TGF-beta/Smad signaling and accelerated hepatocyte proliferation through down-regulation of p21

267 rmal growth factor receptor (EGFR)-dependent hepatocyte proliferation through integrin alpha6-mediate

268 es show that increased HNF6 levels stimulate hepatocyte proliferation through transcriptional inducti

269 beta1 (TGF-beta1), a powerful suppressor of hepatocyte proliferation, through signaling by mitogen-a

270 y inhibiting carcinogen-induced compensatory hepatocyte proliferation, thus limiting the expansion of

271 ce after PH rescues CYCLIN D1 expression and hepatocyte proliferation to wild-type levels.

272 oncluded that FFAs can shift insulin-induced hepatocyte proliferation toward hepatocyte apoptosis by

273 echanisms of HNF4alpha-induced inhibition of hepatocyte proliferation using a novel tamoxifen (TAM)-i

274 Thus, platelets stimulate hepatocyte proliferation via a mechanism that is depende

275 A significant elevation of hepatocyte proliferation was also seen 7 days after RF a

276 No defect in the initiation of hepatocyte proliferation was apparent.

277 Hepatocyte proliferation was assessed by Ki67 labeling i

278 Hepatocyte proliferation was decreased in CXCR1(-/-) mic

279 We found that serum-stimulated hepatocyte proliferation was dependent on calcium, and t

280 However, a rebound increase in hepatocyte proliferation was evident in the knockout mic

281 When PXR was absent, the second wave of hepatocyte proliferation was severely suppressed, which

282 Hepatocyte proliferation was unaffected by treatment wit

283 ll cycle progression during TCPOBOP-mediated hepatocyte proliferation, was greatly attenuated in [MET

284 DEN, and JNK activity is required for normal hepatocyte proliferation, we examined whether increased

285 To identify the mechanism for FGF19-induced hepatocyte proliferation, we explored similarities and d

286 ations that Myc is unnecessary for long-term hepatocyte proliferation, we have now examined its role

287 rovide conditions permissive for deregulated hepatocyte proliferation, we investigated the consequenc

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

289 Markers of hepatocyte proliferation were 10-fold higher after ALPPS

290 However, the impairments to hepatocyte proliferation were compensated by a response

291 jury as well as basal and mitogen-stimulated hepatocyte proliferation were not modulated by BID.

292 porter-1 and glucose-6-phosphatase mRNA, and hepatocyte proliferation were observed in ArntDeltaEC em

293 ting more severe liver injury and/or reduced hepatocyte proliferation when compared with wild-type mi

294 howed the least amount of liver recovery and hepatocyte proliferation, whereas CXCR2(Hep-/My-) mice h

295 ct ligation because of significantly greater hepatocyte proliferation, which led to a larger liver ma

296 HGF-mediated signaling pathways cooperate in hepatocyte proliferation, which may be crucial in liver

297 oninvasive imaging technique to assess donor hepatocyte proliferation with a preparative regimen of p

298 rto unrecognized role for eNOS activation in hepatocyte proliferation with implications for targeted

299 NF4alpha in adult mice resulted in increased hepatocyte proliferation, with a significant increase in

300 at extending the original model by including hepatocyte proliferation yields a more realistic model w