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

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

2 , showing delayed regeneration and decreased hepatocyte proliferation.

3 ation plays an important role in suppressing hepatocyte proliferation.

4 fibronectin is not essential for subsequent hepatocyte proliferation.

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

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

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

8 erokine which regulates liver metabolism and hepatocyte proliferation.

9 levation determines the extent of subsequent hepatocyte proliferation.

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

11 This treatment significantly inhibited hepatocyte proliferation.

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

13 5 led to diminished p15(INK4B) and increased hepatocyte proliferation.

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

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

16 iptional regulator of FoxM1 and compensatory hepatocyte proliferation.

17 is specifically related to liver growth and hepatocyte proliferation.

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

19 ote or diminish hepatic steatosis, influence hepatocyte proliferation.

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

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

22 modulating lipid homeostasis and regulating hepatocyte proliferation.

23 rentiation and maturation, but also enhanced hepatocyte proliferation.

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

25 obiotic and endobiotic metabolism as well as hepatocyte proliferation.

26 ntiate to myofibroblasts and did not support hepatocyte proliferation.

27 mixture resulted in moderate suppression of hepatocyte proliferation.

28 ression and Stat3 activation, and suppressed hepatocyte proliferation.

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

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

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

32 orts liver regeneration through promotion of hepatocyte proliferation.

33 egeneration only during inhibition of innate hepatocyte proliferation.

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

35 eration and molecular events associated with hepatocyte proliferation.

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

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

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

39 liver tumors also implicates this pathway in hepatocyte proliferation.

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

41 otrophic effect secondary to increased basal hepatocyte proliferation.

42 nt in transgenic mice secondary to increased hepatocyte proliferation.

43 ntrolobular lesions rather than a deficit in hepatocyte proliferation.

44 th anti-SCF antibodies inhibits IL-6-induced hepatocyte proliferation.

45 ocked the stimulating effect of platelets on hepatocyte proliferation.

46 hereas insulin triggered EGFR activation and hepatocyte proliferation.

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

48 ostasis and for linking mtDNA expansion with hepatocyte proliferation.

49 SP1 expression plasmid also led to decreased hepatocyte proliferation.

50 howed a marked reduction in regeneration and hepatocyte proliferation.

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

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

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

54 vel type of serotonin receptor implicated in hepatocyte proliferation.

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

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

57 miR-221 overexpression accelerates hepatocyte proliferation.

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

59 by histologic assessment and measurement of hepatocyte proliferation.

60 key regeneration-linked processes including hepatocyte proliferation.

61 d signaling pathways related to these benign hepatocyte proliferations.

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

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

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

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

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

73 clear p21 expression, which resulted in less hepatocyte proliferation, an exaggerated ductular reacti

74 Deletion of Tob1 increases hepatocyte proliferation and accelerates restoration of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 ouse hepatocytes demonstrate that SCF causes hepatocyte proliferation and is induced by IL-6 and that

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

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

93 Erlotinib also decreased hepatocyte proliferation and liver injury.

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

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

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

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

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

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

100 inal kinase (JNK), a known central player in hepatocyte proliferation and liver regeneration.

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

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

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

104 Increased hepatocyte proliferation and liver tumor formation have

105 sis is characterized by a further decline in hepatocyte proliferation and loss of functional liver ma

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

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

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

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

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

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

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

113 Hepatocyte proliferation and regeneration was accelerate

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

115 sults provide evidence for a large amount of hepatocyte proliferation and selection having occurred d

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

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

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

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

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

121 Core protein induces hepatocyte proliferation and the expression of inflammat

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

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

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

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

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

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

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

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

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

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

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

133 se in liver size was attributed to increased hepatocyte proliferation, as monitored by the mitotic in

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

135 inhibitor follistatin resulted in increased hepatocyte proliferation at 120 hours, particularly in R

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

155 y, but significantly blunted ethanol-induced hepatocyte proliferation by more than 50%.

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

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

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

159 nol, but had no effect on Ras activation and hepatocyte proliferation caused by ethanol.

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

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

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

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

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

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

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

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

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

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

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

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

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

173 uced upregulation of hepatocyte p21 inhibits hepatocyte proliferation during the evolution of cirrhos

174 Hepatocyte proliferation early after liver resection is

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

176 , neutrophil infiltration, cholangiocyte and hepatocyte proliferation, extracellular matrix remodelin

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

178 Hepatocyte proliferation following partial hepatectomy a

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

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

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

182 ell-cycle genes, consistent with AGN-induced hepatocyte proliferation having both PPARalpha-dependent

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

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

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

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

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

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

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

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

191 Decreased hepatocyte proliferation in copeb morphants is accompani

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

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

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

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

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

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

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

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

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

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

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

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

204 suggesting that the SCF-induced increase in hepatocyte proliferation in this system is stat3-mediate

205 mitogen that can activate JNK signaling and hepatocyte proliferation in vitro and initiate JNK signa

206 tor beta (TGF-beta) is a potent inhibitor of hepatocyte proliferation in vitro and is suggested to be

207 uclear antigen (PCNA) protein expression and hepatocyte proliferation in vitro.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 a reserve compartment that is activated when hepatocyte proliferation is inhibited.

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

232 er partial hepatectomy (PH), but its role in hepatocyte proliferation is not known.

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

234 Hepatocyte proliferation is required for liver regenerat

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

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

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

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

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

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

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

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

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

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

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

246 e, and p53-deficient mice each have a higher hepatocyte proliferation rate, are less able to detoxify

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

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

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

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

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

252 After partial hepatectomy to stimulate hepatocyte proliferation, retention of vector genomes an

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

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

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

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

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

258 tion, and higher levels of cholangiocyte and hepatocyte proliferation than WT animals after BDL.

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

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

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

262 M1B (FoxM1B) transcription factor regulates hepatocyte proliferation through expression of cell cycl

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

264 onjunction with TNF or LPS, can both inhibit hepatocyte proliferation through the generation of NO an

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

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

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

268 m1b levels are essential for GH to stimulate hepatocyte proliferation, thus providing a mechanism for

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

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

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

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

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

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

275 Hepatocyte proliferation was assessed by Ki67 labeling i

276 ver, by 120 hours after partial hepatectomy, hepatocyte proliferation was back to baseline in both co

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

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

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

280 Hepatocyte proliferation was increased by RAGE blockade,

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

282 However, necrogenic CCL4-induced hepatocyte proliferation was significantly increased in

283 Hepatocyte proliferation was unaffected by treatment wit

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