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1  bipotential facultative hepatic stem cells (hepatoblasts).
2 doptive transfer of primary precursor cells (hepatoblasts).
3 m cell niche in supporting the proliferating hepatoblast.
4 ng with proliferation and differentiation of hepatoblasts.
5 ntenance, and suppressing ST18 expression in hepatoblasts.
6 gallbladder epithelia but not in fetal liver hepatoblasts.
7  generate cholangiocytes from HepaRG-derived hepatoblasts.
8 replication in Huh-7 cells and primary human hepatoblasts.
9 of Dlk1, concomitant with Dlk1 expression by hepatoblasts.
10 ripotent progenitors: hepatic stem cells and hepatoblasts.
11 ss of Hnf4alpha and Hnf6 expression in early hepatoblasts.
12 alpha-fetoprotein enhancer to ablate Jag1 in hepatoblasts.
13 ) livers exhibit diminished proliferation of hepatoblasts.
14 development, also produce albumin-expressing hepatoblasts.
15 o functional mature hepatocytes via immature hepatoblasts.
16 c mutations and a common cell of origin, the hepatoblast, across patients.
17 dence of a KDR+ hepatic progenitor for fetal hepatoblasts, adult hepatocytes, and adult cholangiocyte
18 n occurs in mild forms of liver failure, and hepatoblast amplification occurs in forms of cirrhosis.
19 embryonic stem cells, pancreatic beta cells, hepatoblast and multipotent hematopoietic cells, as well
20 ll fates and morphogenesis in both embryonic hepatoblasts and adult hepatocytes rely on canonical Not
21 tegrated gene expression data from rat fetal hepatoblasts and adult hepatocytes with HCC from human a
22 atic stem cells and hepatoblasts and between hepatoblasts and adult parenchyma are observed.
23 intermediates between hepatic stem cells and hepatoblasts and between hepatoblasts and adult parenchy
24 specification and morphogenesis of embryonic hepatoblasts and biliary conversion of adult hepatocytes
25 strates functional heterogeneity within E9.5 hepatoblasts and identifies Lgr5 as a marker for a subpo
26 e surface of the liver, intermingle with the hepatoblasts and incorporate to the sinusoidal walls.
27 onstrate the antigenic profile of clonogenic hepatoblasts and proof of their bipotency.
28 HBC-3 cells behave in culture as bipotential hepatoblasts and provide a model system to identify fact
29 pha is much reduced and the proliferation of hepatoblasts and RXRalpha-positive cells is significantl
30                   The phenotypic identity of hepatoblasts and the clonal culture system have relevanc
31 main of Notch was conditionally expressed in hepatoblasts and their progeny (hepatocytes and cholangi
32 hHpSCs), which are pluripotent precursors of hepatoblasts and thence of hepatocytic and biliary epith
33 tamyl-transpeptidase (GGT, a marker of fetal hepatoblasts) and glucose-6-phosphatase (G6Pase, a marke
34  (E)8.5 endoderm, E14.5 Dlk1(+) liver cells (hepatoblasts), and adult liver by employing Illumina seq
35  hepatic progenitor cells, lineage-committed hepatoblasts, and differentiated adult hepatocytes with
36                           Using hepatocyte-, hepatoblast- and ductal cell-derived organoids we demons
37                                          The hepatoblasts are contiguous to the niches, decline in nu
38                     Bilateral populations of hepatoblasts are detectable in rargb morphants, indicati
39                           Here, we show that hepatoblasts are not only transcriptionally but also fun
40 and flow cytometry were used to identify rat hepatoblasts as being classical MHC class I, RT1A(l-), O
41 eased, and CK14 and CK19 were abrogated from hepatoblasts at 14 to 16 weeks' gestation.
42 ub-populations of transcriptionally distinct hepatoblasts at E11.5.
43 ells as well as somatic epithelial cells and hepatoblasts/biliary precursors differentiated from thes
44 that other factors are necessary to maintain hepatoblast bipotency.
45  derived not only from adult hepatocytes and hepatoblasts but also hepatic stem/progenitors.
46 dicted targets are expressed highly in E14.5 hepatoblasts but low in the endoderm.
47  to rapid biliary specification of embryonic hepatoblasts, but also-when expressed in up to 6-month-o
48 able neither in normal liver nor in cultured hepatoblasts, but were readily expressed after subcutane
49                Furthermore, isolated Lgr5(+) hepatoblasts can be clonally expanded in vitro into embr
50            A line of hepatic endoderm cells, hepatoblast cell line 3 (HBC-3), was derived from the li
51        HBC-3 cells are a clonal fetal murine hepatoblast cell line derived from an e9.5 murine embryo
52  hepatobiliary fate was confirmed in a human hepatoblast cell line, indicating the relevance of this
53 hepatomesenchymal cell type and evidence for hepatoblast collective cell migration.
54       Diminished proliferation of Foxm1b -/- hepatoblasts contributed to abnormal liver development w
55  mitomycin C treated STON+ feeder layer in a hepatoblast culture medium consisting of Dulbecco's modi
56 this factor was examined in embryonic day 13 hepatoblast culture with maturation factor, oncostatin M
57 y was significantly induced by Mist1 in this hepatoblast culture.
58  Knocking down the ST18 mRNA in transplanted hepatoblasts delayed tumor progression.
59 -2 promoted bidirectional differentiation of hepatoblast-derived cells.
60 component of the genetic networks regulating hepatoblast differentiation and intrahepatic bile duct m
61 e of beta-catenin plays a role in regulating hepatoblast differentiation in mouse and human liver, an
62 ese zonally patterned organoids identifies a hepatoblast differentiation trajectory that dictates per
63 otentiates endothelial network formation and hepatoblast differentiation.
64 ow that the gene expression program of fetal hepatoblasts differs profoundly from that of adult hepat
65                       We find that liver bud hepatoblasts diverge from the two-dimensional lineage, a
66                   Prox1 ablation in bipotent hepatoblasts dramatically reduced the expression of mult
67  not only of biliary commitment of embryonic hepatoblasts during development but also of biliary repr
68 lls, which, like hepatocytes, originate from hepatoblasts during embryonic development.
69 ct system of the liver, which originate from hepatoblasts during embryonic liver development.
70 mimic the DNA methylation state of embryonic hepatoblasts (E16.5), indicating that hepatocytes actual
71 eous, and that a subpopulation of E9.5-E10.0 hepatoblasts exhibit a previously unidentified early com
72                                    Moreover, hepatoblasts express Fgfr2b, which strongly suggests the
73  EphrinB1 domains mediate EphB3b-independent hepatoblast extension formation, while EpB3b interaction
74 ial cells exhibit excess proliferation while hepatoblasts fail to mature into hepatocytes, defects th
75 ic bile ducts, and these presumptive biliary hepatoblasts failed to express either biliary cytokerati
76 f the IHBD tree, whereas deletion of Rumi in hepatoblasts frequently results in an increase in the nu
77 nesis, progenitors within the liver known as hepatoblasts give rise to adult hepatocytes and cholangi
78  shared a gene expression pattern with fetal hepatoblasts had a poor prognosis.
79               Hepatic stem/progenitor cells, hepatoblasts, have a high proliferative ability and can
80 or (FP) cells, followed by the generation of hepatoblasts (HBs), cholangiocyte progenitors (CPs) expr
81  liver progenitors residing at the apex of a hepatoblast hierarchy.
82 dying lumenogenesis in differentiating mouse hepatoblasts in vitro, we discovered that adjacent hepat
83  cell-specific genes; (3) genes expressed in hepatoblasts, in hematopoietic cells, and at varying lev
84         By contrast, excessive commitment of hepatoblasts into cholangiocytes, premature intrahepatic
85 r, it is problem that in vitro maturation of hepatoblasts is insufficient in the present culture syst
86 moving one copy of Rumi from either VSMCs or hepatoblasts is sufficient to partially suppress the Jag
87 s proliferated as they dedifferentiated into hepatoblast-like cells; they subsequently differentiated
88                         In conclusion, fetal hepatoblasts (liver stem/progenitor cells) can serve as
89 t proliferation is dramatically reduced when hepatoblasts, liver progenitor cells, differentiate into
90 o liver bud is evident and expression of the hepatoblast marker alpha-fetoprotein (Afp) is lost.
91  process of hepatic morphogenesis, including hepatoblast maturation, expansion, and survival, making
92 ell precursors caused lineage restriction to hepatoblasts, mature endothelia produced differentiation
93                                      Reduced hepatoblast mitosis was associated with decreased protei
94 s controlled by Eph/Ephrin signaling mediate hepatoblast motility and long-distance cell-cell contact
95 of YAP/TAZ induced by loss of Lats1/2 forces hepatoblasts or hepatocytes to commit to the biliary epi
96 ls from 9 to 36 weeks' gestation, but not in hepatoblasts or hepatocytes.
97 lized this information to derive bipotential hepatoblast organoids and then exploited this model syst
98                                 Here, we use hepatoblast organoids derived from human foetal livers t
99 s not sufficient to block differentiation of hepatoblast organoids into hepatocytes or cholangiocytes
100 xpresses phenotypic characteristics of fetal hepatoblasts, oval cells, and fully differentiated hepat
101  that HBC-3 cells retain an undifferentiated hepatoblast phenotype.
102                                              Hepatoblasts play a key role in liver organogenesis by d
103                  These results indicate that hepatoblasts possess unique characteristics as compared
104  results suggest that Foxm1b is critical for hepatoblast precursor cells to differentiate toward bili
105 affect lineage commitment in the bipotential hepatoblast progenitor cell (BHPC) population.
106      Impaired Notch signaling in bipotential hepatoblast progenitor cells (BHPCs) dose-dependently de
107 GFRalpha-blocking antibody, led to decreased hepatoblast proliferation and survival in embryonic live
108 that Wnt signalling activity correlates with hepatoblast proliferation in the human foetal liver, sug
109 bryos died in utero and exhibited diminished hepatoblast proliferation with similar abnormalities in
110                                  EphrinB1 in hepatoblasts regulates directional migration and mediate
111 , and albumin, indicative of early committed hepatoblasts, requires both autocrine Bmp signaling and
112 ession of wild-type PC1 in ADPKD iPS-derived hepatoblasts rescued ciliary PC2 protein expression leve
113 inctly in stellate/myofibroblastic cells and hepatoblasts, respectively.
114 s displayed a 75% reduction in the number of hepatoblasts, resulting from diminished DNA replication
115 tem cells (rHpSCs) versus their descendants, hepatoblasts (rHBs), two lineage stages of multipotent,
116 We first showed that Wnt plays a key role in hepatoblast self-renewal capacity in vitro by maintainin
117                                              Hepatoblast-specific clones and those representing genes
118                           Finally, we used a hepatoblast-specific Cre recombinase transgene to mediat
119 s work were placed into four categories: (1) hepatoblast-specific genes; (2) hematopoietic cell-speci
120      We capture transcriptional profiles for hepatoblast specification and migration, including the e
121                                              Hepatoblast spheroids were reseeded in a high-throughput
122 hepatic endoderm spheroids and stepwise into hepatoblast spheroids.
123  applied to differentiating hESCs at the pre-hepatoblast stage.
124 ' units (HSC PLUS), composed of niche cells (hepatoblasts, stromal cells, endothelial cells, and macr
125 stream of beta-catenin signaling and promote hepatoblast survival.
126  subpopulation constituting 2% of E9.5-E10.0 hepatoblasts that express the adult stem cell marker Lgr
127 egulating TGFbeta signalling, but suppresses hepatoblast to hepatocyte differentiation by repressing
128 ostratified epithelium, which in turn allows hepatoblasts to emerge into the stromal environment and
129       EphB3b in the LPM concomitantly repels hepatoblasts to move leftward into the liver bud.
130 repopulating rat livers with hepatocytes and hepatoblasts transduced with a lentivirus vector express
131 l deletion of beta-catenin in the developing hepatoblasts utilizing Foxa3-cyclization recombination a
132 e beta-catenin activation in and survival of hepatoblasts via FGF10-mediated signaling.
133 ed epidermal growth factor, clonal growth of hepatoblasts was potentiated without epidermal growth fa
134 ough only some of the ductal plate cells and hepatoblasts were OV-6 positive.
135 uctal plate cells, primitive bile ducts, and hepatoblasts were stained with CK-19 and HEA-125 althoug
136 (E12.5-14.5) FL stages, revealing that while hepatoblasts were the primary source of hematopoietic gr
137 nsferred to STO feeders, hHpSCs give rise to hepatoblasts, which are recognizable by cordlike colony
138                                              Hepatoblasts, which are specified at E8.5-E9.0, have bee
139                       They are precursors to hepatoblasts, which differ from hepatic stem cells in si
140 rom Notch signalling, using mice and primary hepatoblasts with liver-specific knockout of Lats1 and L
141 ts to preserve the proliferative capacity of hepatoblasts without being sufficient to maintain their
142 esized that deletion of Pkd1l1 in developing hepatoblasts would lead to cholangiopathy in mice.

 
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