ライフサイエンスコーパス: hepatoblast

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 generate cholangiocytes from HepaRG-derived hepatoblasts.

5 replication in Huh-7 cells and primary human hepatoblasts.

6 of Dlk1, concomitant with Dlk1 expression by hepatoblasts.

7 ntenance, and suppressing ST18 expression in hepatoblasts.

8 ripotent progenitors: hepatic stem cells and hepatoblasts.

9 ss of Hnf4alpha and Hnf6 expression in early hepatoblasts.

10 alpha-fetoprotein enhancer to ablate Jag1 in hepatoblasts.

11 gallbladder epithelia but not in fetal liver hepatoblasts.

12 ) livers exhibit diminished proliferation of hepatoblasts.

13 development, also produce albumin-expressing hepatoblasts.

14 o functional mature hepatocytes via immature hepatoblasts.

15 dence of a KDR+ hepatic progenitor for fetal hepatoblasts, adult hepatocytes, and adult cholangiocyte

16 n occurs in mild forms of liver failure, and hepatoblast amplification occurs in forms of cirrhosis.

17 ll fates and morphogenesis in both embryonic hepatoblasts and adult hepatocytes rely on canonical Not

18 tegrated gene expression data from rat fetal hepatoblasts and adult hepatocytes with HCC from human a

19 atic stem cells and hepatoblasts and between hepatoblasts and adult parenchyma are observed.

20 intermediates between hepatic stem cells and hepatoblasts and between hepatoblasts and adult parenchy

21 specification and morphogenesis of embryonic hepatoblasts and biliary conversion of adult hepatocytes

22 e surface of the liver, intermingle with the hepatoblasts and incorporate to the sinusoidal walls.

23 onstrate the antigenic profile of clonogenic hepatoblasts and proof of their bipotency.

24 HBC-3 cells behave in culture as bipotential hepatoblasts and provide a model system to identify fact

25 pha is much reduced and the proliferation of hepatoblasts and RXRalpha-positive cells is significantl

26 The phenotypic identity of hepatoblasts and the clonal culture system have relevanc

27 main of Notch was conditionally expressed in hepatoblasts and their progeny (hepatocytes and cholangi

28 hHpSCs), which are pluripotent precursors of hepatoblasts and thence of hepatocytic and biliary epith

29 tamyl-transpeptidase (GGT, a marker of fetal hepatoblasts) and glucose-6-phosphatase (G6Pase, a marke

30 (E)8.5 endoderm, E14.5 Dlk1(+) liver cells (hepatoblasts), and adult liver by employing Illumina seq

31 hepatic progenitor cells, lineage-committed hepatoblasts, and differentiated adult hepatocytes with

32 The hepatoblasts are contiguous to the niches, decline in nu

33 Bilateral populations of hepatoblasts are detectable in rargb morphants, indicati

34 and flow cytometry were used to identify rat hepatoblasts as being classical MHC class I, RT1A(l-), O

35 eased, and CK14 and CK19 were abrogated from hepatoblasts at 14 to 16 weeks' gestation.

36 ells as well as somatic epithelial cells and hepatoblasts/biliary precursors differentiated from thes

37 derived not only from adult hepatocytes and hepatoblasts but also hepatic stem/progenitors.

38 dicted targets are expressed highly in E14.5 hepatoblasts but low in the endoderm.

39 to rapid biliary specification of embryonic hepatoblasts, but also-when expressed in up to 6-month-o

40 able neither in normal liver nor in cultured hepatoblasts, but were readily expressed after subcutane

41 A line of hepatic endoderm cells, hepatoblast cell line 3 (HBC-3), was derived from the li

42 HBC-3 cells are a clonal fetal murine hepatoblast cell line derived from an e9.5 murine embryo

43 Diminished proliferation of Foxm1b -/- hepatoblasts contributed to abnormal liver development w

44 mitomycin C treated STON+ feeder layer in a hepatoblast culture medium consisting of Dulbecco's modi

45 this factor was examined in embryonic day 13 hepatoblast culture with maturation factor, oncostatin M

46 y was significantly induced by Mist1 in this hepatoblast culture.

47 Knocking down the ST18 mRNA in transplanted hepatoblasts delayed tumor progression.

48 -2 promoted bidirectional differentiation of hepatoblast-derived cells.

49 component of the genetic networks regulating hepatoblast differentiation and intrahepatic bile duct m

50 e of beta-catenin plays a role in regulating hepatoblast differentiation in mouse and human liver, an

51 otentiates endothelial network formation and hepatoblast differentiation.

52 ow that the gene expression program of fetal hepatoblasts differs profoundly from that of adult hepat

53 We find that liver bud hepatoblasts diverge from the two-dimensional lineage, a

54 Prox1 ablation in bipotent hepatoblasts dramatically reduced the expression of mult

55 not only of biliary commitment of embryonic hepatoblasts during development but also of biliary repr

56 lls, which, like hepatocytes, originate from hepatoblasts during embryonic development.

57 ct system of the liver, which originate from hepatoblasts during embryonic liver development.

58 Moreover, hepatoblasts express Fgfr2b, which strongly suggests the

59 EphrinB1 domains mediate EphB3b-independent hepatoblast extension formation, while EpB3b interaction

60 ial cells exhibit excess proliferation while hepatoblasts fail to mature into hepatocytes, defects th

61 ic bile ducts, and these presumptive biliary hepatoblasts failed to express either biliary cytokerati

62 f the IHBD tree, whereas deletion of Rumi in hepatoblasts frequently results in an increase in the nu

63 shared a gene expression pattern with fetal hepatoblasts had a poor prognosis.

64 Hepatic stem/progenitor cells, hepatoblasts, have a high proliferative ability and can

65 or (FP) cells, followed by the generation of hepatoblasts (HBs), cholangiocyte progenitors (CPs) expr

66 cell-specific genes; (3) genes expressed in hepatoblasts, in hematopoietic cells, and at varying lev

67 By contrast, excessive commitment of hepatoblasts into cholangiocytes, premature intrahepatic

68 r, it is problem that in vitro maturation of hepatoblasts is insufficient in the present culture syst

69 moving one copy of Rumi from either VSMCs or hepatoblasts is sufficient to partially suppress the Jag

70 s proliferated as they dedifferentiated into hepatoblast-like cells; they subsequently differentiated

71 In conclusion, fetal hepatoblasts (liver stem/progenitor cells) can serve as

72 t proliferation is dramatically reduced when hepatoblasts, liver progenitor cells, differentiate into

73 o liver bud is evident and expression of the hepatoblast marker alpha-fetoprotein (Afp) is lost.

74 process of hepatic morphogenesis, including hepatoblast maturation, expansion, and survival, making

75 ell precursors caused lineage restriction to hepatoblasts, mature endothelia produced differentiation

76 Reduced hepatoblast mitosis was associated with decreased protei

77 s controlled by Eph/Ephrin signaling mediate hepatoblast motility and long-distance cell-cell contact

78 of YAP/TAZ induced by loss of Lats1/2 forces hepatoblasts or hepatocytes to commit to the biliary epi

79 ls from 9 to 36 weeks' gestation, but not in hepatoblasts or hepatocytes.

80 xpresses phenotypic characteristics of fetal hepatoblasts, oval cells, and fully differentiated hepat

81 that HBC-3 cells retain an undifferentiated hepatoblast phenotype.

82 These results indicate that hepatoblasts possess unique characteristics as compared

83 results suggest that Foxm1b is critical for hepatoblast precursor cells to differentiate toward bili

84 affect lineage commitment in the bipotential hepatoblast progenitor cell (BHPC) population.

85 Impaired Notch signaling in bipotential hepatoblast progenitor cells (BHPCs) dose-dependently de

86 GFRalpha-blocking antibody, led to decreased hepatoblast proliferation and survival in embryonic live

87 bryos died in utero and exhibited diminished hepatoblast proliferation with similar abnormalities in

88 EphrinB1 in hepatoblasts regulates directional migration and mediate

89 , and albumin, indicative of early committed hepatoblasts, requires both autocrine Bmp signaling and

90 ession of wild-type PC1 in ADPKD iPS-derived hepatoblasts rescued ciliary PC2 protein expression leve

91 inctly in stellate/myofibroblastic cells and hepatoblasts, respectively.

92 s displayed a 75% reduction in the number of hepatoblasts, resulting from diminished DNA replication

93 tem cells (rHpSCs) versus their descendants, hepatoblasts (rHBs), two lineage stages of multipotent,

94 Hepatoblast-specific clones and those representing genes

95 Finally, we used a hepatoblast-specific Cre recombinase transgene to mediat

96 s work were placed into four categories: (1) hepatoblast-specific genes; (2) hematopoietic cell-speci

97 stream of beta-catenin signaling and promote hepatoblast survival.

98 egulating TGFbeta signalling, but suppresses hepatoblast to hepatocyte differentiation by repressing

99 ostratified epithelium, which in turn allows hepatoblasts to emerge into the stromal environment and

100 EphB3b in the LPM concomitantly repels hepatoblasts to move leftward into the liver bud.

101 repopulating rat livers with hepatocytes and hepatoblasts transduced with a lentivirus vector express

102 l deletion of beta-catenin in the developing hepatoblasts utilizing Foxa3-cyclization recombination a

103 e beta-catenin activation in and survival of hepatoblasts via FGF10-mediated signaling.

104 ed epidermal growth factor, clonal growth of hepatoblasts was potentiated without epidermal growth fa

105 ough only some of the ductal plate cells and hepatoblasts were OV-6 positive.

106 uctal plate cells, primitive bile ducts, and hepatoblasts were stained with CK-19 and HEA-125 althoug

107 nsferred to STO feeders, hHpSCs give rise to hepatoblasts, which are recognizable by cordlike colony

108 They are precursors to hepatoblasts, which differ from hepatic stem cells in si

109 rom Notch signalling, using mice and primary hepatoblasts with liver-specific knockout of Lats1 and L