ライフサイエンスコーパス: hepatocytic

1 ent precursors of hepatoblasts and thence of hepatocytic and biliary epithelia, are located in ductal

2 red to host hepatocytes, differentiated into hepatocytic and biliary epithelial cells, and generated

3 ar1-positive, or CK19-positive, has revealed hepatocytic and biliary poles, respectively, in the DRs.

4 zo-p-dioxin (TCDD), causes increases in both hepatocytic and cholangiocytic tumors.

5 iron-restricted media, reduced its growth in hepatocytic and epithelial cells, and impaired its acqui

6 y enables differentiation transition between hepatocytic and liver progenitor cell types, which is as

7 s-related gene expression and thereby reduce hepatocytic apoptosis after burn injury.

8 dary inflammatory cellular reaction, induces hepatocytic apoptosis and suggest that future therapeuti

9 V/HIV envelope proteins cooperatively induce hepatocytic apoptosis by activating a novel downstream S

10 In this model, hepatocytic apoptosis is the main pathological component

11 Here, we have defined the mechanism of this hepatocytic apoptosis.

12 ant role in HDL metabolism; yet, the role of hepatocytic ATF3 in the development of steatohepatitis r

13 Mechanistically, hepatocytic ATF3 induces hepatic lipolysis and fatty aci

14 According to this model, hepatocytic bilirubin glucuronide can follow a liver-to-

15 ) of F. tularensis grown in the FL83B murine hepatocytic cell line compared to that of F. tularensis

16 uman HBV nucleocapsids in a variety of human hepatocytic cell lines and in primary rat hepatocytes an

17 These were predifferentiated in vitro into hepatocytic cells and delivered to the liver by splenic

18 Cotransfection into AFP-producing hepatocytic cells repressed AFP reporter expression, sug

19 storation of DDD expression in DDD-deficient hepatocytic cells, we found that both caspase-3 sites in

20 zed duck HBV (DHBV) nucleocapsids in chicken hepatocytic cells.

21 uciferase reporter gene and transfected into hepatocytic cells.

22 In normal liver, FLEP cells formed: 1) hepatocytic clusters ranging in size up to approximately

23 ate lobular lymphoplasmacytic hepatitis with hepatocytic coagulative necrosis, but the hydrogenase mu

24 Mice with hepatocytic deletion of Pten develop NASH and HCC later

25 ure hepatocyte markers are expressed; mature hepatocytic differentiation and cell size are also augme

26 9.2% displayed histological diversity: focal hepatocytic differentiation and ductular areas (mixed-IC

27 ividually throughout the liver, resulting in hepatocytic differentiation by tumor cells with concomit

28 Sustained activation of mTOR impaired the hepatocytic differentiation capability of these cells as

29 the human HepaRG cells, which possess potent hepatocytic differentiation capability.

30 l to study factors that may be important for hepatocytic differentiation from precursor cells and a m

31 and a fibroblast feeder layer that supports hepatocytic differentiation from precursor epithelial (o

32 ome P450 (CYP) enzymes, and other markers of hepatocytic differentiation in SHPCs during the protract

33 but differentially express tumorigenicity or hepatocytic differentiation in the liver depending on ho

34 cell pool, impaired migration, and decreased hepatocytic differentiation in vivo, as demonstrated by

35 dged by high expression of c-kit and lack of hepatocytic differentiation markers, whereas OV1(high) c

36 Knockdown of miR-23b miRNAs during hepatocytic differentiation of a fetal liver stem cell l

37 a microRNA signature associated with HCC and hepatocytic differentiation of progenitor cells.

38 further identified miR-148a as an inducer of hepatocytic differentiation that is down-regulated in HC

39 e alpha/NUMB/NOTCH pathway and an inducer of hepatocytic differentiation that when deregulated promot

40 e-like cells also expressed other markers of hepatocytic differentiation, including albumin, transfer

41 ted genes posttranscriptionally regulated on hepatocytic differentiation.

42 ll feeder layer was essential for supporting hepatocytic differentiation.

43 equires an assay system that is conducive to hepatocytic differentiation.

44 cyte-like cells showing different degrees of hepatocytic differentiation.

45 sulfoxide or sodium butyrate induces a rapid hepatocytic differentiation.

46 monolayered Madin-Darby canine kidney cells, hepatocytic epithelial cells, which typically feature ti

47 ation, mainly cells with a single phenotype, hepatocytic (expressing AFP and albumin) or bile ductula

48 suggest that Mist1 partially induces mature hepatocytic expression and function accompanied by the d

49 viremia levels and IFN-alpha therapy reduced hepatocytic expression of HCV RNA.

50 oper morphology, marker gene expression, and hepatocytic functions.

51 Columnar MDCK and Par1b-depleted hepatocytic HepG2 cells featured high RhoA activity that

52 es were transcribed equivalently in Sp3-rich hepatocytic HepG2 cells.

53 c steatohepatitis significantly up-regulated hepatocytic HRG expression, which was associated with M1

54 Therefore, further understanding of the hepatocytic ISG regulation machinery will guide us to an

55 ociated with characteristic liver lesions of hepatocytic karyomegaly and oval cell hyperplasia.

56 ontrast, cotransfection into an AFP-negative hepatocytic line produced moderate activation of the AFP

57 or (rat liver epithelial [RLE]) cells toward hepatocytic lineage affects the response to TNFalpha-med

58 ed hESC- or HepaRG-cholangiocytes, separates hepatocytic lineage from cholangiocyte lineage.

59 in cell culture and differentiated along the hepatocytic lineage in the presence of dexamethasone, ex

60 three markers are transitional cells in the hepatocytic lineage.

61 factor, Mist1, induced expression of mature hepatocytic markers such as carbamoyl-phosphate syntheta

62 chemistry was performed with biliary/HPC and hepatocytic markers.

63 Hepatocytic maturation in iPS-HPCs was significantly inc

64 PS-HSCs with iPS-HPCs significantly improved hepatocytic maturation in iPS-HPCs, such as their capaci

65 s repressed by Hippo pathway activation upon hepatocytic maturation in vitro.

66 that LHX2 upregulation in iPS-HSCs promotes hepatocytic maturation of iPS-HPCs, and indicates that g

67 transmission electron microscopy, and fewer hepatocytic microvilli were evident, indicating impaired

68 f human fetal hepatocytes (HFHs) that retain hepatocytic morphology and gene expression patterns for

69 ve (HNF4alpha(+)) biphenotypic cells showing hepatocytic morphology appeared near EpCAM(+) ductular s

70 culture system, these cells acquired typical hepatocytic morphology.

71 Primary liver cancer arises either from hepatocytic or biliary lineage cells, giving rise to hep

72 C engrafted into the parenchyma exhibited an hepatocytic phenotype and generated new hepatic cord str

73 These problems include the rapid loss of the hepatocytic phenotype in primary culture and the limited

74 cell clusters, very few of which exhibited a hepatocytic phenotype.

75 ficient generation of cells with an immature hepatocytic phenotype.

76 more proliferative, and acquired more mature hepatocytic phenotype.

77 stem cells derived from the bone marrow have hepatocytic potential, a topic that has been covered ext

78 In contrast to hepatocytic potential, duct-like structures and biliary

79 Oval cells are hepatocytic precursors that proliferate in late-stage ci

80 receptor system to elucidate the pathway of hepatocytic processing of ligands such as asialoorosomuc

81 ic-transplant recipients are allowed to age, hepatocytic progeny of BAG2-GN6TF cells proliferate to f

82 f oval cells in an environment inhibitory to hepatocytic proliferation.

83 ncy and is also a determinant factor for the hepatocytic response to antiviral treatment.

84 , hydroxamic acid 14 demonstrates good human hepatocytic stability and good oral bioavailability in r