ライフサイエンスコーパス: embryonal carcinoma cell

1 ng RA-driven differentiation of human NT2/D1 embryonal carcinoma cells.

2 ic stem cells or their malignant equivalent, embryonal carcinoma cells.

3 noic acid/cAMP induced differentiation of F9 embryonal carcinoma cells.

4 ional activation of the same reporter in P19 embryonal carcinoma cells.

5 nd murine mammary stem/progenitor cells, and embryonal carcinoma cells.

6 ouse embryonic stem (mES) cells and in human embryonal carcinoma cells.

7 erum/cytokine-free expansion of leukemic and embryonal carcinoma cells.

8 ctodermal differentiation of pluripotent P19 embryonal carcinoma cells.

9 colocalizing with OCT4 in Ntera2 testicular embryonal carcinoma cells.

10 ons of dorsal root ganglion (DRG) and in P19 embryonal carcinoma cells.

11 platin in testicular germ cell-derived human embryonal carcinoma cells.

12 vity that accompanies the differentiation of embryonal carcinoma cells.

13 s the specificity of RNA interference in p19 embryonal carcinoma cells.

14 f RA-induced neuronal differentiation in p19 embryonal carcinoma cells.

15 fferentiation and cell cycle arrest in human embryonal carcinoma cells.

16 mElf-3 mRNA during the differentiation of F9 embryonal carcinoma cells.

17 y recombinant nodal protein treatment of P19 embryonal carcinoma cells.

18 of retinoic acid-induced differentiation of embryonal carcinoma cells.

19 potent mouse embryonic stem cells or NTERA-2 embryonal carcinoma cells.

20 ferentiation and cell cycle control of human embryonal carcinoma cells.

21 ng retinoid-induced differentiation of human embryonal carcinoma cells.

22 ferentiation and growth suppression of human embryonal carcinoma cells.

23 tion signals has been devised with mouse P19 embryonal carcinoma cells.

24 fic inhibitor of histone deacetylase, on P19 embryonal carcinoma cells.

25 In P19 embryonal carcinoma cells, activation of EphB1 (ELK) by

26 (IPE) element that is inactive in murine F9 embryonal carcinoma cells and active in the parietal end

27 predominant form in embryonic stem cells and embryonal carcinoma cells and can also be detected from

28 lated during neuronal differentiation in P19 embryonal carcinoma cells and epigenetic changes play an

29 or beta2 (RAR(beta2)) gene expression in P19 embryonal carcinoma cells and for reporters driven by th

30 y the activation of STAT1 and STAT3 in mouse embryonal carcinoma cells and human T cells.

31 ted knockdown of USP2a in NTERA-2 testicular embryonal carcinoma cells and MCF7 breast cancer cells c

32 re methylated de novo to a high level in the embryonal carcinoma cells and that the B1 elements acted

33 rget of GATA-6 regulation in differentiating embryonal carcinoma cells and that, in vivo, the express

34 These studies employed F9 embryonal carcinoma cells and their differentiated cells

35 use embryonic stem cells, in differentiating embryonal carcinoma cells, and in transgenic mice.

36 sttranscriptionally in embryonic stem cells, embryonal carcinoma cells, and primary tumors.

37 cardiomyocyte differentiation in pluripotent embryonal carcinoma cells, and we show that this involve

38 Undifferentiated human embryonal carcinoma cells are characterized by high expr

39 , new markers, eg, FGF4, CD30, and OCT-4, of embryonal carcinoma cells are identifying alternative wa

40 d in mES cells and in Ntera-2 or NCCIT human embryonal carcinoma cells, as compared with cells growin

41 ot only in differentiated cells derived from embryonal carcinoma cells, but also in choriocarcinoma c

42 Sox-2 is also highly expressed in F9 embryonal carcinoma cells, but becomes undetectable foll

43 protein synthesis-independent manner in P19 embryonal carcinoma cells by inactivation of NF-kappa B.

44 P19 mouse embryonal carcinoma cells can be stimulated to different

45 wn of Cripto-1 expression in human and mouse embryonal carcinoma cells desensitized the ligand-induce

46 protein affects mdm-2 gene expression as F9 embryonal carcinoma cells differentiate into parietal en

47 FoxA proteins are induced when F9 embryonal carcinoma cells differentiate into visceral en

48 pluripotent embryonic stem cells (ESCs) and embryonal carcinoma cells (ECCs) have some but not all c

49 c acid (RA)-induced differentiation of human embryonal carcinoma cells engages p53.

50 In P19 mouse embryonal carcinoma cells, expression of the MOR was gre

51 ansfection of TFIIB and IRF-1 cDNAs into P19 embryonal carcinoma cells, further demonstrating functio

52 on of Pax3 expression in differentiating P19 embryonal carcinoma cells have been localized.

53 rmation of primitive endoderm from mouse P19 embryonal carcinoma cells in response to retinoic acid,

54 Differentiation of P19 embryonal carcinoma cells in response to the morphogen r

55 neural cells derived from embryonic stem and embryonal carcinoma cells in vitro and neural stem cells

56 st cancer cells and suppressed the growth of embryonal carcinoma cells in vitro.

57 footprinting analysis was performed with P19 embryonal carcinoma cells, in which transcription of the

58 ression following transfection into mouse F9 embryonal carcinoma cells indicated that only Adh-2 poss

59 L1 RNA in extracts from both mouse and human embryonal carcinoma cells indicated that ORF1 protein bi

60 Studies of miR-125b function in mouse P19 embryonal carcinoma cells induced to develop into neuron

61 erization partner E12, can convert mouse P19 embryonal carcinoma cells into differentiated neurons.

62 e Bmp2 mRNA during the differentiation of F9 embryonal carcinoma cells into parietal endoderm.

63 s demonstrated that differentiation of mouse embryonal carcinoma cells leads to transcriptional up-re

64 beta) in neurons (NT2N) derived from a human embryonal carcinoma cell line (NT2) by steady state meta

65 rated that NT2N neurons derived from a human embryonal carcinoma cell line (NT2) constitutively proce

66 Treatment of the undifferentiated parental embryonal carcinoma cell line NT2 with soluble Tax1 did

67 rans-retinoic acid (RA) treatment, the human embryonal carcinoma cell line NT2/D1 exhibits a progress

68 In the embryonal carcinoma cell line NT2/D1, ectopic DeltaN-p63

69 oth mouse embryonic stem cells and the human embryonal carcinoma cell line NT2/D1.

70 After RA-treatment the multipotent human embryonal carcinoma cell line NTERA-2 clone D1 (NT2/D1)

71 iggers terminal differentiation in the human embryonal carcinoma cell line NTERA-2 clone D1 (NT2/D1),

72 Differentiation of the human embryonal carcinoma cell line NTERA-2 is characterized b

73 oters in mouse central nervous system and an embryonal carcinoma cell line P19 was confirmed in a rib

74 xamined in transgenic mouse embryos, a mouse embryonal carcinoma cell line P19, and a mouse embryonic

75 ct4 gene locus in retinoic acid (RA)-treated embryonal carcinoma cell line P19, which involves recept

76 quired for suppressive activity in the mouse embryonal carcinoma cell line P19.

77 Incubation of a human embryonal carcinoma cell line with NMM reduces its stem

78 transactivation function of p53 in the human embryonal carcinoma cell line, NT2/D1, in a retinoid rec

79 Both species are repressed when the human embryonal carcinoma cell line, NT2/D1, is induced to dif

80 Here we show that a embryonal carcinoma cell line, P19, transfected with a S

81 clude two regions of promoter activity in an embryonal carcinoma cell line, Tera2EC.

82 ell lines, five normal human tissues, and an embryonal carcinoma cell line.

83 r into a de novo methylation-competent mouse embryonal carcinoma cell line.

84 significantly greater levels in human ES and embryonal carcinoma cell lines than in control samples.

85 Comparison of human embryonal carcinoma cell lines with breast/ovarian cance

86 nd no alpha subunit message, is expressed in embryonal carcinoma cell lines, F9 and Nulli-SSC1, and i

87 alyzed the activity of 4HPR on a panel of F9 embryonal carcinoma cell lines, which includes wild-type

88 pattern of ARP1 in several mouse tissues and embryonal carcinoma cell lines.

89 of the expressing differentiated cells with embryonal carcinoma cells or by treatment of the differe

90 Removal of endogenous OAZ from pluripotent embryonal carcinoma cells prevents the induction of Smad

91 Here, we report that human embryonal carcinoma cells proliferate and produce differ

92 we show that in mouse embryoid bodies or F9 embryonal carcinoma cells, RARs occupy a large repertoir

93 that overexpressing Hoxa2 in cultures of P19 embryonal carcinoma cells reduced the frequency of spont

94 ion of p53 and p53 pathway genes and renders embryonal carcinoma cells relatively resistant to cispla

95 Embryonal carcinoma cells represent the pluripotent enti

96 t growth factor 4 (FGF-4) gene expression in embryonal carcinoma cells requires a synergistic interac

97 ines showed many similarities with the human embryonal carcinoma cell samples and more distantly with

98 rentiation, whereas studies with pluripotent embryonal carcinoma cells suggest that this pathway prom

99 f RA-induced neuronal differentiation of p19 embryonal carcinoma cells, supporting a role for this pr

100 the Hoxa1, RARbeta2, and Cyp26A1 RAREs in F9 embryonal carcinoma cells (teratocarcinoma stem cells) d

101 ed large sets of genes in embryonic stem and embryonal carcinoma cells that are associated with the t

102 bers of the MEF2 family are expressed in P19 embryonal carcinoma cells that have been induced to form

103 We show here, using P19 embryonal carcinoma cells, that the combination of RA an

104 coupled to the effective maturation of human embryonal carcinoma cells, the described co-transfection

105 We previously reported that, in P19 embryonal carcinoma cells, the expression of kinase-nega

106 which regulates inducibility of the gene in embryonal carcinoma cells through a pattern of DNA-prote

107 Retinoic acid induces P19 mouse embryonal carcinoma cells to differentiate to endoderm a

108 we demonstrate that differentiation of mouse embryonal carcinoma cells to parietal endoderm-like cell

109 the action of retinoic acid, inducing these embryonal carcinoma cells to primitive endoderm.

110 tutive levels of this BH3-only protein prime embryonal carcinoma cells to undergo rapid and massive a

111 ffold protein (GRASP), was isolated from P19 embryonal carcinoma cells using a subtractive screening

112 hylation upon stable transfection into mouse embryonal carcinoma cells was examined.

113 o DNA methylation-associated inactivation in embryonal carcinoma cells were transfected into differen

114 We have studied the function of LINC in F9 embryonal carcinoma cells, which are distinguished by a

115 We showed previously that HL-60 and F9 mouse embryonal carcinoma cells will take up and deblock perac