ライフサイエンスコーパス: megakaryoblastic

1 G-actin-associated transcriptional cofactor, megakaryoblastic acute leukemia factor-1 (MKL).

2 , initiation of differentiation of the human megakaryoblastic cell line CHRF-288-11 with phorbol 12-m

3 acetate (PMA)-mediated maturation of a human megakaryoblastic cell line CMK.

4 We used the human megakaryoblastic cell line MEG-01 as an in vitro model f

5 telet-like particles (PLPs) derived from the megakaryoblastic cell line MEG-01 stimulate proliferatio

6 Restoring NF-E2 activity in a megakaryoblastic cell line or in NF-E2-deficient primary

7 ively activated Mek or Erk cDNA into a human megakaryoblastic cell line, CMK, by electroporation.

8 In the SET-2 human megakaryoblastic cell line, heterozygous for the JAK2 V6

9 sufficient to induce differentiation in this megakaryoblastic cell line.

10 Expression of GPVI is increased in the megakaryoblastic cell lines HEL and CMK on differentiati

11 ses in human platelets as well as in several megakaryoblastic cell lines.

12 In human megakaryoblastic cells (MEG-01), transfection with const

13 exes from phorbol ester-induced L8057 murine megakaryoblastic cells and identified the ets transcript

14 croscopy to determine that platelets, MEG-01 megakaryoblastic cells, and bone marrow megakaryocytes c

15 row, human megakaryocytes, and MEG-01 clonal megakaryoblastic cells.

16 ate acetate (PMA)-induced differentiation of megakaryoblastic cells; NMDA receptor blockade by specif

17 The megakaryoblastic CHRF-288 cell line was used to investig

18 rly changes in gene expression necessary for megakaryoblastic commitment and differentiation.

19 a cell line is bipotential for erythroid and megakaryoblastic differentiation.

20 hibition produced a fulminant but reversible megakaryoblastic disorder reminiscent of the transient m

21 sorder (age 0-24 days) and in all with acute megakaryoblastic leukaemia (age 14-38 months).

22 r transient myeloid disorder (n=10) or acute megakaryoblastic leukaemia (n=6).

23 of the mechanosensitive transcription factor megakaryoblastic leukaemia 1 (MKL1), a myocardin family

24 tations in GATA1 have been reported in acute megakaryoblastic leukaemia in Down's syndrome.

25 tions do not necessarily predict later acute megakaryoblastic leukaemia.

26 markedly increased risk of developing acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic

27 (DS) have a greatly increased risk of acute megakaryoblastic leukemia (AMKL) and acute lymphoblastic

28 cal and biologic features of pediatric acute megakaryoblastic leukemia (AMKL) and to identify prognos

29 cases of Down syndrome (DS)-associated acute megakaryoblastic leukemia (AMKL) and transient leukemia

30 actor 1 receptor (CSF1R) kinase in the acute megakaryoblastic leukemia (AMKL) cell line MKPL-1.

31 Acute megakaryoblastic leukemia (AMKL) comprises between 4% an

32 ly death and subsequent development of acute megakaryoblastic leukemia (AMKL) have been reported.

33 Acute megakaryoblastic leukemia (AMKL) is a form of acute myel

34 Acute megakaryoblastic leukemia (AMKL) is a heterogeneous dise

35 Acute megakaryoblastic leukemia (AMKL) is a heterogeneous dise

36 Acute megakaryoblastic leukemia (AMKL) is a rare subtype of AM

37 Acute megakaryoblastic leukemia (AMKL) is a subtype of acute m

38 Acute megakaryoblastic leukemia (AMKL) is a subtype of acute m

39 Acute megakaryoblastic leukemia (AMKL) is more frequently obse

40 ndrome (DS) are predisposed to develop acute megakaryoblastic leukemia (AMKL), characterized by expre

41 TMD may be a precursor to acute megakaryoblastic leukemia (AMKL), with an estimated 30%

42 ), and 20% to 30% of those progress to acute megakaryoblastic leukemia (AMKL).

43 clonal preleukemia, and/or who develop acute megakaryoblastic leukemia (AMKL).

44 trisomic for Hsa21, are predisposed to acute megakaryoblastic leukemia (AMKL).

45 myeloproliferative disorder (TMD) and acute megakaryoblastic leukemia (AMKL).

46 myeloproliferative disorder (TMD), and acute megakaryoblastic leukemia (AMKL).

47 k of developing leukemia, particularly acute megakaryoblastic leukemia (AMKL).

48 es of acute lymphoblastic leukemia and acute megakaryoblastic leukemia (AMKL); DS newborns present wi

49 in the vast majority of patients with acute megakaryoblastic leukemia (DS-AMKL) and in nearly every

50 drome (DS) are at high risk to develop acute megakaryoblastic leukemia (DS-AMKL) and the related tran

51 striction is achieved in Down syndrome acute megakaryoblastic leukemia (DS-AMKL), characterized by th

52 of these infants subsequently develop acute megakaryoblastic leukemia (DS-AMKL).

53 ative disorder (TMD) and Down syndrome-acute megakaryoblastic leukemia (DS-AMKL).

54 ttention as a candidate oncogene in DS-acute megakaryoblastic leukemia (DS-AMKL).

55 ed transient leukemia) and the related acute megakaryoblastic leukemia (DS-AMKL, also called DS-AML M

56 Megakaryoblastic leukemia (MKL)/serum-response factor (S

57 mutation spectrum in non-Down syndrome acute megakaryoblastic leukemia (non-DS-AMKL), we performed tr

58 um response factor (SRF) and its coactivator megakaryoblastic leukemia 1 (MKL1) had increased express

59 Megakaryoblastic leukemia 1 (MKL1) is a myocardin-relate

60 Megakaryoblastic leukemia 1 (MKL1) is a myocardin-relate

61 utrophil immunodeficiency disorder caused by megakaryoblastic leukemia 1 (MKL1) mutation.

62 ocytosis of ACs by splenic MZMs required the megakaryoblastic leukemia 1 (MKL1) transcriptional coact

63 Moreover, megakaryoblastic leukemia 1 (MKL1), a well-known actor i

64 Megakaryoblastic leukemia 1 (MKL1), also known as MAL or

65 Megakaryoblastic leukemia 1 (MKL1), identified as part o

66 and a mechanosensitive transcription factor, megakaryoblastic leukemia 1 (MKL1), that coordinately re

67 ctivation of the transcriptional coactivator megakaryoblastic leukemia 1 (MKL1), which targets the se

68 regulate Srf in part via a pathway involving megakaryoblastic leukemia 1 (Mkl1, also known as myocard

69 protein 15 (RBM15) is involved in the RBM15-megakaryoblastic leukemia 1 fusion in acute megakaryobla

70 Z macrophages (MZMs), which in turn disrupts megakaryoblastic leukemia 1-mediated (MKL1-mediated) mec

71 ignificant proportion of children with acute megakaryoblastic leukemia acquire a translocation that c

72 of hematologic malignancies, including acute megakaryoblastic leukemia and a subset of myeloprolifera

73 wn syndrome (DS) have had significantly more megakaryoblastic leukemia and have experienced better ou

74 megakaryocytic differentiation of the human megakaryoblastic leukemia cell line UT7-MPL.

75 of HPIP in K562 cells, a multipotent erythro-megakaryoblastic leukemia cell line, led to an induction

76 ty of myocardin to physically associate with megakaryoblastic leukemia factor-1 (MKL1) and characteri

77 d possibly increasing ability to distinguish megakaryoblastic leukemia from lymphoid leukemia.

78 formed by the t(1;22) translocation of acute megakaryoblastic leukemia had a markedly increased abili

79 hildren with Down syndrome who develop acute megakaryoblastic leukemia harbor mutations in GATA1 that

80 proliferative disease (MPD) with features of megakaryoblastic leukemia in a murine transplant model.

81 sregulation of GATA-2 is a hallmark of acute megakaryoblastic leukemia in children with Down syndrome

82 to identify chromosome 21 genes that promote megakaryoblastic leukemia in children with DS.

83 o cooperate with GATA1 mutations to initiate megakaryoblastic leukemia in vivo.

84 platelet counts, more antecedent MDS, acute megakaryoblastic leukemia or undifferentiated AML, and a

85 ethod to gene expression profiling for acute megakaryoblastic leukemia shows that our method detects

86 Megakaryoblastic leukemia was unfavorable in others but

87 ies that human GATA1 mutations promote acute megakaryoblastic leukemia, a clonal malignancy with feat

88 s part of the t(1;22) translocation in acute megakaryoblastic leukemia, and plays a critical role in

89 oprotein, which is found in aggressive acute megakaryoblastic leukemia, confers megakaryocytic identi

90 the t(1;22) translocation specific to acute megakaryoblastic leukemia, is highly expressed in differ

91 cation involving 14 cases of pediatric acute megakaryoblastic leukemia, MIST more robustly identified

92 contribute to Diamond-Blackfan anemia, acute megakaryoblastic leukemia, transient myeloproliferative

93 er preleukemic disorders together with acute megakaryoblastic leukemia, whereas quantitative or quali

94 g gene with homology to Drosophila spen, and Megakaryoblastic Leukemia-1 (MKL1), a gene encoding an S

95 ogic disruption of the transcription factors megakaryoblastic leukemia-1 (MKL1)/serum response factor

96 ocardin and the related transcription factor megakaryoblastic leukemia-1 (MKL1/MAL/MRTF-A) can strong

97 n the serum response factor (SRF) co-factors Megakaryoblastic Leukemia-1 and -2 (MKL1 and MKL2) and t

98 ctin polymerization, nuclear accumulation of megakaryoblastic leukemia-1 protein, and SRF activation.

99 ansient myeloproliferative disease and acute megakaryoblastic leukemia.

100 nsient myeloproliferative disorder and acute megakaryoblastic leukemia.

101 e disorder, and increased incidence of acute megakaryoblastic leukemia.

102 in the pathogenesis of trisomy 21-associated megakaryoblastic leukemia.

103 -megakaryoblastic leukemia 1 fusion in acute megakaryoblastic leukemia.

104 th MKL in the t(1;22) translocation of acute megakaryoblastic leukemia.

105 ;22) is the principal translocation of acute megakaryoblastic leukemias.

106 ally, we compared the microRNA expression of megakaryoblastic leukemic cell lines with that of in vit

107 Genetic and pharmacological studies in human megakaryoblastic MEG-01 cells showed that DREAM is impor

108 horylation-regulated kinase 1A, was a potent megakaryoblastic tumor-promoting gene that contributed t

109 In contrast, tie-1 expression on megakaryoblastic UT-7 cells was unaffected by PMA or TNF