ライフサイエンスコーパス: BFU-E

1 BFU-E and CFU-GM values did not increase in the femur bu

2 BFU-E from peripheral blood were cultured in methylcellu

3 ere higher in less mature precursors (day 10 BFU-E-derived cells) compared with more differentiated (

4 In nuclear extracts from day 10 BFU-E-derived cells, p50, p52, and p65 were able to form

5 evaluable patients; including CFU-GEMM (12), BFU-E (8), and CFU-GM (6).

6 heterozygous for CALR del 52 bp, and 1 of 31 BFU-E was homozygous for CALR del 52 bp.

7 in 31 of the 37 colonies examined; 30 of 31 BFU-E were heterozygous for CALR del 52 bp, and 1 of 31

8 The JAK2 mutation status of 6495 BFU-E, grown in low erythropoietin conditions, was deter

9 cells formed significantly more CFU-GEMM and BFU-E colonies than did the controls.

10 Trauma plasma suppressed CFU-GM and BFU-E colony growth by 40% to 60% at all time periods af

11 essive effect of trauma plasma on CFU-GM and BFU-E colony growth during the early but not late time p

12 trast, there was little effect on CFU-GM and BFU-E formulation or on long term culture initiating cel

13 row yields a marked separation of CFU-GM and BFU-E progenitors, select CCE SBA(-) fractions contain s

14 numbers as well as production of CFU-GM and BFU-E.

15 ombination with carboplatin, than CFU-GM and BFU-E.

16 (6)/kg), GM-CFC (20.5 v 5.0 x 10(4)/kg), and BFU-E (36.9 v 8.9 x 10(4)/kg) in patients receiving r-me

17 essed and secreted by CFU-GM-, CFU-Meg-, and BFU-E-derived cells.

18 l blood were cultured in methylcellulose and BFU-E-derived colonies were harvested on day 10.

19 s, in addition to promoting adhesion of both BFU-E and CFU-E, supported the highest levels of CFU-E m

20 ver or yolk sac cells, hemoglobin-containing BFU-E colonies were detected in cultures treated with re

21 Knockdown of ZFP36L2 in cultured BFU-E cells did not affect the rate of cell division but

22 ites and presumably facilitates GR-dependent BFU-E self-renewal.

23 man and rabbit bone marrow erythroid (CFU-E, BFU-E) and myeloid (CFU-GM) colony growth.

24 of the ACK2 antibody reduced femoral CFU-E, BFU-E, and CFU-GM content to less than half that found i

25 that glucocorticoids stimulate the earliest (BFU-E) progenitors to undergo limited self-renewal, whic

26 /p52, and p65 were highly expressed in early BFU-E-derived precursors, which are rapidly proliferatin

27 a receptor kinase inhibitor increases early BFU-E cell self-renewal and total erythroblast productio

28 promotes TGF-beta signaling during the early BFU-E to late BFU-E transition.

29 "Early" BFU-E cells forming large BFU-E colonies presumably have

30 ermissive for the development of erythbroid (BFU-E), myeloid (CFU-GM), and primitive progenitor (CFU-

31 observed in burst-forming unit-erythrocytes (BFU-E)-derived erythroblasts from a 7-day culture of CD3

32 D34+-derived myeloid (CFU-GM) and erythroid (BFU-E) progenitors.

33 f glucocorticoid action, inhibits erythroid (BFU-E), multipotential (CFU-GEMM), and granulocyte-macro

34 id progenitor, burst-forming unit erythroid (BFU-E), and increase the production of terminally differ

35 = .0008), and burst-forming unit-erythroid (BFU-E) (median slope per day, -1.18; P = .006) were obse

36 cells impaired burst-forming unit-erythroid (BFU-E) and colony-forming unit-erythroid (CFU-E) formati

37 id (CFU-E) and burst-forming unit-erythroid (BFU-E) colonies were not present in cultures derived fro

38 Burst-forming unit-erythroid (BFU-E) colony-formation was also assessed in 7 PV patien

39 Normal burst forming unit-erythroid (BFU-E) growth (>30 bursts/10(5) marrow mononuclear cells

40 newal of early burst-forming unit-erythroid (BFU-E) progenitors.

41 ith progeny of burst-forming unit-erythroid (BFU-E) suggest that the FRET technique is sufficiently s

42 tion from late burst forming unit-erythroid (BFU-E) to basophilic erythroblast stages.

43 e (CFU-M), and burst-forming unit-erythroid (BFU-E) was markedly decreased in Mll -/- cultures, while

44 hage (CFU-GM), burst-forming unit-erythroid (BFU-E), and CFU-erythroid (CFU-E).

45 hage (CFU-GM), burst-forming unit-erythroid (BFU-E), and colony-forming unit-granulocyte, -erythrocyt

46 n of primitive burst-forming unit-erythroid (BFU-E), mature BFU-E, and colony-forming unit-erythroid

47 determined in burst-forming unit-erythroid (BFU-E)-derived cells at different stages of differentiat

48 Burst-forming unit-erythroid (BFU-E)-derived colony growth was not affected.

49 essed in early burst-forming unit-erythroid (BFU-E)-derived erythroid precursors (day 7) and decrease

50 U-GM)-derived, burst forming unit-erythroid (BFU-E)-derived, and CFU-megakaryocyte (CFU-Meg)-derived

51 ; in contrast, burst-forming unit-erythroid (BFU-E)-forming cells were concentrated in the SBA(-) fra

52 ed individual burst-forming units-erythroid (BFU-E) and nonerythroid colony-forming unit-granulocyte-

53 normal human burst-forming units-erythroid (BFU-E) contained Mpl receptor mRNA, and flow cytometric

54 Single burst-forming units-erythroid (BFU-E) from 1 patient were grown in vitro and genotyped:

55 er numbers of burst-forming units-erythroid (BFU-E) in the Wnt-expressing cocultures compared with th

56 Burst-forming units-erythroid (BFU-E) increased in the same time frame as those of CFU-

57 (GM-CFC), and burst-forming units-erythroid (BFU-E) per kilogram in the apheresis product was similar

58 the number of burst-forming units-erythroid (BFU-E), whereas lenalidomide specifically increased colo

59 17% inhibition burst forming unit-erythroid [BFU-E]) and 3.44 micromol/L (24% inhibition of CFU-GM; 5

60 d progenitors (burst-forming unit-erythroid [BFU-E]) were significantly decreased in frequency among

61 [CFU-Meg], and burst-forming unit-erythroid [BFU-E]), and CD34(+) cells showed differential expressio

62 ]), erythroid (burst-forming unit-erythroid [BFU-E]), and granulocyte-macrophage (colony-forming unit

63 e [CFU-GM] and burst-forming unit-erythroid [BFU-E]).

64 ed erythroid (burst-forming units-erythroid [BFU-E]), myeloid (colony-forming units-granulocyte/macro

65 l precursors, burst-forming unit-erythroid- (BFU-E) derived cells.

66 roma severely suppressed growth of 98% of FL BFU-E by inducing apoptosis of cells beyond early erythr

67 receptor (GR) in BFU-Es and is required for BFU-E self-renewal.

68 d and myeloid lineages, including functional BFU-E, CFU-GM, and CFU-MIX progenitors.

69 tured for hematopoietic progenitors (CFU-GM, BFU-E, and CFU-E colonies).

70 Bone marrow CFU-GM, BFU-E, and CFU-E colony formation was significantly redu

71 antly reduced while peripheral blood CFU-GM, BFU-E, and CFU-E was increased in the trauma patients co

72 Proliferative capacities of CFU-GM, BFU-E, and CFU-GEMM were intact as colonies generated re

73 6% and yielded 2 degrees colonies of CFU-GM, BFU-E, and CFU-GEMM.

74 However, BFU-E responses to SCF and erythropoietin were suppresse

75 ssion was erythroid-specific and detected in BFU-E colonies and the erythroid progenies of CFU-GEMM.

76 lucocorticoids induce expression of genes in BFU-E cells that contain promoter regions highly enriche

77 ivision but disrupted glucocorticoid-induced BFU-E self-renewal, and knockdown of ZFP36L2 in transpla

78 The Vav-targeted AS ODN inhibited BFU-E colony formation in all by a mean +/- SD of 81% +/

79 /L (24% inhibition of CFU-GM; 57% inhibition BFU-E) of depsipeptide for 4 hours, followed by a 14-day

80 "Early" BFU-E cells forming large BFU-E colonies presumably have higher capacities for sel

81 eta signaling during the early BFU-E to late BFU-E transition.

82 ee Wnt genes had threefold to fourfold lower BFU-E colony numbers than the Wnt-5A- or Wnt-2B-expressi

83 Trauma plasma inhibits bone marrow BFU-E and CFU-GM colony growth for up to 2 weeks after i

84 burst-forming unit-erythroid (BFU-E), mature BFU-E, and colony-forming unit-erythroid (CFU-E).

85 in cultures grown in the absence of Epo, no BFU-E or CFU-GEMM colonies grew.

86 Hematocrit, red blood cell number, BFU-E-derived colony number,and size were significantly

87 We found that only 10% to 15% of BFU-E bound to FN or to the RGDS sequence in contrast to

88 Approximately 50% to 70% of BFU-E and 60% to 80% of CFU-E bound to the carboxy-termi

89 The appearance of BFU-E was followed by the development of later stage def

90 The binding of BFU-E and CFU-E to the RGDS and CS-1 sites was blocked b

91 s report, we demonstrate that the control of BFU-E cycling is encoded by a gene linked to, but distin

92 The fraction of BFU-E and CFU-GM retrieved from the marrow and spleen of

93 ABM) microenvironment, we compared growth of BFU-E and CFU-GM from 7-14-wk-old FL, 11-20-wk-old fetal

94 , the authors showed that this inhibition of BFU-E and CFU-GM colony growth was mediated by bone marr

95 TE patients showed significant inhibition of BFU-E growth with 10 ng/ml enalaprilat, but controls sho

96 prilat, but controls showed no inhibition of BFU-E growth with ACEI.

97 in mouse strains that exhibit high levels of BFU-E cell cycling.

98 er, there was no difference in the number of BFU-E colonies between PTE patients and controls.

99 on of the CFU-Mix, and a minor population of BFU-E.

100 ocytic lineage, but also includes progeny of BFU-E.

101 No rescue of BFU-E and CFU-E growth was observed when NmU peptide was

102 glucocorticoids, PHI-induced stimulation of BFU-E progenitors thus represents a conceptually new the

103 there is increased expression of the AT1R on BFU-E-derived cells of patients with PTE, which might co

104 or replace the effect of glucocorticoids on BFU-E self-renewal.

105 Only BFU-E colonies were positive for EPO mRNA.

106 Lysates from pooled BFU-E colonies stained positively for EPO by immunoblott

107 he earliest erythroid-restricted precursors (BFU-E [burst-forming unit-erythroid]) is also detected i

108 cted at 21 and 25 ml/min contained primarily BFU-E forming cells, similar to that observed with whole

109 progeny of all early erythroid progenitors (BFU-E colony-forming cells) exhibited the same propensit

110 ferential activity on erythroid progenitors (BFU-E) compared with Wnt-5A and Wnt-2B.

111 earance of definitive erythroid progenitors (BFU-E) that were first detectable at 1-7 somite pairs (E

112 the glucocorticoid receptor (GR) to promote BFU-E self-renewal.

113 ions as part of a molecular switch promoting BFU-E self-renewal and a subsequent increase in the tota

114 Rescued BFU-E colonies expressed adult beta-globin and c-MPL and

115 or c-myb siRNA-treated CD34(+) cells rescued BFU-E and yielded a greater number of CFU-E than observe

116 ned by all tested GR agonists that stimulate BFU-E self-renewal, and the GR binds to several potentia

117 the expansion and differentiation of stress BFU-E during the recovery from acute anemia.

118 cannot recapitulate the expansion of stress BFU-E observed in vivo, which suggests that other signal

119 did we recapitulate the expansion of stress BFU-E observed in vivo.

120 CF are necessary for the expansion of stress BFU-E, but only when spleen cells were cultured in BMP4

121 n a severe defect in the expansion of stress BFU-E, indicating a role for the Kit/SCF signaling pathw

122 rus results in the rapid expansion of stress BFU-E, providing abundant target cells for viral infecti

123 trated that these progenitors, termed stress BFU-E, are targets for Friend virus in the spleen.

124 ation of erythroid progenitors termed stress BFU-E.

125 t the decision to variegate occurs after the BFU-E stage of erythroid differentiation.

126 ed during erythroid differentiation from the BFU-E stage, but its expression is maintained by all tes

127 in bone marrow cells causes a defect in the BFU-E colony formation.

128 transduced human alpha-globin gene in their BFU-E and CFU-GEMM and the lack of its transcript.

129 In contrast to BFU-E from FBM, UCB, or ABM, soluble factor(s) produced

130 6(-) bone marrow cells as EEP giving rise to BFU-E, and Lin(-)CD34(+/-)CD38(+)CD45RA(-)CD123(-)CD71(+

131 , both in control and corticosteroid-treated BFU-E cells, PPAR-alpha co-occupies many chromatin sites

132 id burst- and erythroid colony-forming unit (BFU-E and CFU-E) colonies, the clonogenic assays that qu

133 Using erythroid burst-forming unit (BFU-E) and CFU-E progenitors purified by a new technique

134 ransduction of erythroid burst-forming unit (BFU-E) and colony-forming unit-granulocyte macrophage (C

135 te decrease in erythroid burst-forming unit (BFU-E) and erythroid colony-forming unit (CFU-E) numbers

136 t (CFU-GM) and erythroid burst-forming unit (BFU-E) colonies.

137 s encompassing erythroid burst-forming unit (BFU-E) differentiation to proerythroblast.

138 t (CFU-GM) and erythroid burst-forming unit (BFU-E) growth.

139 % reduction in erythroid blast-forming unit (BFU-E), erythroid colony-forming unit (CFU-E), and colon

140 blast-forming unit and colony-forming unit (BFU-E/CFU-E) activities were significantly reduced in th

141 of both early (erythroid burst-forming unit [BFU-E]) and late erythroid progenitors (erythroid colony

142 of both early (erythroid burst-forming unit [BFU-E]) and late erythroid progenitors (erythroid colony

143 Erythroid burst-forming units (BFU-E) were isolated from peripheral blood using standar

144 (CFU-GM) and erythroid burst-forming units (BFU-E) were performed on each harvest.

145 n contrast, of 8 patients with poor in vitro BFU-E growth (<6 bursts/10(5) MMNC), 7 failed to respond

146 data suggest that in individuals, from whom BFU-E mature appropriately in culture, immunosuppressive