ライフサイエンスコーパス: BFU

1 BFU showed higher bioaccessibility of phenolic compounds

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

3 BFU-E from peripheral blood were cultured in methylcellu

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

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

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

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

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

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

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

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

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

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

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

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

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

17 (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

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

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

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

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

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

23 e of Fv2 (Fv2(rr)) have few actively cycling BFU-Es.

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

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

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

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

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

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

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

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

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

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

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

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

36 n of wild-type burst-forming unit erythroid (BFU-e) and colony-forming unit erythroid (CFU-e) progeni

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

38 = .0008), and burst-forming unit-erythroid (BFU-E) (median slope per day, -1.18; P = .006) were obse

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 an numbers of burst-forming units-erythroid (BFU-e) were 0.20, 6.94, and 12.78 x 10(4)/kg, and the me

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

63 enriched for burst-forming units-erythroid (BFU-Es) and depleted of colony-forming units--granulocyt

64 17% inhibition burst forming unit-erythroid [BFU-E]) and 3.44 micromol/L (24% inhibition of CFU-GM; 5

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

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

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

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

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

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

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

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

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

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

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

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

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

78 6% and yielded 2 degrees colonies of CFU-GM, BFU-E, and CFU-GEMM.

79 (P = .022) and, strikingly, V617F-homozygous BFU-Es were detected in all 17 patients with PV, but in

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

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

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

83 arget of the glucocorticoid receptor (GR) in BFU-Es and is required for BFU-E self-renewal.

84 e CFU assay showed a significant increase in BFU-E and CFU-G, but a decrease in CFU-GM in FL-HSCs fro

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

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

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

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

89 s a marker that distinguishes early and late BFU-Es.

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

91 r capacities for self-renewal than do "late" BFU-Es forming small colonies, but the mechanism underly

92 cells in cultures of both mouse fetal liver BFU-Es and mobilized human adult CD34(+) peripheral bloo

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

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

95 In Dhh-deficient spleen and bone marrow, BFU-Es and erythroblast populations were increased compa

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

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

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

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

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

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

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

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

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

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

106 onal antibody, reduced bone marrow homing of BFU-Es.

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

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

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

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

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

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

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

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

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

116 ith inulin (BIU) or fructo-oligosaccharides (BFU) or polydextrose (BPU).

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

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

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

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

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

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

123 yocyte (CFU-Mk) and erythrocyte progenitors (BFU-e) were present during the entire period of the cult

124 e number of committed erythroid progenitors (BFU-E and CFU-E) and erythroblast differentiation in the

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

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

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

128 Burst-forming unit erythroid progenitors (BFU-Es) are so named based on their ability to generate

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

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

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

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

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

134 We show EPO expression in the EMP-stimulated BFU-Es at both mRNA and protein levels.

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

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

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

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

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

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

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

142 ation of erythroid progenitors termed stress BFU-E.

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

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

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

146 the SP600125 inhibited proliferation of the BFU-e's.

147 units (CFU-e's), and SP600125 protected the BFU-e's from apoptosis induced by cytosine arabinoside,

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

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

150 6(-) bone marrow cells as EEP giving rise to BFU-E, and Lin(-)CD34(+/-)CD38(+)CD45RA(-)CD123(-)CD71(+

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

152 but a low proportion of burst-forming unit (BFU)e.

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

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

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

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

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

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

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

160 % reduction in erythroid blast-forming unit (BFU-E), erythroid colony-forming unit (CFU-E), and colon

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

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

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

164 timulates erythroid (E) (burst-forming unit [BFU]-E and colony-forming unit [CFU]-E) and myeloid (CFU

165 unit-erythroid [CFU-E], burst-forming unit [BFU]-E, and CFU-granulocyte-macrophage [GM]) were quanti

166 the number of erythroid burst-forming units (BFU-e's) but not the more differentiated erythroid colon

167 finitive-type erythroid burst-forming units (BFU-e's), erythroid colony-forming units (CFU-e's), gran

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

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

170 d bone marrow erythroid burst-forming units (BFU-Es) and colony-forming units-erythroid (CFU-Es) acti

171 c progenitors erythroid burst-forming units (BFU-Es) and granulocyte-macrophage colony-forming units

172 617F-positive erythroid burst-forming units (BFU-Es) were more frequent in patients with PV compared

173 progenitors (erythroid blast-forming units [BFU-Es]).

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

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