ライフサイエンスコーパス: fetal hemoglobin

1 s an oxygen affinity that is comparable with fetal hemoglobin.

2 ia cell line K562 resulted in an increase of fetal hemoglobin.

3 PD98059) demonstrated significant effects on fetal hemoglobin.

4 sickle cell anemia are aimed at reactivating fetal hemoglobin.

5 obin expression, and hence the production of fetal hemoglobin.

6 effects largely attributable to induction of fetal hemoglobin.

7 otential target for therapeutic induction of fetal hemoglobin.

8 , and produced large cumulative increases in fetal hemoglobin.

9 nclude chronic hydroxyurea therapy to induce fetal hemoglobin.

10 ydrogenase and bilirubin and negatively with fetal hemoglobin.

11 d several genetic loci involved in silencing fetal hemoglobin.

12 kb of LCR sequences expressed high levels of fetal hemoglobin (17%-33%), with an average vector copy

13 Because the mouse does not have a true fetal hemoglobin, a delayed switching human gamma to bet

14 F cells measure the presence of fetal hemoglobin, a heritable quantitative trait in adul

15 ts after 2 years (difference, 6 g/L), as was fetal hemoglobin (absolute difference, 3.2%).

16 Fetal hemoglobin achieved levels of 68.6 +/- 3.9% in the

17 Increased levels of fetal hemoglobin (alphagamma;HbF), such as occurs with h

18 n study results for the levels of A1, A2 and fetal hemoglobins, analyzed for the first time concurren

19 nsequence of a weakened relationship between fetal hemoglobin and 2,3-diphosphoglycerate.

20 f infants in association with lower total or fetal hemoglobin and higher white blood cell or reticulo

21 inks that are already known (such as between fetal hemoglobin and malaria risk) and those that are no

22 duction of treatments that induce protective fetal hemoglobin and reduce infectious complications has

23 ion of DNMT1-targeted therapy is to increase fetal hemoglobin and treat hemoglobinopathy.

24 bin synthesis, with persistent expression of fetal hemoglobin and, most remarkably, expression of lar

25 djusting for sex, age, asthma, percentage of fetal hemoglobin, and alpha-globin gene deletion.

26 throblasts, that are smaller, express mostly fetal hemoglobin, and can enucleate.

27 Hydroxyurea is a potent inducer of fetal hemoglobin, and evidence over the past 25 years ha

28 (n = 65) and demonstrate that high levels of fetal hemoglobin (assessed as F cells) are associated wi

29 homozygous CA mice survive solely upon human fetal hemoglobin at birth.

30 rify the mechanism of cytotoxic drug-induced fetal hemoglobin augmentation.

31 In the absence of PD98059, levels of fetal hemoglobin averaged 27.4% +/- 7.9% in EPO+SCF comp

32 tation modifies the ligand-binding pocket of fetal hemoglobin by means of two mechanisms.

33 of developmental gene regulation and because fetal hemoglobin can significantly ameliorate the clinic

34 nclude sickle cell type, severity of anemia, fetal hemoglobin concentration, and hypoxemia from upper

35 leotide polymorphisms (SNPs) associated with fetal hemoglobin concentration.

36 Fetal hemoglobin concentrations increased with increasin

37 a-thalassemias and hereditary persistence of fetal hemoglobin conditions are most likely to be due to

38 he levels of gamma mRNA and the frequency of fetal hemoglobin-containing erythroblasts in erythroid b

39 the relationships among PS externalization, fetal hemoglobin content, hydration state, and cell age.

40 heritable variations in RBC traits, such as fetal hemoglobin content.

41 oglobin switching were better understood and fetal hemoglobin could be more fully reactivated in adul

42 eletion and a rare hereditary persistence of fetal hemoglobin deletion with identical downstream brea

43 Since increased fetal hemoglobin diminishes the severity of beta-thalass

44 ll crises that are independent of the drug's fetal hemoglobin-elevating properties and probably invol

45 increased HbF by 4%-9% (P < 0.001), doubling fetal hemoglobin-enriched red blood cells (F-cells) up t

46 s study, we investigated the role of NRF2 in fetal hemoglobin expression and the pathophysiology of s

47 logy with an emphasis upon the modulation of fetal hemoglobin expression during the maturation of adu

48 peutic and butyrate therapeutics that induce fetal hemoglobin expression generally also suppress eryt

49 Increased fetal hemoglobin expression in adulthood is associated w

50 c trichostatin A for their ability to induce fetal hemoglobin expression in erythroid cells.

51 progenitors may provide a method to activate fetal hemoglobin expression in individuals with beta-tha

52 Furthermore, fetal hemoglobin expression was inhibited during erythro

53 ments inhibit HbS polymerization by inducing fetal hemoglobin expression, prevent or repair erythrocy

54 rin A) expression, and exclusively embryonic/fetal hemoglobin expression.

55 end joining pathway may induce compensatory fetal hemoglobin expression.

56 er haplotypes, alpha-globin gene number, and fetal hemoglobin expression.

57 Tetrameric fetal hemoglobin F in the liganded state was found to di

58 limiting the production of cells containing fetal hemoglobin (F cells).

59 intergenic region required for gamma-globin (fetal hemoglobin) gene silencing.

60 Fetal hemoglobin genes are genetically regulated, and th

61 roved understanding of the regulation of the fetal hemoglobin genes holds promise for the development

62 Increases in fetal hemoglobin have been identified after birth in sev

63 f these mutants with Hb S versus mixtures of fetal hemoglobin (Hb F) and Hb A with Hb S.

64 concerns with pharmacological stimulation of fetal hemoglobin (Hb F) as a therapeutic option for the

65 Three recombinant mutants of human fetal hemoglobin (Hb F) have been constructed to determi

66 The favorable effects of high levels of fetal hemoglobin (Hb F) in sickle cell disease have been

67 Mean corpuscular volume and percent fetal hemoglobin (Hb F) increased from 87% +/- 6% to 98%

68 Induction of fetal hemoglobin (Hb F) is an important therapeutic tool

69 Fetal hemoglobin (Hb F) levels increase in most patients

70 ll disease, is thought to indirectly promote fetal hemoglobin (Hb F) production by perturbing the mat

71 High levels of fetal hemoglobin (Hb F) protect from many of the complic

72 ased hemoglobin concentration, percentage of fetal hemoglobin (Hb F), and mean corpuscular volume (MC

73 A recombinant mutant of human fetal hemoglobin (Hb F), named rHb Oscar, has been const

74 r significantly in average HU dose, baseline fetal hemoglobin (Hb F), or maximum Hb F response.

75 2,3-biphosphosphoglycerate (BPG) binding to fetal hemoglobin (Hb F), we engineered and produced norm

76 Increased fetal hemoglobin (Hb F; alpha(2)gamma(2)) production in

77 recombinant analysis of the adult hemoglobin/fetal hemoglobin (HbA/HbF) systems.

78 of Plasmodium falciparum in cells containing fetal hemoglobin (HbF = alpha2gamma2) is retarded, but i

79 Elevated fetal hemoglobin (HbF) ameliorates the clinical severity

80 Hydroxyurea (HU) has been shown to increase fetal hemoglobin (HbF) and decrease painful episodes in

81 Hydroxyurea increases levels of fetal hemoglobin (HbF) and decreases morbidity from vaso

82 here is delayed switching and persistence of fetal hemoglobin (HbF) and elevation of embryonic hemogl

83 , have attempted to augment the synthesis of fetal hemoglobin (HbF) and improve current treatment.

84 atty acid butyrate has been shown to elevate fetal hemoglobin (HbF) by inducing expression of the gam

85 of experiments explored the possibility that fetal hemoglobin (HbF) content influences the in vivo de

86 Fetal hemoglobin (HbF) content was determined in isolate

87 Fetal hemoglobin (HbF) decreases polymerization of sickl

88 Furthermore, several PHIs induced fetal hemoglobin (HbF) expression in primary human eryth

89 Interindividual variation in fetal hemoglobin (HbF) expression is a known and potenti

90 Pharmacologic induction of fetal hemoglobin (HbF) expression is an effective treatm

91 cells (HSCs) results in sufficient postnatal fetal hemoglobin (HbF) expression to correct sickle cell

92 e levels, MAGE1A CpG island methylation, and fetal hemoglobin (HbF) expression.

93 Reactivation of fetal hemoglobin (HbF) holds therapeutic potential for s

94 Reactivation of fetal hemoglobin (HbF) in adults ameliorates the severit

95 sity changes of HDE cells; (2) the amount of fetal hemoglobin (HbF) in labeled cells after magnetic i

96 EVs are related mechanistically to cellfree fetal hemoglobin (HbF) in maternal plasma.

97 5-azacytidine (5-Aza) is a potent inducer of fetal hemoglobin (HbF) in people with beta-thalassemia a

98 harmacologic strategies for the induction of fetal hemoglobin (HbF) in people with sickle cell diseas

99 Hydroxyurea (HU) can increase fetal hemoglobin (HbF) in sickle cell anemia (HbSS).

100 Current techniques for identifying fetal hemoglobin (HbF) inducers are complex and time con

101 Fetal hemoglobin (HbF) induction can ameliorate the clin

102 Fetal hemoglobin (HbF) interferes with this polymerizati

103 Fetal hemoglobin (HbF) is a potent genetic modifier of t

104 Fetal hemoglobin (HbF) is heterogeneously distributed am

105 Fetal hemoglobin (HbF) is regulated as a multigenic trai

106 Fetal hemoglobin (HbF) is the major genetic modulator of

107 Fetal hemoglobin (HbF) is the major modifier of the clin

108 genetic variation at BCL11A associated with fetal hemoglobin (HbF) level lies in noncoding sequences

109 moglobin level, mean corpuscular volume, and fetal hemoglobin (HbF) level, whereas significant decrea

110 omosome 6q that are associated with elevated fetal hemoglobin (HbF) levels and alterations of other c

111 To evaluate the association between fetal hemoglobin (HbF) levels and morbidity in beta-thal

112 Strategies to increase fetal hemoglobin (HbF) levels can ameliorate symptoms an

113 Increased fetal hemoglobin (HbF) levels diminish the clinical seve

114 Although increased fetal hemoglobin (HbF) levels have proven benefit for pe

115 emethylase 1 (LSD1) has been shown to induce fetal hemoglobin (HbF) levels in cultured human erythroi

116 5-aza-2'-deoxycytidine (decitabine) augments fetal hemoglobin (HbF) levels in patients with sickle ce

117 Higher fetal hemoglobin (HbF) levels in red blood cells of SCD

118 Augmentation of the fetal hemoglobin (HbF) levels is of therapeutic benefit

119 half of patients show elevated age-adjusted fetal hemoglobin (HbF) levels.

120 The level of fetal hemoglobin (HbF) modifies the severity of the comm

121 To assess whether fetal hemoglobin (HbF) modulates the adhesion of sickle

122 Fetal hemoglobin (HbF) modulates the phenotype of sickle

123 rs was developed to identify determinants of fetal hemoglobin (HbF) modulation during adult erythropo

124 Induction of fetal hemoglobin (HbF) production in adult erythrocytes

125 Although butyrate was shown to induce fetal hemoglobin (HbF) production in patients with hemog

126 Recent molecular studies of fetal hemoglobin (HbF) regulation have reinvigorated the

127 Reducing expression of the fetal hemoglobin (HbF) repressor BCL11A leads to a simul

128 n) knock-in mice that demonstrate a distinct fetal hemoglobin (HbF) stage, where gamma-globin is the

129 Strategies to induce fetal hemoglobin (HbF) synthesis for the treatment of be

130 ense sickle cells have a lower percentage of fetal hemoglobin (HbF) than PS- cells in the same densit

131 Differences in the amount of fetal hemoglobin (HbF) that persists into adulthood affe

132 A transition from fetal hemoglobin (HbF) to adult hemoglobin (HbA) normall

133 tolerated dose (MTD), hydroxyurea increases fetal hemoglobin (HbF) to levels ranging from 10% to 40%

134 rtance of the distribution or "packaging" of fetal hemoglobin (HbF) within erythrocytes of persons wi

135 at replacement of sickle hemoglobin (HbS) by fetal hemoglobin (HbF) would have major clinical benefit

136 is approach to pharmacologic reactivation of fetal hemoglobin (HbF), hematopoietic cells from patient

137 patients with sickle-cell disease increases fetal hemoglobin (HbF), which reduces hemoglobin S polym

138 ainly been attributed to increased levels of fetal hemoglobin (HbF), which reduces the tendency for s

139 blood, using flow cytometric enumeration of fetal hemoglobin (HbF)-containing cells.

140 versus high levels of gamma-globin mRNA and fetal hemoglobin (HbF).

141 ection with increased levels of antisickling fetal hemoglobin (HbF).

142 obinopathies by augmenting the production of fetal hemoglobin (HbF).

143 at 26.2 +/- 4.9 mg/kg/d with 29.1% +/- 6.7% fetal hemoglobin (HbF).

144 ia (SCA), primarily through the induction of fetal hemoglobin (HbF).

145 F-B) had synergistic effects with respect to fetal hemoglobin (HbF): average HbF/HbF + adult hemoglob

146 Increased levels of fetal hemoglobin (HbF, alpha(2)gamma(2)) are of no conse

147 Persistence of human fetal hemoglobin (HbF, alpha(2)gamma(2)) in adults lesse

148 Individual variation in fetal hemoglobin (HbF, alpha(2)gamma(2)) response underl

149 Patients with elevated levels of fetal hemoglobin (HbF, alpha2gamma2) as adults exhibit r

150 ell patients, the presence of high levels of fetal hemoglobin (HbF, alpha2gamma2) can compensate for

151 Fetal hemoglobin (HbF, alpha2gamma2) induction is a well

152 Maximum percentage fetal hemoglobin (%HbF) is 20.6% +/- 8.0% and percentage

153 ave a phenotype of hereditary persistence of fetal hemoglobin (HPFH) but, when the CACCC box of the -

154 e and generate the hereditary persistence of fetal hemoglobin (HPFH) condition.

155 deletion types of hereditary persistence of fetal hemoglobin (HPFH) is thought to be mediated by enh

156 , showing that the hereditary persistence of fetal hemoglobin (HPFH) phenotype was maintained in thes

157 ich heterocellular hereditary persistence of fetal hemoglobin (HPFH) segregates is described.

158 ns associated with hereditary persistence of fetal hemoglobin (HPFH) was due to greater interactions

159 For example, in hereditary persistence of fetal hemoglobin (HPFH), a benign genetic condition, mut

160 to as pancellular hereditary persistence of fetal hemoglobin (HPFH).

161 alled non-deletion hereditary persistence of fetal hemoglobin (HPFH).

162 f individuals with hereditary persistence of fetal hemoglobin (HPFH).

163 mutant that causes hereditary persistence of fetal hemoglobin (HPFH).

164 ed from -117 Greek hereditary persistence of fetal hemoglobin human beta-globin locus yeast artificia

165 ta indicate that in addition to induction of fetal hemoglobin, hydroxyurea attenuates leukocyte-endot

166 er, Hb Felix has some features that resemble fetal hemoglobin, i.e. its significantly decreased tetra

167 switching and the potential reactivation of fetal hemoglobin in adult hematopoietic cells remain elu

168 adult hemoglobin is incomplete; the residual fetal hemoglobin in adults is restricted to a subset of

169 BCL11A is a potent silencer of fetal hemoglobin in both mouse and humans.

170 These compounds induced fetal hemoglobin in both primary erythroid cell cultures

171 Agamma-globin gene promoter results in 4-10% fetal hemoglobin in heterozygotes.

172 The persistence of fetal hemoglobin in many patients with deletion type bet

173 been identified as robustly associated with fetal hemoglobin in patients with sickle cell disease, p

174 the maintenance and therapeutic induction of fetal hemoglobin in pediatric sickle cell disease.

175 CL11 gene expression and additively increase fetal hemoglobin in primary human erythroid cells.

176 CL11 gene expression and additively increase fetal hemoglobin in primary human erythroid cells.

177 especially the use of hydroxyurea to elevate fetal hemoglobin in sickle cell disease.

178 velopment and evaluation of drugs to elevate fetal hemoglobin in the treatment of the genetic disease

179 g protein (CREB), are intimately involved in fetal hemoglobin induction by these agents.

180 yte density, pulmonary artery pressures, and fetal hemoglobin induction deserve study.

181 pment of targeted therapeutic approaches for fetal hemoglobin induction in the beta-hemoglobinopathie

182 phosphatase (PP2A) and correlated well with fetal hemoglobin induction.

183 AC1 and HDAC2 as molecular targets mediating fetal hemoglobin induction.

184 Induction of fetal hemoglobin is a validated strategy to improve symp

185 Embryonic hemoglobins are the weakest; fetal hemoglobin is of intermediate strength, and adult

186 Although hydroxyurea (HU), an inducer of fetal hemoglobin, is the main therapy for treatment of S

187 lobin-expressing red cells and the amount of fetal hemoglobin, leading to resolution of anemia.

188 Fetal hemoglobin level is a heritable complex trait that

189 The fetal hemoglobin level, white-cell count, and platelet c

190 (rs766432) in BCL11A, a gene known to affect fetal hemoglobin levels (P = 2.6E-21) and in Thailand an

191 Very different fetal hemoglobin levels among adult sickle cell anemia p

192 3 patients who had the highest or the lowest fetal hemoglobin levels and 7 patients whose fetal hemog

193 In sickle cell anemia, different fetal hemoglobin levels are associated with distinct bet

194 subset of children on hydroxyurea, baseline fetal hemoglobin levels explained 33% of the variance in

195 otide polymorphisms associated with baseline fetal hemoglobin levels in adult sickle cell disease wer

196 lap between baseline and hydroxyurea-induced fetal hemoglobin levels in pediatric disease.

197 se genome wide association studies including fetal hemoglobin levels in sickle cell anemia and a samp

198 of the mechanism of 6q QTL as a modifier of fetal hemoglobin levels in the beta hemoglobinopathies.

199 fetal hemoglobin levels and 7 patients whose fetal hemoglobin levels were atypical of their haplotype

200 al (eg, nutrition) and nonenvironmental (eg, fetal hemoglobin levels, alpha-thalassemia status) facto

201 ons, pharmacologic interventions to increase fetal hemoglobin levels, and stem cell transplantation.

202 ciated with red-blood-cell traits, including fetal hemoglobin levels.

203 oxyurea treatment, preceding the increase in fetal hemoglobin levels.

204 disorders that would benefit from increased fetal hemoglobin levels.

205 ponse to pharmacological agents that elevate fetal hemoglobin, may be expected to involve either chan

206 ns in these areas are uncommon mechanisms of fetal hemoglobin modulation in sickle cell anemia.

207 olled adults reported a relative increase in fetal hemoglobin of 4% to 20% and a relative reduction i

208 difficult, strategies to increase levels of fetal hemoglobin or reverse sickle erythrocyte dehydrati

209 lar volume, mean corpuscular hemoglobin, and fetal hemoglobin parameters, and decreases in white bloo

210 mmunomodulatory drug, was proposed to induce fetal hemoglobin production by an unknown mechanism.

211 n studies may provide methods for modulating fetal hemoglobin production enough to attenuate stroke r

212 Among the genetic elements that may enhance fetal hemoglobin production is an artificial zinc-finger

213 sion and may explain the previously observed fetal hemoglobin production that occurs during early adu

214 ing human CD34(+) cells in culture increases fetal hemoglobin production with a concomitant decrease

215 globin S within erythrocytes, by stimulating fetal hemoglobin production, increasing cell water, or i

216 ent and prevention of these events using the fetal hemoglobin-reactivating agent hydroxyurea are curr

217 mechanisms by which pomalidomide reactivates fetal hemoglobin, reinforcing its potential as a treatme

218 fold increased tetramer strength of liganded fetal hemoglobin relative to that of adult hemoglobin be

219 JCML/JMML, (3) suggest that the elevation in fetal hemoglobin seen in JCML/JMML is a result of primar

220 We found that a critical fetal hemoglobin silencing factor, BCL11A, and its partn

221 s other surrounding sequences, and maintains fetal hemoglobin silencing.

222 the delta-globin gene that is necessary for fetal hemoglobin silencing.

223 ion in human HPFH (hereditary persistence of fetal hemoglobin) syndrome, and we show that this mutati

224 tant clinical implications for de-repressing fetal hemoglobin synthesis to treat sickle cell anemia a

225 de between the effects of acetylation of the fetal hemoglobin tetramer on the strength of its subunit

226 p64-HA showed up to 16-fold higher levels of fetal hemoglobin than the native K562 cell line.

227 found that 31 SNPs in 12 genes interact with fetal hemoglobin to modulate the risk of stroke.

228 A linear dose response in levels of fetal hemoglobin to PD98059 was detected (0.16 microM =

229 rategy for the identification of inducers of fetal hemoglobin transcripts in primary human erythroid

230 t human stress erythroid progenitors express fetal hemoglobin upon differentiation.

231 Acetylation of fetal hemoglobin weakens its unusually strong subunit in

232 Target residues in these recombinant fetal hemoglobins were replaced with the corresponding a

233 corresponding sequence of the gamma-chain of fetal hemoglobin with the remaining sequence of the beta

234 antly increased hemoglobin concentration and fetal hemoglobin, with decreased leukocytes and reticulo