ライフサイエンスコーパス: fetal hemoglobin

1 d several genetic loci involved in silencing fetal hemoglobin.

2 up to 60% efficiency, causing persistence of fetal hemoglobin.

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

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

5 PD98059) demonstrated significant effects on fetal hemoglobin.

6 s was an effective strategy for induction of fetal hemoglobin.

7 d in individuals who have elevated levels of fetal hemoglobin.

8 O(2)-independent antisickling properties of fetal hemoglobin.

9 sickle cell anemia are aimed at reactivating fetal hemoglobin.

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

11 effects largely attributable to induction of fetal hemoglobin.

12 otential target for therapeutic induction of fetal hemoglobin.

13 , and produced large cumulative increases in fetal hemoglobin.

14 nclude chronic hydroxyurea therapy to induce fetal hemoglobin.

15 ydrogenase and bilirubin and negatively with fetal hemoglobin.

16 were estimated quantitatively for adult and fetal hemoglobins.

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

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

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

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

21 and HBG2 were significantly associated with fetal hemoglobin (absolute value of Z = 4.00 to 20.66; P

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

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

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

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

26 Gene variants regulating fetal hemoglobin and alpha-thalassemia (important marker

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

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

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

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

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

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

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

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

35 S with pancellular hereditary persistence of fetal hemoglobin are both relatively benign conditions.

36 nt and stable induction of fetal hemoglobin (fetal hemoglobin as a percentage of total hemoglobin, 19

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

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

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

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

41 ge of total hemoglobin, 19.0 to 26.8%), with fetal hemoglobin broadly distributed in red cells (F cel

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

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

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

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

46 Fetal hemoglobin concentrations increased with increasin

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

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

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

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

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

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

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

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

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

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

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

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

59 Increased fetal hemoglobin expression in adulthood is associated w

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

61 92, increases PGC-1alpha leading to enhanced fetal hemoglobin expression in human erythroid cells, be

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

63 ly install natural mutations that upregulate fetal hemoglobin expression in the BCL11A enhancer or in

64 Furthermore, fetal hemoglobin expression was inhibited during erythro

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

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

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

68 end joining pathway may induce compensatory fetal hemoglobin expression.

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

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

71 ants had engraftment and stable induction of fetal hemoglobin (fetal hemoglobin as a percentage of to

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

73 Fetal hemoglobin genes are genetically regulated, and th

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

75 s diminishes CHD4 levels and derepresses the fetal hemoglobin genes.

76 moglobin level was 11.9 g per deciliter, and fetal hemoglobin had a pancellular distribution (>=94% o

77 would be survivable once the nonpolymerizing fetal hemoglobin has been replaced by adult hemoglobin S

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

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

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

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

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

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

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

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

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

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

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

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

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

91 2,3-biphosphosphoglycerate (BPG) binding to fetal hemoglobin (Hb F), we engineered and produced norm

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

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

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

95 Elevated fetal hemoglobin (HbF) ameliorates the clinical severity

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

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

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

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

100 based strategies for reactivating endogenous fetal hemoglobin (HbF) are also promising, because eleva

101 limited, and innovative treatments to induce fetal hemoglobin (HbF) are needed.

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

103 gamma-globin expression leading to increased fetal hemoglobin (HbF) by targeting BCL11A.

104 Increased production of fetal hemoglobin (HbF) can ameliorate the severity of si

105 Fetal hemoglobin (HbF) can blunt the pathophysiology, te

106 A high level of erythrocyte fetal hemoglobin (HbF) comprising a- and y-globins may a

107 A high level of erythrocyte fetal hemoglobin (HbF) comprising alpha- and gamma-globi

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

109 Fetal hemoglobin (HbF) content was determined in isolate

110 Essential for fetal hemoglobin (HbF) control is a non-redundant subcom

111 Fetal hemoglobin (HbF) decreases polymerization of sickl

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

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

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

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

116 A goal of this approach is to increase fetal hemoglobin (HbF) expression while coordinately red

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

118 , leading to the anticipated reactivation of fetal hemoglobin (HbF) expression.

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

120 enhancer within the BCL11A gene reactivates fetal hemoglobin (HbF) in adult erythroid cells, serving

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

122 ematopoietic stem cells (HSCs) to reactivate fetal hemoglobin (HbF) in erythroid progeny offers an al

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

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

125 5-azacytidine (5-Aza) is a potent inducer of fetal hemoglobin (HbF) in people with beta-thalassemia a

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

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

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

129 Fetal hemoglobin (HbF) induction can ameliorate the clin

130 rythroid enhancer is a validated approach to fetal hemoglobin (HbF) induction for beta-hemoglobinopat

131 Fetal hemoglobin (HbF) induction in erythroid progeny af

132 Fetal hemoglobin (HbF) interferes with this polymerizati

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

134 Fetal hemoglobin (HbF) is heterogeneously distributed am

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

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

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

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

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

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

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

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

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

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

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

146 5-aza-2'-deoxycytidine (decitabine) augments fetal hemoglobin (HbF) levels in patients with sickle ce

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

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

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

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

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

152 Fetal hemoglobin (HbF) modulates the clinical severity o

153 Fetal hemoglobin (HbF) modulates the phenotype of sickle

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

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

156 HRI has recently been found to inhibit fetal hemoglobin (HbF) production in adult erythroid cel

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

158 Fetal hemoglobin (HbF) reactivation expression through C

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 he induction of gamma-globin, a component of fetal hemoglobin (HbF).

177 h that results in silencing of expression of fetal hemoglobin (HbF).

178 the BCL11A erythroid enhancer to reactivate fetal hemoglobin (HbF).

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

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

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

182 BCL11A, the major regulator of fetal hemoglobin (HbF, a(2)y(2)) level, represses y-glob

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

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

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

186 e (SCD) and beta-thalassemia by induction of fetal hemoglobin (HbF, alpha(2)gamma(2))(1).

187 ne for gamma-globin, which is a component of fetal hemoglobin (HbF, alpha(2)gamma(2)); however, gamma

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

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

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

191 Reversing the developmental switch from fetal hemoglobin (HbF, alpha2gamma2) to adult hemoglobin

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

193 n gene that expresses a potent anti-sickling fetal hemoglobin, HbF(G16D).

194 Hereditary persistence of fetal hemoglobin (HPFH) ameliorates B-hemoglobinopathies

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

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

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

198 aturally occurring hereditary persistence of fetal hemoglobin (HPFH) mutations, editing of transcript

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 r that represses gamma-globin expression and fetal hemoglobin in erythroid cells.

215 actor that represses y-globin expression and fetal hemoglobin in erythroid cells.

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

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

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

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

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

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

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

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

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

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

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

227 fficiency, higher specificity, and increased fetal hemoglobin induction potential compared with SpCas

228 High-level fetal hemoglobin induction was observed in erythroid pro

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

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

231 ngraftment, gene marking, and vector-derived fetal hemoglobin induction.

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

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

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

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

236 Fetal hemoglobin level is a heritable complex trait that

237 in level of 9.0 g or more per deciliter or a fetal hemoglobin level of 20% or more after 24 months.

238 level was 13.1 g per deciliter and the mean fetal hemoglobin level was 11.9 g per deciliter, and fet

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

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

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

242 3 patients who had the highest or the lowest fetal hemoglobin levels and 7 patients whose fetal hemog

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

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

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

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

247 Elevated fetal hemoglobin levels in red cells protect against com

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

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

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

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

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

253 t present a pharmacologic target for raising fetal hemoglobin levels.

254 disorders that would benefit from increased fetal hemoglobin levels.

255 ificant increases in both the hemoglobin and fetal hemoglobin levels.

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

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

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

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

260 2a mimics multiple hereditary persistence of fetal hemoglobin mutations.

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

262 transfer strategies to induce expression of fetal hemoglobin or other nonsickling hemoglobin isoform

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

264 , genome editing could restore expression of fetal hemoglobin or target specific mutations to restore

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

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

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

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

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

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

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

272 s been implicated in the regulation of human fetal hemoglobin production.

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

274 Fetal hemoglobin reactivation is a promising therapy for

275 Hydroxyurea therapy increases fetal hemoglobin (reducing ischemia), and chronic blood

276 ed gene silencing by NuRD in a cell model of fetal hemoglobin regulation.

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

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

279 Reactivation of fetal hemoglobin remains a critical goal in the treatmen

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

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

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

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

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

285 nonviral cell therapy designed to reactivate fetal hemoglobin synthesis by means of ex vivo clustered

286 nonviral cell therapy designed to reactivate fetal hemoglobin synthesis through ex vivo clustered reg

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

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

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

290 iting in bone marrow and blood, increases in fetal hemoglobin that were distributed pancellularly, tr

291 al pharmacologic agents to induce sufficient fetal hemoglobin to diminish clinical severity is an unm

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

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

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

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

296 nding site at the HBG1/2 promoters to induce fetal hemoglobin using either SpCas9 or AsCas12a mimics

297 Acetylation of fetal hemoglobin weakens its unusually strong subunit in

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

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

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