ライフサイエンスコーパス: erythroid

1 Nuclear factor, erythroid 2 like 2 (Nrf2)-regulated genes were overexpre

2 pharmacological activation of nuclear factor erythroid 2 p45-related factor 2 (NRF2) can be deployed

3 eat shock factor 1 (HSF1) and nuclear factor-erythroid 2 p45-related factor 2 (NRF2), is not well und

4 of transcription factor Nrf2 (nuclear factor-erythroid 2 p45-related factor 2).

5 ssociating protein 1 (Keap1), nuclear factor erythroid 2 related factor 2 (Nrf2) and glutathione pero

6 The nuclear factor (erythroid 2)-like (NRF) transcription factors are a subs

7 The nuclear factor (erythroid 2)-like 2 (NRF2 or NFE2L2) transcription facto

8 or Y subunit alpha (NFYa) and nuclear factor erythroid 2-like 1 (NFE2L1) transcription factors, which

9 While transcription factor nuclear factor-erythroid 2-like 2 (NRF2) protects cells from oxidative,

10 By exposing nuclear factor erythroid 2-related factor (Nrf2) knockout (Nrf2(-/-)) m

11 of rat enteric neurons and in nuclear factor erythroid 2-related factor (Nrf2) knockout mice.

12 nitric oxide synthase (eNOS), nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1

13 Nuclear factor erythroid 2-related factor 2 (Nrf2) dissociates from its

14 tivation of the transcription factor nuclear erythroid 2-related factor 2 (Nrf2) enables idebenone to

15 ased nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2) in the mutant, sugge

16 (KSHV)-induced activation of nuclear factor erythroid 2-related factor 2 (Nrf2) is essential for bot

17 Nuclear factor erythroid 2-related factor 2 (Nrf2) is ubiquitously expr

18 The nuclear factor erythroid 2-related factor 2 (Nrf2) signaling axis is a

19 ECH-associated protein 1 and nuclear factor erythroid 2-related factor 2 (NRF2) signaling pathway in

20 ox1) and transcription factor nuclear factor-erythroid 2-related factor 2 (Nrf2)).

21 methyl, a potent activator of nuclear factor erythroid 2-related factor 2 (Nrf2), is effective in inc

22 ociated protein 1, activating nuclear factor erythroid 2-related factor 2 (Nrf2), which stimulates tr

23 ween oxidative stress and the nuclear factor erythroid 2-related factor 2 (Nrf2)-dependent antioxidan

24 associated with reduced transcription of NF erythroid 2-related factor 2 (NRF2)-dependent antioxidat

25 l hydrocarbon receptor (AhR)- nuclear factor erythroid 2-related factor 2 (Nrf2)-dependent pathways t

26 ulator of antioxidant defense nuclear factor erythroid 2-related factor 2 (Nrf2).

27 ange in the expression of the nuclear factor-erythroid 2-related factor 2 and its downstream targets

28 Increased nuclear factor erythroid 2-related factor 2 expression was also found i

29 esponse guided by a defective Nuclear Factor Erythroid 2-Related Factor 2 pathway confirmed an unbala

30 cological activation of NRF2 (nuclear factor erythroid 2-related factor 2) arises from blocking the i

31 s the activation of the Nrf2 (nuclear factor erythroid 2-related factor 2) pathway, which provides a

32 oxia-inducible factor-1alpha, nuclear factor erythroid 2-related factor 2) suggesting superior mitoch

33 rganization and activation of nuclear factor erythroid 2-related factor 2-mediated oxidative stress r

34 protective expression of the nuclear factor, erythroid 2.

35 The transcription factor nuclear factor erythroid-2-related factor 2 (Nrf2) plays a critical rol

36 suggesting a compensatory mechanism by other erythroid ABC transporters.

37 ring gestation away from being predominantly erythroid, accompanied by a parallel change in different

38 a reduction in the early burst-forming unit-erythroid and an expansion of late-stage erythroblasts t

39 ion of myeloid populations at the expense of erythroid and B lymphoid fractions.

40 ineage committed progenitors of the myeloid, erythroid and lymphoid lineages specified an altered com

41 e inflammasome regulates the balance between erythroid and myeloid differentiation in model systems,

42 Gene expression analysis reveals erythroid and myeloid priming in the NEO1(+) fraction an

43 Erythroid and reticulocyte-specific signatures were mark

44 protein 7 (CHD7) expanded phenotypic HSPCs, erythroid, and myeloid lineages in zebrafish and mouse e

45 gata2a(-) runx1(+) cells abundantly contain erythroid- and/or myeloid-primed progenitors.

46 " and "criteria" for hematologic improvement-erythroid assessment and a new categorization of transfu

47 s-erythroid (CFU-Es), as well as myeloid and erythroid blood cells.

48 Loss of ZNF410 in adult-type human erythroid cell culture systems and xenotransplantation s

49 or that globally activates genes involved in erythroid cell development.

50 Recent studies suggest that decreased erythroid cell differentiation and survival also contrib

51 ological manipulations of iron metabolism or erythroid cell differentiation and survival have been sh

52 oietin response to anemia, and inhibition of erythroid cell differentiation by inflammatory mediators

53 n essential role of TH during terminal human erythroid cell differentiation; specific depletion of TH

54 om patients are confounded by poor levels of erythroid cell expansion, aberrant or incomplete erythro

55 We have previously identified 2 in vitro erythroid cell growth phenotypes for primary CD34(+) cel

56 R/Cas9 gene editing in an immortalised human erythroid cell line (BEL-A2) abolishes MAM expression.

57 non-F cells (A cells) from the human HUDEP2 erythroid cell line and primary human erythroid cultures

58 In this study we generate an immortalised erythroid cell line from peripheral blood stem cells of

59 Treatment with deferiprone of UROS-deficient erythroid cell lines and peripheral blood CD34+-derived

60 esis, and consequently improved thalassaemic erythroid cell pathology.

61 itosis in highly purified, synchronous mouse erythroid cell populations.

62 erythroid-related factor 2 (Nrf2)/kelch-like erythroid cell-derived protein 1 (Keap1) pathway is dysr

63 e IV, characterized by severe anemia and non-erythroid-cell-related symptoms.

64 In later erythroid cells (CD71(+)Ter119(lo-hi)), heme decreases G

65 Our studies demonstrate that in early erythroid cells (CD71(+)Ter119(neg-lo)), heme increases

66 ssed mainly in hepatocytes and in developing erythroid cells and is an important focal point in syste

67 ulating transferrin-bound iron to developing erythroid cells and other cell types.

68 equired for repression of HbF in adult-stage erythroid cells but are dispensable in non-erythroid cel

69 entadactyl DNA-binding protein that in human erythroid cells directly activates only a single gene, t

70 duction of ATF4 protein synthesis in vivo in erythroid cells during ID.

71 ence of avascular blood islands of primitive erythroid cells expressing hemangioblast markers (Flk1,

72 RNA transcript analyses of erythroid cells from controls and patients with RP or GA

73 Approaches to derive erythroid cells from induced pluripotent stem cells (iPS

74 ncrease the production of mature, enucleated erythroid cells from umbilical cord blood derived CD34(+

75 al continuum dictates the absolute number of erythroid cells generated from each transit-amplifying p

76 e high-level expression of GATA1 in maturing erythroid cells have been studied extensively, the initi

77 ve in reducing the globin chain imbalance in erythroid cells hence improving the clinical outcome of

78 n the globin chain and the heme synthesis in erythroid cells of DBA patients.

79 e molecular mechanism of URE inactivation in erythroid cells through loss of TF binding represents a

80 e erythroid cells but are dispensable in non-erythroid cells(2-6).

81 kably selective transcriptional activator in erythroid cells, and its perturbation might offer new op

82 Pu.1 itself directly regulate Pu.1 levels in erythroid cells, and loss of both factors is critical fo

83 Mature erythrocytes, immature erythroid cells, and phagocytes accounted for the larges

84 te enhancer that drives globin expression in erythroid cells, before the divergence of jawless and ja

85 leading to inhibition of TAL1 expression in erythroid cells, but not T-ALL cells.

86 , in confirmatory studies using human marrow erythroid cells, ribosomal protein transcripts and prote

87 ma-globin expression and fetal hemoglobin in erythroid cells.

88 or in various solid tumours, is expressed in erythroid cells.

89 and resulting in decreased apoptosis of DBA erythroid cells.

90 ression in adults prevents the maturation of erythroid cells.

91 and impair the growth and differentiation of erythroid cells.

92 enic endothelial cells capable of generating erythroid cells.

93 ce-mediated downregulation of ALAS2 in human erythroid cellular models of CEP disease.

94 +CD71hiCD105med immature colony-forming unit-erythroid (CFU-E) population.

95 enitors (PreMegEs), and colony-forming units-erythroid (CFU-Es), as well as myeloid and erythroid blo

96 d-specification bias, evident from increased erythroid colony-forming ability and decreased megakaryo

97 This expansion of the erythroid compartment coincided with increased erythrofe

98 ell lines and peripheral blood CD34+-derived erythroid cultures from a patient with CEP inhibited iro

99 HUDEP2 erythroid cell line and primary human erythroid cultures.

100 Nuclear factor erythroid derived-2-related factor 2 (Nrf2)(-/-) and cor

101 red glutathione synthesis and nuclear factor erythroid-derived 2 related factor 2 (NRF2)-dependent ge

102 aturation protein (POMP) and nuclear factor (erythroid-derived 2)-like 2 (NRF2) expression.

103 Nuclear factor (erythroid-derived 2)-like 2 (NRF2) is a transcription fa

104 The nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is the most potent an

105 zipper transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2) plays a critical role

106 activating transcription of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) responsive genes duri

107 The nuclear factor (erythroid-derived 2)-like 2 (Nrf2) transcription factor

108 eptors can attenuate altered Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), neuronal Nitric Oxid

109 se kinase 3 beta (GSK-3beta)/nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/tetrahydrobiopterin (

110 e oxygenase-1 expression via nuclear factor (erythroid-derived 2)-like 2 signalling pathway.

111 ranscriptional activation of nuclear factor (erythroid-derived 2)-like 2, the master protector agains

112 of the transcription factor nuclear factor, erythroid-derived 2, like 2 (Nfe2l2 or Nrf2) and up-regu

113 is inhibited by silencing of nuclear factor erythroid-derived 2-like 2 (Nrf2), supporting a key role

114 t is due to binding of Nrf2 (nuclear factor [erythroid-derived 2]-like 2) to 2 AREs (antioxidant resp

115 tion by activating the NRF2 (nuclear factor [erythroid-derived 2]-like 2) transcription factor.

116 n this receptor is associated with increased erythroid development and expression of EPO and ERFE in

117 The roles of PCBP, ferritin, and NCOA4 in erythroid development remain unclear.

118 at lose chromatin accessibility during early erythroid development.

119 Dexamethasone treatment of erythroid-differentiated PB, but not CB, CD34+ progenito

120 e culture medium completely blocked terminal erythroid differentiation and enucleation.

121 hroid cell expansion, aberrant or incomplete erythroid differentiation and foetal/embryonic rather th

122 es in cohesin complex levels are critical to erythroid differentiation and how perturbations can cont

123 ly attenuated the impact of dexamethasone on erythroid differentiation and inhibited the expansion of

124 Erythropoietin (EPO) stimulates erythroid differentiation and maturation.

125 eIF2alphaP and ATF4 are necessary to promote erythroid differentiation and to reduce oxidative stress

126 ) and shorter (S) splicing variants regulate erythroid differentiation in a manner unexplainable by t

127 in accumulation, driving heme production and erythroid differentiation in committed CD71+ progenitors

128 Its expression during erythroid differentiation is regulated by alternative pr

129 e demonstrate that enasidenib enhanced human erythroid differentiation of hematopoietic progenitors.

130 Overexpression of human SIX1 stimulated erythroid differentiation of human erythroleukemia TF1 c

131 gical inhibition of the inflammasome altered erythroid differentiation of human erythroleukemic K562

132 eme as the comaster regulators of the normal erythroid differentiation program.

133 at one highly differentially expressed gene, erythroid differentiation regulator-1 (Erdr1), is induce

134 penia that is characterized by a blockade in erythroid differentiation related to impaired ribosome b

135 ein pathway suppressor 2 (GPS2) in promoting erythroid differentiation through stabilizing the erythr

136 We report that the sensitivity of erythroid differentiation to dexamethasone is dependent

137 Furthermore, miR-17-92 negatively influences erythroid differentiation, a process that depends on gen

138 nd hemoglobin content in the blood, improved erythroid differentiation, and reduced splenomegaly of i

139 e defect in erythroid proliferation, delayed erythroid differentiation, increased apoptosis, and decr

140 Depletion of cohesin severely impairs erythroid differentiation, particularly at Etv6-prebound

141 and HMG20B or of GSE1 blocks GFI1B-mediated erythroid differentiation, phenocopying impaired differe

142 nts Pu.1 down-regulation and blocks terminal erythroid differentiation, resulting in extensive ex viv

143 arasite-derived extracellular vesicles delay erythroid differentiation, thereby allowing gametocyte m

144 nd temporal resolution through in vivo mouse erythroid differentiation.

145 and S to restrict autophagic degradation and erythroid differentiation.

146 n BFUe lacking a URE fails to block terminal erythroid differentiation.

147 aintain mitochondrial function and to enable erythroid differentiation.

148 and redox homeostasis, as well as to enable erythroid differentiation.

149 slow induction of genes that drive terminal erythroid differentiation.

150 xpected synergy between CBL and CNN1 driving erythroid differentiation.

151 GATA1 protein in mouse HSPC promoting their erythroid differentiation.

152 es at active regulatory elements only during erythroid differentiation.

153 itting more cell divisions prior to terminal erythroid differentiation.

154 tal requirement for subsequent initiation of erythroid differentiation.

155 progenitors modifies their granulocytic and erythroid differentiation.

156 y MDS stroma enhanced its ability to support erythroid differentiation.

157 l as autophagy, possibly thereby fine-tuning erythroid differentiation.

158 ession, impeding hemoglobin switching during erythroid differentiation.

159 articular relating to megakaryocyte (Mk) and erythroid (E) development.

160 ieved with combined disruption of the BCL11A erythroid enhancer and correction of the HBB -28A>G prom

161 locks long-range interaction between the +51 erythroid enhancer and TAL1 promoter-1 leading to inhibi

162 have shown that core sequences at the BCL11A erythroid enhancer are required for repression of HbF in

163 on-target cytosine base edits at the BCL11A erythroid enhancer at +58 with few indels.

164 ithin a GATA1 binding site at the +58 BCL11A erythroid enhancer results in highly penetrant disruptio

165 ical and genetic inhibition of NLK increases erythroid expansion in mouse and human progenitors, incl

166 we screen for small molecules that increase erythroid expansion in mouse models of DBA.

167 nanomolar concentrations without perturbing erythroid expansion, viability, differentiation or the t

168 oxygen species and this initiated a nuclear erythroid factor 2-like 2 signaling response, downstream

169 Nuclear factor-erythroid factor 2-related factor 2 (Nrf2) may either am

170 transfusion, suggesting the presence of >=1 erythroid factor with the ability to modulate iron metab

171 ogenitor cells can irreversibly commit to an erythroid fate well before EPO acts, risking inefficienc

172 monstrate that m(6)A MTase activity promotes erythroid gene expression programs through selective tra

173 We show KLF3 can displace KLF1 from key erythroid gene promoters and enhancers in vivo.

174 us retrovirus activated transcription of key erythroid genes and modulated ex vivo erythropoiesis.

175 required for dynamic expression at critical erythroid genes during differentiation and how this may

176 expression levels of TfR1, GATA1, and other erythroid genes.

177 vascular isolated cells expressing primitive erythroid, hemangioblast and endothelial makers were vis

178 f differentiation and is not observed in non-erythroid hematopoietic lineages or healthy erythroblast

179 rates a wave of new erythrocytes to maintain erythroid homeostasis until steady-state erythropoiesis

180 als induce stress erythropoiesis to maintain erythroid homeostasis when inflammation inhibits steady-

181 h stabilizing the erythroid master regulator erythroid Kruppel-like factor (EKLF, also known as KLF1)

182 Acute erythroid leukemia (AEL) commonly involves both myeloid

183 Acute erythroid leukemia (AEL) is a high-risk leukemia of poor

184 studies provide new molecular insights into erythroid leukemia and suggest potential therapeutic tar

185 of ALK and NTRK1, the latter of which drives erythroid leukemogenesis sensitive to TRK inhibition.

186 ex 1 (mTORC1) signaling, specifically in the erythroid lineage as a feedback mechanism of erythropoie

187 Analysis of erythroid lineage cells of A20 deficient mice indicated

188 ematopoiesis by directly repressing critical erythroid lineage specifiers.

189 mia (AEL) commonly involves both myeloid and erythroid lineage transformation.

190 s are produced via a shared pathway with the erythroid lineage, also shared in its early stages with

191 sis of hematopoietic specification along the erythroid lineage, which reveals a role for the EGF rece

192 RNA embedded in a microRNA (shmiR), allowing erythroid lineage-specific knockdown.

193 lated expression of Cebpa and Gata1, myeloid/erythroid lineage-specific transcription factors.

194 ifferentiation-proliferation pathways of the erythroid lineage.

195 screen for genes affecting expression of the erythroid marker CD235a/GYPA.

196 roid differentiation through stabilizing the erythroid master regulator erythroid Kruppel-like factor

197 s such as luspatercept that are promising as erythroid maturation agents to alleviate anemia and rela

198 factor beta superfamily ligands, may enhance erythroid maturation and reduce the transfusion burden (

199 rediction and perturb the pathway to improve erythroid maturation from human pluripotent stem cells.

200 from 3 patients showed that genes related to erythroid maturation were down-regulated during acute in

201 peding a key step required for commitment to erythroid maturation.

202 thways in MDSs causes anemia due to impaired erythroid maturation.

203 d other conditions characterized by impaired erythroid maturation.

204 the transcriptomes of naive progenitors and erythroid-, megakaryocyte-, and leukocyte-committed prog

205 de spectrum of leukemias, including myeloid, erythroid, megakaryocytic and lymphoid, at age 9-14 mont

206 However, the full repertoire of erythroid miR-144/451 target messenger RNAs (mRNAs) and

207 To comprehensively and accurately identify erythroid miR-144/451 target mRNAs, we compared gene kno

208 characterised by excessive proliferation of erythroid, myeloid, and megakaryocytic components in the

209 nally, some HSCs gave rise to megakaryocytic-erythroid or myeloid precursors.

210 ntracellular iron levels and by accelerating erythroid output as reflected by increased maturation of

211 f GFI1B in K562 erythroleukemia cells favors erythroid over megakaryocytic differentiation, providing

212 The line differentiates along the erythroid pathway to orthochromatic erythroblasts and re

213 This erythroid-permissive chromatin conformation is retained

214 ATA1, as SIX1 overexpression failed to drive erythroid phenotypes and gene expression patterns in GAT

215 on in the KLF1 zinc finger exerts effects on erythroid physiology in CDA type IV.

216 ss, respectively, thereby installing ectopic erythroid potential.

217 expressed by mature hematopoietic cells, and erythroid precursor cell expression of Gdf11 has been im

218 age in mice does not alter erythropoiesis or erythroid precursor cell frequency under normal conditio

219 iatric B-ALL cell line, SEM, and an immortal erythroid precursor cell line, HUDEP-2, to allow for acu

220 nd traps or neutralizing antibodies promotes erythroid precursor cell maturation and red blood cell f

221 nias, characteristic vacuoles in myeloid and erythroid precursor cells, dysplastic bone marrow, neutr

222 a KY1070 modulates ferroportin expression on erythroid precursor cells, thereby lowering potentially

223 scue assay in murine Samd14-Enh(-/-) primary erythroid precursor cells.

224 ovides the major survival signal to maturing erythroid precursors (EPs) and is essential for terminal

225 ss from HbF repression in both primary human erythroid precursors and transgenic mice.

226 per cell (VCN) of 0.58 (range 0.10-1.97) in erythroid precursors at 1 year, in absence of clonal dom

227 cal iron accumulation in the mitochondria of erythroid precursors.

228 ing sequences comprehensively in human adult erythroid precursors.

229 ng approach to treating CEP is to reduce the erythroid production of porphyrins through substrate red

230 s with excessive heme in colony-forming unit-erythroid/proerythroblasts, explain why these anemias ar

231 activation is initiated at the Megakaryocyte/Erythroid Progenitor (MEP) stage of differentiation and

232 mmon myeloid progenitor (CMP), megakaryocyte-erythroid progenitor (MEP), and granulocyte-macrophage p

233 ify a unique glucocorticoid-responsive human erythroid progenitor and provide new insights into gluco

234 B19 has a strong tropism to erythroid progenitor cells and is able to cause a series

235 Splenic erythroid progenitor cells and mesenchymal stromal cells

236 potential of the vector was demonstrated in erythroid progenitor cells derived from beta(IVS2-654)-t

237 Furthermore, cultured erythroid progenitor cells from MAM-negative individuals

238 arrow cellularity and decreased frequency of erythroid progenitor cells in the bone marrow consistent

239 B19 (B19V) takes place exclusively in human erythroid progenitor cells of bone marrow and fetal live

240 transgenic Eto2 null mice and in human CD34+ erythroid progenitor cells with reduced ETO2, loss of ET

241 IE is an abnormal expansion of the number of erythroid progenitor cells with unproductive synthesis o

242 lentiviral short hairpin RNA transduction of erythroid progenitor cells, with global surface proteomi

243 binding to erythropoietin receptor (Epor) on erythroid progenitor cells.

244 Erythroid progenitor daughter cell pairs have similar tr

245 e marrow and spleen, but it had no effect on erythroid progenitor frequency.

246 SCF/proto-oncogene c-Kit (c-Kit) signaling, erythroid progenitor function, and erythrocyte regenerat

247 ng cells (EPCs), leading to expansion of the erythroid progenitor pool and robust splenic erythropoie

248 d with decreased levels and functionality of erythroid progenitor populations, defects ameliorated by

249 tained in human umbilical cord blood-derived erythroid progenitor-2 cells, in which beta-globin expre

250 biases the commitment of megakaryocytic (Mk)-erythroid progenitors (MEPs) toward the Mk lineage in bo

251 marrow environment affects the megakaryocyte-erythroid progenitors (MEPs).

252 Immature stress erythroid progenitors (SEPs) are derived from short-term

253 igands that initiate the expansion of stress erythroid progenitors (SEPs) in the spleen.

254 displayed an increase in colony-forming unit-erythroid progenitors and in all erythroblast population

255 transcriptional activity and accumulation of erythroid progenitors and that it may do so in an AhR-de

256 ion factor (TF) that plays critical roles in erythroid progenitors by promoting proliferation and blo

257 P1 knock-in premegakaryocyte/erythroid progenitors demonstrate an erythroid-specifica

258 Using purified erythroid progenitors in vitro, we show that IL-33 direc

259 homeostasis in the body, TFR2's function in erythroid progenitors remains controversial.

260 ds to expansion of myeloid cells and reduced erythroid progenitors resulting in anemia, with dysregul

261 Early erythroid progenitors were closely associated with peris

262 2, is expressed preferentially and highly on erythroid progenitors.

263 ex vivo proliferation and immortalization of erythroid progenitors.

264 proteins in dexamethasone-treated PB and CB erythroid progenitors.

265 Fetal hemoglobin (HbF) induction in erythroid progeny after base editing or nuclease editing

266 ng and ameliorated globin chain imbalance in erythroid progeny from sickle cell disease and beta-thal

267 Erythroid progeny of edited engrafting SCD HSCs express

268 ned lymphoid, neutrophilic/monocytic, and/or erythroid progeny outputs from >1000 index-sorted CD34(+

269 Erythroid proliferation in culture and ribosome profile

270 TA1, is a major contributor to the defect in erythroid proliferation, delayed erythroid differentiati

271 found that the cytoprotective nuclear factor erythroid-related factor 2 (Nrf2)/kelch-like erythroid c

272 sed GSH/GSSG ratio, augmented nuclear factor erythroid-related factor 2, and increased 8-oxo-7,8-dihy

273 Most suggestions relate to erythroid response assessment, which are refined in an o

274 Y1070 and recombinant human EPO improved the erythroid response compared with either monotherapy in a

275 The primary end point was erythroid response, defined as hemoglobin increase of >=

276 al of them, especially for the evaluation of erythroid response.

277 e SEPs are capable of self-renewal, they are erythroid restricted.

278 generated a novel mouse model (eAA) with the erythroid-specific ablation of eIF2alphaP and demonstrat

279 of the fetal gamma-globin gene requires the erythroid-specific eIF2alpha kinase heme-regulated inhib

280 Functional analysis demonstrates that an erythroid-specific enhancer is located in intron 7 of la

281 onors, with CRISPR-Cas9 targeting the BCL11A erythroid-specific enhancer.

282 hemoglobin switching as well as high-level, erythroid-specific expression of genes at the B-globin l

283 This raises the question of whether erythroid-specific expression of HB also evolved twice i

284 ransduction at the HSC level and high-level, erythroid-specific expression with long-term persistence

285 nherited frameshift indel mutations of human erythroid-specific isozyme ALAS2, within a C-terminal (C

286 in dramatic loss of H3K4me3 marks across key erythroid-specific KLF1 transcriptional targets (e.g., H

287 esis by using G1E-ER4 cells, which carry the erythroid-specific transcription factor GATA-binding pro

288 Formation of an erythroid-specific, protein 4.1R-dependent membrane skel

289 f their mRNAs targets are required for human erythroid specification in primary bone-marrow derived p

290 ryocyte/erythroid progenitors demonstrate an erythroid-specification bias, evident from increased ery

291 lyses of the spatiotemporal configuration of erythroid super-enhancers and promoter-centric interacti

292 oid transcription factor (TF) expression and erythroid TF chromatin access, respectively, thereby ins

293 Mice with Epor restricted to erythroid tissue exhibit reduced bone and increased marr

294 itors is sufficient to deviate cells from an erythroid to a megakaryocyte trajectory, showing that qu

295 1-dependent manner to control acquisition of erythroid traits by K562 cells.

296 and Gata2 mutations synergize by increasing erythroid transcription factor (TF) expression and eryth

297 We propose a unifying model in which the erythroid transcriptional program works in concert with

298 on of p53 may not explain all aspects of DBA erythroid tropism, involvement of GATA1/HSP70 and globin

299 ausing opposite shifts in the frequencies of erythroid versus myelomonocytic progenitors following Te

300 cile genome-wide DNAme changes with specific erythroid versus myelomonocytic skews, we provide eviden