ライフサイエンスコーパス: erythroid

1 ference in the regulation of nuclear factor, erythroid 2 (Nfe2) and core-binding factor, runt domain,

2 lated the expression of NRF2 (nuclear factor erythroid 2 [NF-E2]-related factor 2) and its target enz

3 y of the transcription factor nuclear factor-erythroid 2 p45-derived factor 2 (NRF2) is orchestrated

4 Wild-type (Control) and nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) null mice were s

5 went on to identify the AMPK-nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) pathway as a mec

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

7 ER-bound transcription factor nuclear factor erythroid 2 related factor-1, Nrf1/Nfe2L1, as a critical

8 , 4), a negative regulator of nuclear factor erythroid 2-like 2 (NFE2L2; hereafter NRF2), which is th

9 ministration or activation of nuclear factor erythroid 2-like 2 (Nrf2), a transcriptional regulator o

10 haracterized by up-regulated nuclear factor, erythroid 2-like 2 activity; high lin-28 homolog B, high

11 amined here the expression of nuclear factor-erythroid 2-related factor (Nrf-2), a master antioxidant

12 We determined if activating nuclear factor erythroid 2-related factor (Nrf2), a potential therapeut

13 1, respectively) and improved nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1

14 his phenomenon was partially dependent on NF erythroid 2-related factor 2 (NRF2) but not on nuclear l

15 WT mice showed increased antioxidant and NF erythroid 2-related factor 2 (Nrf2) gene expression, Nrf

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

17 The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial regulat

18 Nuclear erythroid 2-related factor 2 (Nrf2) is a redox-sensitive

19 NF erythroid 2-related factor 2 (Nrf2) is a transcription f

20 on through down-regulation of nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in oPMN, des

21 haracterized by activation of nuclear factor erythroid 2-related factor 2 (NRF2) target genes, suppor

22 tenuated GSH/GSSG, total GSH, nuclear factor erythroid 2-related factor 2 (Nrf2), and processes downs

23 l hydrocarbon receptor (AhR), nuclear factor erythroid 2-related factor 2 (Nrf2), and tumor suppresso

24 scription was mediated by the nuclear factor erythroid 2-related factor 2 (Nrf2), as evidenced by the

25 Nuclear factor erythroid 2-related factor 2 (Nrf2), the master transcri

26 is was confirmed by silencing nuclear factor-erythroid 2-related factor 2 (Nrf2), which decreased MRP

27 n receptor-alpha activity and nuclear factor erythroid 2-related factor 2 activity, anti-oxidative ac

28 (ROS) production, with the involvement of NF-erythroid 2-related factor 2 and heme oxygenase-1.

29 ein kinase (AMPK) pathway and nuclear factor-erythroid 2-related factor 2 target genes, and show enha

30 through competition of Nrf2 (nuclear factor erythroid 2-related factor 2) for Keap1 binding.

31 Notably, expression of nuclear factor erythroid 2-related factor 2-dependent antioxidant genes

32 Nuclear factor-erythroid 2-related factor-2 (Nrf2) is a master regulato

33 Nuclear factor erythroid-2-related factor 1 (NRF1) and NRF2 are essenti

34 argets transcriptional factor nuclear factor erythroid-2-related factor 2 (NRF2) for degradation.

35 Nuclear factor erythroid-2-related factor 2 (Nrf2) is a key transcripti

36 The nuclear factor-erythroid-2-related factor 2 (Nrf2)-mediated antioxidant

37 s via focal amplification and nuclear factor erythroid-2-related factor 2 (NRF2)-mediated up-regulati

38 n of the antioxidant transcription factor NF erythroid-2-related factor 2 level and DNA binding activ

39 ation end products (RAGE) via nuclear factor erythroid-2-related-factor-2 (Nrf2)-dependent pathway.

40 el regulator underpining the pathogenesis of erythroid abnormalities caused by TRalpha1 mutants.

41 mutations, via dominant negative mode, cause erythroid abnormalities in patients.

42 The absence of erythroid ACKR1 altered mouse hematopoiesis including st

43 roughout differentiation into megakaryocytic-erythroid and granulocytic-monocytic lineages.

44 tes with Sf3b1(K700E) to cause a more severe erythroid and LT-HSC phenotype.

45 ly assessed IR in primary maturing mammalian erythroid and megakaryocyte (MK) lineages as well as the

46 ce marker expression observed in standard 2D erythroid and megakaryocyte cultures.

47 GATA1 organizes erythroid and megakaryocytic differentiation by orchestr

48 preleukemic Pre-Meg/Es display dysregulated erythroid and megakaryocytic fate-determining factors in

49 tion of rRNA synthesis in cell lines of both erythroid and non-erythroid origin.

50 We next addressed the importance of LMO2 in erythroid and thymocyte development, two lineages in whi

51 macrophage, burst-forming unit-erythroid/CFU-erythroid, and CFU-granulocyte/erythroid/macrophage/MK)

52 sion changes associated with early lymphoid, erythroid, and granulocyte-macrophage differentiation.

53 severely decreased bone-marrow cellularity, erythroid anemia and B cell lymphopenia.

54 eased differentiation of HSCs toward myeloid/erythroid-associated MPP2s.

55 rs exclude H3K27me3 from extended regions in erythroid blood cells.

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

57 uman pluripotent stem cells allowed enhanced erythroid cell expansion with preserved differentiation.

58 nd common as well as unique sites within the erythroid cell genome by ChIP-seq.

59 n1b transcription by approximately 70% in an erythroid cell line.

60 EPO mutant is less effective at stimulating erythroid cell proliferation and differentiation, even a

61 Although the principal erythroid cell transcription factors are known, mechanis

62 Interestingly, bdh2-inactivated erythroid cells also exhibit genomic alterations as indi

63 Our results uncover in chorea-acanthocytosis erythroid cells an association between accumulation of a

64 and genes with an overwhelming loss of IR in erythroid cells and MKs compared to MEPs.

65 Despite the common origin of erythroid cells and MKs, and overlapping gene expression

66 ill poorly understood and studies on patient erythroid cells are hampered by their paucity.

67 In human hematopoiesis, megakaryocytes and erythroid cells differentiate from a shared precursor, t

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

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

70 mutations in the transcription factor GATA1 Erythroid cells from patients with DBA have not been wel

71 pomalidomide induces HbF in differentiating erythroid cells from people with sickle cell disease and

72 Nucleated erythroid cells had high expression of ACKR1, which faci

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

74 Macrophages and erythroid cells in the fetal liver (FL) were also decrea

75 largely mediate enhancer-promoter looping in erythroid cells independent of mediator and cohesin.

76 Mechanistic studies in erythroid cells indicate that LDB1, as part of a GATA1/T

77 , shRNAmiR-mediated suppression of BCL11A in erythroid cells led to stable long-term engraftment of g

78 d that RNF41 expression decreased in primary erythroid cells of lenalidomide-responding patients, sug

79 did not disrupt the generation of primitive erythroid cells or erythro-myeloid progenitors (EMPs) in

80 Amassing of PPIX in erythroid cells promotes erythropoietic protoporphyria (

81 in methylcellulose culture large colonies of erythroid cells that consist of "bursts" of smaller eryt

82 e complex controls the massive production of erythroid cells that ensures organismal survival in home

83 n (HbS) synthesis as well as sickling of SCD erythroid cells under hypoxic conditions.

84 In human primary erythroid cells USF1/2, H3K4me3 and the NURF complex wer

85 ineage-specific BCL11A shRNAmiR gave rise to erythroid cells with up to 90% reduction of BCL11A prote

86 mast cells, eosinophils, megakaryocytes and erythroid cells, and a pathway lacking expression of tha

87 induce a differentiation defect in wild-type erythroid cells, and genetic inactivation of S100a8 expr

88 ctively abolishes the expression of ACKR1 in erythroid cells, causing a Duffy-negative phenotype.

89 f X-chromosome inactivation (Lyonisation) in erythroid cells, may have low G6PD activity in the major

90 In adult erythroid cells, the LCR can be redirected from the adul

91 n edited CD34+ cells are differentiated into erythroid cells, we observe the expected reduction in al

92 do not express NR4A1 primarily develop into erythroid cells.

93 the silenced PU.1 promoter in differentiated erythroid cells.

94 A1, TAL1, LMO2, LDB1 and Pol II at least, in erythroid cells.

95 shown to facilitate direct iron transfer in erythroid cells.

96 f relevant cell surface markers in Eklf(-/-) erythroid cells.

97 of the strongest putative super-enhancers in erythroid cells.

98 atients with DBA and differentiate them into erythroid cells.

99 the potential of MPPS to differentiate into erythroid cells.

100 bin gene expressed specifically in primitive erythroid cells.

101 U-granulocyte/macrophage, burst-forming unit-erythroid/CFU-erythroid, and CFU-granulocyte/erythroid/m

102 id cells that consist of "bursts" of smaller erythroid colonies derived from the later colony-forming

103 pressed erythroid surface markers and formed erythroid colonies.

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

105 Reduced definitive erythroid colony-forming activity was found in the blood

106 ing erythropoiesis at the burst-forming unit-erythroid/colony-forming unit-erythroid transition, but

107 ent for Setd1a, an H3K4 trimethylase, in the erythroid compartment exhibited reduced Ter119/CD71 posi

108 We describe a 3D erythroid culture system that utilises a porous polyuret

109 n in K562 cells and in human primary ex vivo erythroid cultures enhances erythroid differentiation an

110 macrophages--is functionally involved in the erythroid defect caused by the Rps14 deletion, as additi

111 how NCOR1 could regulate TRalpha1 mutants in erythroid defects in vivo is not known.

112 e expression of key erythroid genes, causing erythroid defects.

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

114 y of keratinocytes to sustain nuclear factor erythroid-derived 2 related factor 2-dependent (NRF2-dep

115 The nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a transcription fa

116 Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is the master regulat

117 ffects via activation of the nuclear factor (erythroid-derived 2)-like 2 (NRF2) pathway.

118 idative transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway.

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

120 Furthermore, TKE2 activated nuclear factor (erythroid-derived 2)-like 2 (NRF2) signaling pathway, re

121 affected genes belong to the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) transcription factor

122 llular antioxidant response, nuclear factor (erythroid-derived 2)-like 2 (NRF2), shuttled to the nucl

123 Activation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), the "master regulato

124 rotein 1 (Keap1) to regulate nuclear factor (erythroid-derived 2)-like 2 (Nrf2).

125 Nuclear factor (erythroid-derived 2)-like 2 and its Caenorhabditis elega

126 ession of the redox regulator nuclear factor-erythroid-derived 2-like 2 (NFE2L2 alias NRF-2).

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

128 ve stress and address whether nuclear factor-erythroid-derived 2-related factor 2 (Nrf2) can reverse

129 binding to and deacetylating nuclear factor erythroid-derived 2-related factor 2 (NRF2) on lysines 5

130 e transcription factor NRF2 (nuclear factor [erythroid-derived 2]-like 2) plays crucial roles in the

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

132 The erythroid-derived hormone erythroferrone appears to be a

133 ective transcription factor, nuclear factor (erythroid-derived-2)-like 2 (Nrf2), aggravates cardiotox

134 Disruption of nuclear factor (erythroid-derived-2)-like 2 antioxidant signaling: a mec

135 Erythroid development and differentiation from multiprog

136 itored the impact of Salmonella infection on erythroid development and found that systemic infection

137 e profound effect of Salmonella infection on erythroid development and suggest that the modulation of

138 velopment and suggest that the modulation of erythroid development has both positive and negative con

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

140 remature mitochondrial degradation, promotes erythroid development, and reverses altered gene express

141 Salmonella infection profoundly affects host erythroid development, but the mechanisms responsible fo

142 e II (CDAII), a disease limited to defective erythroid development.

143 mmunication with the nucleus is critical for erythroid development.

144 ed to BATF as a candidate novel regulator of erythroid development.

145 oiesis and indicates that ASXL1 loss hinders erythroid development/maturation, which could be of prog

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

147 low cytometric analysis showed impairment of erythroid differentiation and expansion of megakaryocyti

148 primary ex vivo erythroid cultures enhances erythroid differentiation and leads to hemoglobinization

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

150 In this study, we used erythroid differentiation as a model to analyze how the

151 vels of RBM39, whose expression rises during erythroid differentiation as exon 16 inclusion increases

152 collaboration of malignant proliferation and erythroid differentiation blockage.

153 nactivation of S100a8 expression rescued the erythroid differentiation defect of Rps14-haploinsuffici

154 al inactivation of Rps14 and demonstrated an erythroid differentiation defect that is dependent on th

155 100A9 expression, leading to a p53-dependent erythroid differentiation defect.

156 hroid stages in the spleen thereby excluding erythroid differentiation defects.

157 s showed decreased proliferation and delayed erythroid differentiation in comparison with controls.

158 Its expression during erythroid differentiation is regulated by alternative pr

159 proliferation defect with minimal effect on erythroid differentiation potential, suggesting the mech

160 regulating the sequential steps of terminal erythroid differentiation remain largely undefined, yet

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

162 arly complex patterns were observed in human erythroid differentiation, but not involving the murine

163 Using a cultured cell model of erythroid differentiation, depletion of PCBP1 or NCOA4 i

164 se cultures indicates lymphoid, myeloid, and erythroid differentiation, indicating that CHEST cells a

165 tal requirement for subsequent initiation of erythroid differentiation.

166 ression of ARID3a inhibited both myeloid and erythroid differentiation.

167 to EPO inhibits their migration and enhances erythroid differentiation.

168 GATA1 via inhibiting PU.1, thereby improving erythroid differentiation.

169 elease, chromatin condensation, and terminal erythroid differentiation.

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

171 bition of gene transcription and blockade of erythroid differentiation.

172 progenitors modifies their granulocytic and erythroid differentiation.

173 taID) mice led to partial rescue of terminal erythroid differentiation.

174 n capacity; "E-MEP," strongly biased towards erythroid differentiation; and "MK-MEP," a previously un

175 ements proximal to other genes implicated in erythroid disorders, and show that targeted disruption o

176 pathogenicity of noncoding variants in human erythroid disorders.

177 ult hematopoietic system recapitulates fetal erythroid-dominant hematopoiesis.

178 e to a terminal erythroid maturation defect, erythroid dysplasia, and long-term hematopoietic stem ce

179 kout mice showed cell-autonomous anaemia and erythroid dysplasia, mimicking dyserythropoiesis in MDS.

180 rogeny limited to the megakaryocyte (Mk) and erythroid (E) lineages.

181 is prevalent at dynamic enhancers and drives erythroid enhancer commissioning.

182 l globin expression, display hallmarks of an erythroid enhancer in cell lines and transgenic mice.

183 eotide polymorphisms lie within an essential erythroid enhancer of the BCL11A gene.

184 from validated and predicted LDB1-regulated erythroid enhancer-gene pairs.

185 cell-sorting scheme to resolve myeloid (My), erythroid (Er), and megakaryocytic (Mk) fates from singl

186 as part of a GATA1/TAL1/LMO2 complex, brings erythroid-expressed genes into proximity with enhancers

187 f SOX17 instead directed the cells toward an erythroid fate.

188 le transcription factors are associated with erythroid gene expression, and have created predictive m

189 n a chronic anemia mouse model by regulating erythroid gene expression.

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

191 ith alterations in NURF complex occupancy at erythroid gene promoters and reduced chromatin accessibi

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

193 De-repression of key erythroid genes in Thra1 (PV/+) Ncor1 (DeltaID/DeltaID)

194 co-enriched at transcription start sites of erythroid genes, and their binding was associated with p

195 d directly to suppress the expression of key erythroid genes, causing erythroid defects.

196 ns that accompany fetal development, such as erythroid globin chain switching, play important roles i

197 ing Group-defined haematological improvement-erythroid (HI-E), defined as a haemoglobin concentration

198 Regardless of the presence of erythroid hyperplasia, calculating the percentage of BM

199 rvival than did patients with RAEB-1 without erythroid hyperplasia.

200 otal nucleated cells (TNCs), unless there is erythroid-hyperplasia (erythroblasts >/= 50%), calculate

201 one marrow failure syndrome characterized by erythroid hypoplasia, usually without perturbation of ot

202 d a differential proteomic analysis on human erythroid K562 cells overexpressing Sox6.

203 Erythroid Kruppel-like Factor (EKLF/KLF1) is a master tr

204 Acute erythroid leukemia (AEL) is characterized by lower incid

205 he cellular hierarchy in human megakaryocyte/erythroid lineage commitment and highlights the importan

206 lastic syndrome (MDS), lenalidomide promotes erythroid lineage competence and effective erythropoiesi

207 CM expression induces marked deficiencies in erythroid lineage differentiation and early preleukemic

208 and TET2 share common effects on myeloid and erythroid lineage differentiation, however, their role i

209 erythroid promoter chromatin dynamics during erythroid lineage differentiation.

210 ribosomal protein function and linked to the erythroid lineage in 5q deletion myelodysplastic syndrom

211 rogram is entirely distinct from that of the erythroid lineage with regards to introns, genes, and af

212 uts depend on the expression of ACKR1 in the erythroid lineage, findings with major implications for

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

214 ferentiation potential of progenitors in the erythroid lineage.

215 presses mTORC1 signaling specifically in the erythroid lineage.

216 for studies on gene expression in the MK and erythroid lineages.

217 terized by distinct primitive and definitive erythroid lineages.

218 erythroid/CFU-erythroid, and CFU-granulocyte/erythroid/macrophage/MK) irrespective of their mutationa

219 nd the body to sites of utilization with the erythroid marrow having particularly high iron requireme

220 Although defective erythroid maturation and anemia are associated with the

221 ated that exosome complex subunits confer an erythroid maturation barricade, and the erythroid transc

222 The basis for this erythroid maturation defect is not known.

223 develop macrocytic anemia due to a terminal erythroid maturation defect, erythroid dysplasia, and lo

224 transcription factor induced during terminal erythroid maturation.

225 plex IR patterns were seen throughout murine erythroid maturation.

226 horein and autophagic vesicle trafficking in erythroid maturation.

227 leads to hemoglobinization, the hallmark of erythroid maturation.

228 , folding and trafficking, key processes for erythroid maturation.

229 inct subpopulations: "Pre-MEP," enriched for erythroid/megakaryocyte progenitors but with residual my

230 hematopoietic cells from zebrafish to define erythroid, myeloid, B, and T cell lineages.

231 commitment of blood progenitor cells to the erythroid or myeloid lineage is preceded by the destabil

232 esis in cell lines of both erythroid and non-erythroid origin.

233 d erythroferrone, suggesting that the strong erythroid phenotype in Ex12 mutant mice is favored by ch

234 Exosome complex integrity in erythroid precursor cells ensures Kit receptor tyrosine

235 ng protein 3 (RIP3)-dependent necroptosis in erythroid precursor cells.

236 Ex vivo differentiation of erythroid precursors from Pcbp1-deficient mice confirmed

237 cytopenia and marked reduction or absence of erythroid precursors from the bone marrow.

238 F2alpha kinase (HRI) is a key hemoprotein in erythroid precursors that sense intracellular heme conce

239 on is inherently critical for enucleation of erythroid precursors, thereby demonstrating a direct fun

240 poiesis, we studied in vitro CD34(+)-derived erythroid precursors.

241 d only slightly increased TfR1 expression in erythroid precursors.

242 athological mitochondrial iron deposition in erythroid precursors.

243 and demonstrated the presence of a primitive erythroid primed hemogenic endothelial cell population i

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

245 e from a shared precursor, the megakaryocyte-erythroid progenitor (MEP), which remains poorly defined

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

247 modimers signal to promote the maturation of erythroid progenitor cells.

248 were also present in downstream myeloid and erythroid progenitor cells.

249 arly steps in the differentiation of myeloid-erythroid progenitor cells.

250 s derived from the later colony-forming unit erythroid progenitor erythropoietin (Epo)-dependent prog

251 Burst-forming unit erythroid progenitors (BFU-Es) are so named based on the

252 Bipotent megakaryocyte/erythroid progenitors (MEPs) give rise to progeny limite

253 cytic progenitors (GMPs), and megakaryocytic-erythroid progenitors (MEPs).

254 romote increased quiescence in megakaryocyte-erythroid progenitors (MEPs).

255 Erythroid progenitors and precursors were increased in h

256 Abnormality in Meg/E or erythroid progenitors could potentially be considered an

257 Lowering LMO2 levels in erythroid progenitors delays G1-S progression and arrest

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

259 Culture of erythroid progenitors from the patient and his parents r

260 poietic stem cells (HSCs) and megakaryocytic erythroid progenitors identified highly up-regulated gen

261 mice harbor significantly higher numbers of erythroid progenitors in the spleen compared with wild-t

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

263 re activated in P1 knock-in premegakaryocyte/erythroid progenitors, presumably accounting for the inc

264 opoietic stem/progenitor cells and committed erythroid progenitors.

265 ically targeted to and coordinately regulate erythroid promoter chromatin dynamics during erythroid l

266 The erythroid proteome undergoes a rapid transition at the r

267 trum ubiquitinating enzyme that remodels the erythroid proteome.

268 o 80% cellularity), with an elevated myeloid:erythroid ratio of 5:1, increased megakaryocytes includi

269 ted erythropoiesis, an obligate step towards erythroid recovery in response to supplementation.

270 hroferrone (ERFE) has been identified as the erythroid regulator that inhibits hepcidin in stress ery

271 pecific transcription factors, including the erythroid regulators Klf1 and Epor, is upregulated in do

272 is assay identifies elements with endogenous erythroid regulatory activity.

273 ed hemoglobin formation, and perturbation of erythroid regulatory systems.

274 cycle stages with a specific augmentation of erythroid related genes in the G2/M phase.

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

276 Results Erythroid response to ESAs was 61.5%, and median respons

277 at their peak response, surprisingly, their erythroid response was not compromised and was similar t

278 ysplastic syndrome (MDS) patients achieve an erythroid response with lenalidomide in 25% of cases.

279 acterized, and the mechanisms underlying the erythroid specific effects of either RP or GATA1 associa

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

281 At a transcriptional level, multiple erythroid-specific genes are upregulated and megakaryocy

282 Erythroid-specific overexpression of IGF2BP1 caused a ne

283 KLF1 directly activates the Klf3 gene via an erythroid-specific promoter.

284 We find that RBM38, an erythroid-specific RNA-binding protein previously implic

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

286 ormal Pre-Meg/E progenitors with compromised erythroid specification and differentiation capacity.

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

288 by avid extramedullary erythropoiesis at all erythroid stages in the spleen thereby excluding erythro

289 % (physiologic; normalized by treatment with erythroid-stimulating agent).

290 e detailed observations at baseline and post-erythroid stress (E-stress) in 2 mouse models with genet

291 Induced erythroblasts expressed erythroid surface markers and formed erythroid colonies.

292 t neonates are physiologically enriched with erythroid TER119(+)CD71(+) cells.

293 tors that cooperate with TRbeta during human erythroid terminal differentiation, we conducted RNA-seq

294 Here we investigated in primary human erythroid tissues a downstream element of the heterochro

295 r an erythroid maturation barricade, and the erythroid transcription factor GATA-1 dismantles the bar

296 Key erythroid transcription factors, GATA1 and TAL1, coopera

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

298 t-forming unit-erythroid/colony-forming unit-erythroid transition, but without affecting terminal dif

299 lls, thus unraveling potential regulators of erythroid translational programs.

300 GATA1 precedes and initiates megakaryocytic-erythroid versus granulocytic-monocytic lineage decision