ライフサイエンスコーパス: erythroblast

1 ransition from proerythroblast to basophilic erythroblast.

2 of murine proerythroblast to orthochromatic erythroblast.

3 oprotein (RhAG) were found in the basophilic erythroblast.

4 es had a higher actin turnover compared with erythroblasts.

5 nsition from polychromatic to orthochromatic erythroblasts.

6 gulation of dynamically-increased IR in late erythroblasts.

7 ion of gamma-globin silencing in adult human erythroblasts.

8 rs differentiated to both megakaryocytes and erythroblasts.

9 the midbody formation in dividing wild-type erythroblasts.

10 s physically associated with differentiating erythroblasts.

11 n promoting the formation of hemoglobinizing erythroblasts.

12 ouse erythroid precursors from early to late erythroblasts.

13 ng erythropoiesis, and abundant in very late erythroblasts.

14 e lineage-specific master regulator GATA1 in erythroblasts.

15 distinct morphologic abnormalities of marrow erythroblasts.

16 rplasia composed entirely of Hb Null-derived erythroblasts.

17 g that these cells were differentiating into erythroblasts.

18 ed macrophages surrounded by differentiating erythroblasts.

19 toxicity is not observed in Hb Null-derived erythroblasts.

20 s and aquaporins 1 and 9 in adult definitive erythroblasts.

21 of mesenchymal cells and primitive nucleated erythroblasts.

22 s to low-intensity binary signaling in later erythroblasts.

23 d both were expressed at increased levels in erythroblasts.

24 impairment, but not apoptosis, in dysplastic erythroblasts.

25 and nucleus, in a population of enucleating erythroblasts.

26 ia by promoting binary survival decisions in erythroblasts.

27 ofactor for erythropoiesis and expands early erythroblasts.

28 increased intracellular iron availability of erythroblasts.

29 ously up-regulated in maturing human primary erythroblasts.

30 eduction led to increased FPN1 expression in erythroblasts.

31 rythroid progenitors differentiate into late erythroblasts.

32 oid progenitor cells and more differentiated erythroblasts.

33 in both erythroblast cell lines and primary erythroblasts.

34 ession in T cells, natural killer cells, and erythroblasts.

35 of expanding and terminally differentiating erythroblasts.

36 zed roles supporting enucleation of maturing erythroblasts.

37 nsation, a morphological feature of maturing erythroblasts.

38 l to affect the hemoglobin profiles in human erythroblasts.

39 -erythroid hematopoietic lineages or healthy erythroblasts.

40 ietin (EPO) to favor iron supply to maturing erythroblasts.

41 ic imbalance in ex vivo differentiated human erythroblasts.

42 monstrated that FPN1 was highly expressed in erythroblasts, a cell type that consumes most of the ser

43 In mouse erythroblasts, a similar pattern for KCC3 and KCC1 expre

44 Decreased RhoA activity in erythroblasts abolished localization of NMIIA but not of

45 Immature erythroblasts accumulated in the bone marrow and spleen

46 We hypothesize that FPN1 expression in erythroblasts allows fine-tuning of systemic iron utiliz

47 erythropoiesis by modulating interactions of erythroblast alpha4beta1 with both macrophages and extra

48 reased and were lowest in the orthochromatic erythroblast and reticulocytes.

49 (/) mice also had an increased percentage of erythroblasts and a reduced erythrocyte enucleation in t

50 xpression of aquaporins 3 and 8 in primitive erythroblasts and aquaporins 1 and 9 in adult definitive

51 tes, but do not reach the plasma membrane in erythroblasts and are degraded by the orthochromatic sta

52 antify disrupted F-actin filament network in erythroblasts and demonstrate that reduced expression of

53 hogenesis by reducing viral dissemination to erythroblasts and eliciting an effective cytotoxic T lym

54 Bone marrow studies showed binucleated erythroblasts and erythroblasts with cytoplasmic bridges

55 We performed RNA-seq on circulating erythroblasts and found that human KLF1 acts like mouse

56 somal architectures of fetal and adult human erythroblasts and found that, globally, chromatin struct

57 hibition of RBM38 compromises translation in erythroblasts and impairs their maturation, highlighting

58 ed the expression of Rps19 or Rpl11 in mouse erythroblasts and investigated mRNA polyribosome associa

59 -) fetal livers, with Tmod3 required in both erythroblasts and macrophages.

60 nding and terminally differentiating primary erythroblasts and mature erythrocytes.

61 Indeed, treatment to reduce splenic erythroblasts and mature red blood cells correlated with

62 m and progenitor cells, as well as nucleated erythroblasts and megakaryocytes, reside preferentially

63 xpression, resulting in differentiation into erythroblasts and megakaryocytes.

64 om multilineage precursors to differentiated erythroblasts and megakaryocytes.

65 d proportion of bone marrow (BM) early stage erythroblasts and reduced enucleated erythrocytes compar

66 increased rate of apoptosis in intermediate erythroblasts and reduced release of reticulocytes.

67 long the erythroid pathway to orthochromatic erythroblasts and reticulocytes.

68 c erythroblasts from thalassemic mice and in erythroblasts and sera from subjects with beta-thalassem

69 f each specific developmental stage of human erythroblasts and should provide a powerful means of ide

70 introns that exhibit increased IR in mature erythroblasts, and are enriched in functions related to

71 indicates increased apoptosis of Tmod3(-/-) erythroblasts, and cell-cycle analysis reveals that ther

72 se in red pulp area, the number of nucleated erythroblasts, and expression levels of TfR1, GATA1, and

73 hat FPN1 localizes to the plasma membrane of erythroblasts, and hepcidin treatment leads to decreased

74 to enucleation defects in mouse fetal liver erythroblasts, and in CD34(+) hematopoietic stem and pro

75 nce, nonmammalian red blood cells, mammalian erythroblasts, and platelets have a peripheral ring of m

76 dy reveals novel cross-talk between HSCs and erythroblasts, and sheds a new light on the regulatory m

77 essed SLC25A37 and SF3B1 transcripts in late erythroblasts, and thereby limiting functional mRNA leve

78 ng many genes with undiscovered functions in erythroblasts are a resource for future functional studi

79 l line, we observed that the first primitive erythroblasts are detected in vitro around day 1.5 of bl

80 Our analysis shows that F erythroblasts are not significantly different from non-H

81 criptomic signature and increased numbers of erythroblasts are recorded in patient peripheral blood,

82 In contrast, target genes in erythroblasts are specifically enriched for red cell fun

83 Notably, enucleating Tmod3(-/-) erythroblasts are still in the process of proliferation,

84 Primitive erythroblasts are the first blood cells generated during

85 Here, we identify late erythroblasts as a new host cell for P falciparum sexual

86 e of reticulocytes derived from immortalized erythroblasts as a powerful model system to explore hypo

87 n of biotin to in vitro-differentiated mouse erythroblasts as well as to mature mouse RBCs.

88 ane deformability and stability of primitive erythroblasts, assayed by microfluidic studies and fluor

89 that STEAP3, a metalloreductase expressed in erythroblasts, associates with TfR1 and partially rescue

90 ession at day 8 and a 16% expansion of early erythroblasts at day 10 compared to cultures without NmU

91 devise an effective strategy to distinguish erythroblasts at distinct stages of development.

92 in both reduced and more immature primitive erythroblasts at E9.5 to E10.5.

93 3 and alpha4 integrin enabled us to isolate erythroblasts at specific developmental stages from prim

94 The ratio of erythroblasts at successive stages followed the predicte

95 vestigated Tmod1 function in mouse and human erythroblasts both in vivo and in vitro and found that a

96 ysis, depletes almost all marrow and splenic erythroblasts but leaves peripheral erythrocytes intact.

97 ATA-1 protein expression is decreased in MDS erythroblasts, but restores in the presence of a pan-cas

98 Strikingly, we found that infection of erythroblasts by gametocytes and parasite-derived extrac

99 rected the abnormal ratio of immature/mature erythroblasts by inducing apoptosis of immature erythrob

100 ared gene knockout and wild-type fetal liver erythroblasts by RNA sequencing, quantitative proteomics

101 es of the ERV-9 LTRs and in transgenic mouse erythroblasts carrying a single copy of the primate-spec

102 -specific deletion of ERV-9 lncRNAs in human erythroblasts carrying approximately 4000 copies of the

103 gy is the premature apoptotic destruction of erythroblasts causing ineffective erythropoiesis.

104 attached to them, accumulate in thalassemic erythroblasts causing oxidative stress and the premature

105 ion of an enucleation-competent immortalized erythroblast cell line (BEL-A) support both successful i

106 ate that selective depletion of PABPC4 in an erythroblast cell line inhibits terminal erythroid matur

107 a gene knockout-rescue system in a Brd2-null erythroblast cell line, here we compared a series of mut

108 in intracellular iron concentrations in both erythroblast cell lines and primary erythroblasts.

109 ythroblastic island formation, and defective erythroblast cell-cycle progression and enucleation.

110 In primary human adult erythroblasts, chromatin immunoprecipitation followed by

111 rmore, when compared with autologous control erythroblasts, clonally derived JAK2V617F-positive eryth

112 However, both mouse and human erythroblasts contain an F-actin structure at the rear o

113 on of mRNAs expressed at increased levels in erythroblasts contributes to the erythroid phenotype of

114 oss-of-function strategy in a primary murine erythroblast culture system.

115 expression of BAG1 and CSDE1 was reduced in erythroblasts cultured from DBA patients.

116 n was used to knockdown LIN28B expression in erythroblasts cultured from human umbilical cord CD34+ c

117 hilic, 4 polychromatic, and 8 orthochromatic erythroblasts, currently there is no method to quantitat

118 in enucleation, was also found essential for erythroblast cytokinesis as its deficiency in mice cause

119 ranscriptome profiling of E2F-2-null, mature erythroblasts demonstrated widespread changes in gene ex

120 luated the effects of DZNep in human primary erythroblasts derived from cord blood CD34-positive cell

121 The erythroblast-derived hormone erythroferrone specifically

122 nserved in maturing primitive and definitive erythroblasts despite their respective intravascular and

123 ly, all stages of Hb Null-derived definitive erythroblasts develop normally in vivo in chimeric mice,

124 that additionally acts to support late-stage erythroblast development.

125 nt with TRbeta agonists stimulated premature erythroblast differentiation in vivo and alleviated anem

126 found that Stat5 protein levels decline with erythroblast differentiation, governing the transition f

127 o revealed a critical activating function in erythroblast differentiation, in addition to its known i

128 and 480 primary cord blood cells undergoing erythroblast differentiation.

129 nd ex vivo and that Dhh negatively regulated erythroblast differentiation.

130 Mcm3-deficient erythroblasts display aberrant DNA replication patterns

131 Unlike the Stat5 protein, EpoR expression in erythroblasts does not limit the Stat5 signaling respons

132 method for distinguishing distinct stages of erythroblasts during murine erythropoiesis.

133 ins are sequentially expressed in developing erythroblasts during ontogeny.

134 m (unable to bind STAT-5) on erythropoiesis, erythroblast (EB) expansion cultures of mononuclear cell

135 d cell cycle regulatory pathways, whereas in erythroblasts EKLF is associated with repression of thes

136 In erythroblasts, EKLF is distributed throughout the nucleu

137 These macrophages make physical contact with erythroblasts, enabling signaling and the transfer of gr

138 found that CRIK activity promotes efficient erythroblast enucleation and nuclear condensation.

139 s, FLKO mice show significant enhancement of erythroblast enucleation during definitive erythropoiesi

140 However, the process of erythroblast enucleation has remained provocative and po

141 ogression, and completion of mouse and human erythroblast enucleation in vivo.

142 , Konstantinidis et al provide evidence that erythroblast enucleation is a more complex and multistep

143 of structural and signaling requirements of erythroblast enucleation with the cytokinesis process ha

144 te common cytoskeletal mechanisms underlying erythroblast enucleation, notwithstanding the morphologi

145 skeleton and membrane signaling molecules in erythroblast enucleation, we developed a novel analysis

146 , and F-actin assembly and remodeling during erythroblast enucleation.

147 oth of which undergo dramatic changes during erythroblast enucleation.

148 dentified an unappreciated role for E2F-2 in erythroblast enucleation.

149 iron availability, likely by modulating the erythroblast Epo sensitivity.

150 In later (basophilic) erythroblasts, Epo stimulation triggers a low intensity

151 ry cultured megakaryocytes (MEG) and primary erythroblasts (ERY) from murine fetal liver hematopoieti

152 SCs), common myeloid progenitors (CMPs), and erythroblasts (ERYs).

153 was established in extensively self-renewing erythroblasts (ESREs), a well-characterized, nontransfor

154 Differentiating erythroblasts execute a dynamic alternative splicing pro

155 Erythroblasts express both IRP-repressible ALAS2 and non

156 These early fetal liver erythroblasts express predominantly adult beta-globins a

157 We found that primary primitive erythroblasts express the major membrane skeleton genes

158 he human beta-globin locus, like human fetal erythroblasts, express predominately human gamma-, low b

159 Induced erythroblasts expressed erythroid surface markers and fo

160 assessed by quantitative proteomics, mutant erythroblasts expressed higher levels of proteins involv

161 poietic progenitor cells and then further to erythroblasts expressing normal beta-globin.

162 ession of Lamin isoforms, with primary mouse erythroblasts expressing only Lamin B and primary human

163 d profile differentiation stage-matched late erythroblast F cells and non-F cells (A cells) from the

164 rm switching and protein 4.1R-null primitive erythroblasts fail to establish normal membrane stabilit

165 ipolar microtubule spindle in orthochromatic erythroblasts, followed by Rac-directed formation of a c

166 oblasts:basophilic:polychromatic:orthromatic erythroblasts follows the expected 1:2:4:8 ratio, reflec

167 ads to severe anemia because of a deficit in erythroblast formation.

168 Here, we show that the mouse erythroblast forms large, transient, and recurrent nucle

169 ages on the proliferation and enucleation of erythroblasts from healthy individuals and patients with

170 lysis of clonally derived JAK2V617F-positive erythroblasts from MPN patients also demonstrated impair

171 oblasts, clonally derived JAK2V617F-positive erythroblasts from MPN patients displayed increased ROS

172 immunofluorescence analysis of intermediate erythroblasts from patients with CDA-1 reveals abnormal

173 intra-S checkpoint response was impaired in erythroblasts from polycythemia vera (PV) patients, but

174 ghly expressed in the spleen and in isolated erythroblasts from Tfr2(BMKO) mice.

175 an ActRIIA ligand, was increased in splenic erythroblasts from thalassemic mice and in erythroblasts

176 In RNA-sequencing analysis of erythroblasts, gamma-globin genes were among the most si

177 ernative approach, immortalizing early adult erythroblasts generating a stable line, which provides a

178 NCs), unless there is erythroid-hyperplasia (erythroblasts >/= 50%), calculated from nonerythroid cel

179 Defects of heme biosynthesis in developing erythroblasts have profound medical implications, as rep

180 that during the maturation of human beta-TM erythroblasts, HSP70 interacts directly with free alpha-

181 genitors gives rise to endothelial cells and erythroblasts in a SOX17-dependent manner.

182 ns in mitosis and cytokinesis, as induced in erythroblasts in an E2F-2-dependent manner, and we found

183 tent with appearance of large multinucleated erythroblasts in CDA III patients.

184 Erythroferrone (ERFE) is produced by erythroblasts in response to erythropoietin (EPO) and ac

185 ERFE is produced by erythroblasts in response to erythropoietin.

186 (ERFE) is a glycoprotein hormone secreted by erythroblasts in response to stimulation by erythropoiet

187 ) macrophages markedly reduced the number of erythroblasts in the bone marrow but did not result in o

188 the cell-autonomous development of immature erythroblasts in the bone marrow.

189 retroviruses and limited their spread to the erythroblasts in the red pulp where FVC manifests its pa

190 nt mice increased the ratio of early-to-late erythroblasts in the spleen and bone marrow, and serum L

191 ied DNA methylation in differentiating mouse erythroblasts in vivo by using genomic-scale reduced rep

192 s defective terminal maturation of nucleated erythroblasts in vivo Here, we found that these defects

193 ous hepcidin decreased FPN1 expression in BM erythroblasts in vivo, whereas iron depletion and associ

194 e polychromatophilic and orthochromatophilic erythroblasts, in concert with extensive cellular remode

195 b1 to the beta-globin promoter in GATA1 null erythroblasts, in which the beta-globin locus is relaxed

196 id cell lines and primary CD71(+) Lyn(up/up) erythroblasts, including significant alterations to the

197 LIN28B expression in adult erythroblasts increased the expression of gamma-globin,

198 gamma-globin promoter in primary adult human erythroblasts increases gamma-globin promoter-LCR contac

199 We conclude that maturing primitive erythroblasts initially navigate the embryonic vasculatu

200 s, using exogenous Stat5, we converted later erythroblasts into high-intensity graded signal transduc

201 neral protein synthesis by HRI-eIF2alphaP in erythroblasts is necessary to prevent proteotoxicity and

202 ized by abnormal chromatin ultrastructure in erythroblasts, is caused by abnormalities in codanin-1,

203 During in vivo maturation of human erythroblasts, KCC3a RNA was expressed consistently, whe

204 Here we show that in primary human erythroblasts, lncRNAs transcribed from the LTR retrotra

205 ediated actin remodeling may be required for erythroblast-macrophage adhesion, coordination of cell c

206 tream of cytokine signaling, and in terminal erythroblast maturation and enucleation, as master regul

207 In this system, SetD8 promoted erythroblast maturation and survival, and this did not i

208 Definitive erythroblasts mature and enucleate extravascularly and f

209 ify 1109 polyadenylated lncRNAs expressed in erythroblasts, megakaryocytes, and megakaryocyte-erythro

210 in in mitosis and interphase, using a murine erythroblast model.

211 a8--whose expression was increased in mutant erythroblasts, monocytes and macrophages--is functionall

212 Argonaute bound ~1400 erythroblast mRNAs in a miR-144/451-dependent manner, ac

213 ng at the cell surface constriction in mouse erythroblasts, nor at the membrane protein-sorting bound

214 Mouse erythroblast nuclei acquire a dumbbell-shaped morphology

215 uring enucleation, whereas human bone marrow erythroblast nuclei unexpectedly retain their spherical

216 8 regulates polarization and/or extrusion of erythroblast nuclei.

217 uction of moderate iron deficiency increases erythroblasts number, reduces apoptosis, and enhances er

218 Analysis of gene expression in MDS erythroblasts obtained by ex vivo cultures demonstrates

219 yte-erythroid precursors of mice, and 594 in erythroblasts of humans.

220 Tmod3(-/-) late erythroblasts often exhibit multilobular nuclear morphol

221 ts expressing only Lamin B and primary human erythroblasts only Lamin A/C.

222 tment exhibited reduced Ter119/CD71 positive erythroblasts, peripheral blood RBCs and hemoglobin leve

223 licing program in terminally differentiating erythroblasts plays a major role in regulating gene expr

224 flow-imaging analysis, colchicine inhibited erythroblast polarization, implicating microtubules duri

225 orming unit-erythroid progenitors and in all erythroblast populations regardless of iron overload.

226 cause of 4.1R deficiency, the ratio of these erythroblast populations remains the same as that of wil

227 In addition, we found that erythroblast populations were Dhh-responsive in vitro an

228 deficient spleen and bone marrow, BFU-Es and erythroblast populations were increased compared with WT

229 y E16.5, with profound reduction of maturing erythroblast populations within the fetal liver.

230 transporters, primitive, but not definitive, erythroblasts preferentially accumulate reactive oxygen

231 e migrated into the cytoplasm of normal late erythroblasts prior to and during enucleation, but not i

232 the chromatin structure and transcriptome of erythroblasts, prior to their enucleation.

233 ases early BFU-E cell self-renewal and total erythroblast production, suggesting the usefulness of th

234 f RhoA as a critical regulator for efficient erythroblast proliferation and the p53 pathway as a powe

235 of early erythroid progenitors and enhanced erythroblast proliferation, whereas reduced platelet num

236 Lrf deletion in erythroblasts promoted up-regulation of Dll4 in erythrob

237 -globin expression in cultured primary human erythroblasts provides a robust ex vivo model for beta-t

238 ely, LIN28B overexpression in cultured adult erythroblasts reduced the expression of let-7 and signif

239 opulations of morphologically distinct human erythroblasts, representing the last four cell divisions

240 In particular, maturing erythroblasts required Spi2A for cytoprotection, with ir

241 Moreover, inhibition of p53 in PV erythroblasts resulted in more gamma-H2Ax (gamma-H2Ax)-m

242 ockdown of Xpo7 in primary mouse fetal liver erythroblasts resulted in severe inhibition of chromatin

243 Reexpression of DOCK4 in -7q MDS patient erythroblasts resulted in significant erythropoietic imp

244 Furthermore, Asxl1(/) erythroblasts revealed altered expression of genes invol

245 sized that placenta growth factor (PlGF), an erythroblast-secreted factor that is elevated in SCD, me

246 This capacity for extensive erythroblast self-renewal is temporally associated with

247 throblasts promoted up-regulation of Dll4 in erythroblasts, sensitizing HSCs to T-cell instructive si

248 strated that the intron retention program in erythroblasts shares features with other tissues but ult

249 led analysis of chromatin structure in CDA-1 erythroblasts shows no abnormalities in overall histone

250 Flow cytometry of fetal liver erythroblasts shows that late-stage populations are also

251 rentiation of an erythrocyte, the developing erythroblast shuts down expression of most of its genes

252 reatment of ribosomal protein S-14-deficient erythroblasts significantly reduced cellular p53 and p53

253 F is distributed throughout the nucleus, and erythroblast-specific EKLF occupancy is predominantly in

254 rminal differentiation at the orthochromatic erythroblast stage for Eklf(-/-) cells that proceed beyo

255 ibition of differentiation at the basophilic erythroblast stage.

256 selectively and highly expressed at CFU-e to erythroblast stages.

257 unts without altering relative abundances of erythroblast subpopulations.

258 On acute oxidative stress, Hri(-/-) erythroblasts suffered from increased levels of reactive

259 cRNAs have no detectable expression in human erythroblasts, suggesting that lack of conservation betw

260 genes present in similarly staged definitive erythroblasts, suggesting that the composition and forma

261 nded breaks compared with in like-treated ET erythroblasts, suggesting the defective intra-S checkpoi

262 the number of EBIs as well as the number of erythroblasts surrounding the central macrophage.

263 upregulation of the established regulator of erythroblast survival Bcl-x(L).

264 markedly different response dynamics for two erythroblast survival pathways in vivo.

265 CFU-Es and actively proliferating definitive erythroblasts that clustered around central macrophages,

266 D31, CD34, C-kit, CXCR4, Runx1, and VEGFR2), erythroblasts that expressed embryonic hemoglobin (Hb-ep

267 This was further confirmed in erythroblasts that have a higher basal RhoA activity tha

268 roleukemia, with an accumulation of immature erythroblasts that infiltrated the bone marrow, spleen,

269 nit-erythroid and an expansion of late-stage erythroblasts that was independent of iron overload.

270 In early erythroblasts the binary signal is superseded by a high-

271 We have shown that, in human erythroblasts, the chaperone heat shock protein70 (HSP70

272 th beta-thalassemia, by expanding late-stage erythroblasts through a mechanism distinct from erythrop

273 throblasts by inducing apoptosis of immature erythroblasts through the Fas-Fas ligand pathway.

274 ibits the maturation of late-stage nucleated erythroblasts to anucleate reticulocytes.

275 regulates HbF levels and causes adult human erythroblasts to differentiate with a more fetal-like ph

276 rom high-intensity graded signaling in early erythroblasts to low-intensity binary signaling in later

277 hare similar copy number, mutational status, erythroblast transformation specific (ETS) rearrangement

278 1 ALL-related ETV6 variants clustered in the erythroblast transformation specific domain and were pre

279 200c expression by physically binding to the erythroblast transformation-specific (ETS) motif within

280 protease, serine 2, gene (TMPRSS2) with the erythroblast transformation-specific (ETS)-related gene

281 on differences in the frequency of oncogenic erythroblast transformation-specific family of transcrip

282 and its collaborative transcription factor, erythroblast transformation-specific related gene (ERG),

283 romoter capture Hi-C data suggested that the erythroblast transformation-specific related gene(ERG) e

284 protease, serine 2, gene (TMPRSS2) with the erythroblast transformation-specific-related gene (ERG),

285 Erythroblasts treated with NSC23766, cytochalasin-D, col

286 lenced embryonic globin gene in adult murine erythroblasts triggers its transcriptional reactivation.

287 When differentiated into erythroblasts using a monolayer culture, gene-corrected

288 d into induced endothelial cells and induced erythroblasts using lineage-specific growth factors.

289 rotein translation in vivo in murine primary erythroblasts using ribosome profiling.

290 Cas9-guided loss-of-function screen in human erythroblasts, we identify transcription factor ATF4, a

291 on, maturation, and enucleation of primitive erythroblasts were also impaired by Vegfc deletion.

292 central macrophage surrounded by developing erythroblasts, were described.

293 ellular pools decreased in the polychromatic erythroblast, whereas surface expression increased and w

294 e membrane protein-sorting boundary in human erythroblasts, which do not have a constriction, arguing

295 tant restores terminal maturation of beta-TM erythroblasts, which may provide a rationale for new tar

296 sition of the membrane skeleton in primitive erythroblasts, which progressively mature while circulat

297 studies showed binucleated erythroblasts and erythroblasts with cytoplasmic bridges indicating abnorm

298 uent enucleation were not affected in murine erythroblasts with genetic deletion of Rac1 and Rac2 GTP

299 EPOR-Spi2A serpin-cathepsin axis in maturing erythroblasts, with lysosomal cathepsins as novel therap

300 proerythroblasts with some early basophilic erythroblasts, with no change in morphology over time in