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1 ransition from proerythroblast to basophilic erythroblast.
2 of murine proerythroblast to orthochromatic erythroblast.
3 oprotein (RhAG) were found in the basophilic erythroblast.
4 s physically associated with differentiating erythroblasts.
5 n promoting the formation of hemoglobinizing erythroblasts.
6 ouse erythroid precursors from early to late erythroblasts.
7 ng erythropoiesis, and abundant in very late erythroblasts.
8 e lineage-specific master regulator GATA1 in erythroblasts.
9 distinct morphologic abnormalities of marrow erythroblasts.
10 ession in T cells, natural killer cells, and erythroblasts.
11 rplasia composed entirely of Hb Null-derived erythroblasts.
12 g that these cells were differentiating into erythroblasts.
13 toxicity is not observed in Hb Null-derived erythroblasts.
14 of expanding and terminally differentiating erythroblasts.
15 s and aquaporins 1 and 9 in adult definitive erythroblasts.
16 of mesenchymal cells and primitive nucleated erythroblasts.
17 s to low-intensity binary signaling in later erythroblasts.
18 d both were expressed at increased levels in erythroblasts.
19 impairment, but not apoptosis, in dysplastic erythroblasts.
20 and nucleus, in a population of enucleating erythroblasts.
21 ia by promoting binary survival decisions in erythroblasts.
22 ofactor for erythropoiesis and expands early erythroblasts.
23 increased intracellular iron availability of erythroblasts.
24 ously up-regulated in maturing human primary erythroblasts.
25 eduction led to increased FPN1 expression in erythroblasts.
26 zed roles supporting enucleation of maturing erythroblasts.
27 rythroid progenitors differentiate into late erythroblasts.
28 oid progenitor cells and more differentiated erythroblasts.
29 in both erythroblast cell lines and primary erythroblasts.
30 f clathrin inhibited the enucleation of late erythroblasts.
31 nsation, a morphological feature of maturing erythroblasts.
32 l to affect the hemoglobin profiles in human erythroblasts.
33 ietin (EPO) to favor iron supply to maturing erythroblasts.
34 ic imbalance in ex vivo differentiated human erythroblasts.
35 es had a higher actin turnover compared with erythroblasts.
36 nsition from polychromatic to orthochromatic erythroblasts.
37 gulation of dynamically-increased IR in late erythroblasts.
38 ion of gamma-globin silencing in adult human erythroblasts.
39 rs differentiated to both megakaryocytes and erythroblasts.
40 the midbody formation in dividing wild-type erythroblasts.
42 monstrated that FPN1 was highly expressed in erythroblasts, a cell type that consumes most of the ser
47 erythropoiesis by modulating interactions of erythroblast alpha4beta1 with both macrophages and extra
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
54 somal architectures of fetal and adult human erythroblasts and found that, globally, chromatin struct
55 hibition of RBM38 compromises translation in erythroblasts and impairs their maturation, highlighting
56 ed the expression of Rps19 or Rpl11 in mouse erythroblasts and investigated mRNA polyribosome associa
60 m and progenitor cells, as well as nucleated erythroblasts and megakaryocytes, reside preferentially
63 d proportion of bone marrow (BM) early stage erythroblasts and reduced enucleated erythrocytes compar
65 c erythroblasts from thalassemic mice and in erythroblasts and sera from subjects with beta-thalassem
66 f each specific developmental stage of human erythroblasts and should provide a powerful means of ide
67 introns that exhibit increased IR in mature erythroblasts, and are enriched in functions related to
68 indicates increased apoptosis of Tmod3(-/-) erythroblasts, and cell-cycle analysis reveals that ther
69 hat FPN1 localizes to the plasma membrane of erythroblasts, and hepcidin treatment leads to decreased
70 to enucleation defects in mouse fetal liver erythroblasts, and in CD34(+) hematopoietic stem and pro
71 by miR-451, is up-regulated in miR-451(-/-) erythroblasts, and inhibition of 14-3-3zeta rescues thei
72 nce, nonmammalian red blood cells, mammalian erythroblasts, and platelets have a peripheral ring of m
73 dy reveals novel cross-talk between HSCs and erythroblasts, and sheds a new light on the regulatory m
74 essed SLC25A37 and SF3B1 transcripts in late erythroblasts, and thereby limiting functional mRNA leve
75 ng many genes with undiscovered functions in erythroblasts are a resource for future functional studi
76 of human erythropoiesis in which late-stage erythroblasts are derived directly from human CD34(+) he
77 l line, we observed that the first primitive erythroblasts are detected in vitro around day 1.5 of bl
78 criptomic signature and increased numbers of erythroblasts are recorded in patient peripheral blood,
83 ane deformability and stability of primitive erythroblasts, assayed by microfluidic studies and fluor
84 that STEAP3, a metalloreductase expressed in erythroblasts, associates with TfR1 and partially rescue
85 ession at day 8 and a 16% expansion of early erythroblasts at day 10 compared to cultures without NmU
88 3 and alpha4 integrin enabled us to isolate erythroblasts at specific developmental stages from prim
90 vestigated Tmod1 function in mouse and human erythroblasts both in vivo and in vitro and found that a
91 ysis, depletes almost all marrow and splenic erythroblasts but leaves peripheral erythrocytes intact.
92 ATA-1 protein expression is decreased in MDS erythroblasts, but restores in the presence of a pan-cas
93 rected the abnormal ratio of immature/mature erythroblasts by inducing apoptosis of immature erythrob
94 es of the ERV-9 LTRs and in transgenic mouse erythroblasts carrying a single copy of the primate-spec
95 -specific deletion of ERV-9 lncRNAs in human erythroblasts carrying approximately 4000 copies of the
97 attached to them, accumulate in thalassemic erythroblasts causing oxidative stress and the premature
98 ate that selective depletion of PABPC4 in an erythroblast cell line inhibits terminal erythroid matur
99 ese problems genome-wide in a Gata1 knockout erythroblast cell line that undergoes GATA1-dependent te
101 ythroblastic island formation, and defective erythroblast cell-cycle progression and enucleation.
103 rmore, when compared with autologous control erythroblasts, clonally derived JAK2V617F-positive eryth
104 ocytes, as well as micronucleus formation in erythroblasts, compared with heterozygous and wild-type
106 on of mRNAs expressed at increased levels in erythroblasts contributes to the erythroid phenotype of
109 n was used to knockdown LIN28B expression in erythroblasts cultured from human umbilical cord CD34+ c
110 hilic, 4 polychromatic, and 8 orthochromatic erythroblasts, currently there is no method to quantitat
111 in enucleation, was also found essential for erythroblast cytokinesis as its deficiency in mice cause
112 ranscriptome profiling of E2F-2-null, mature erythroblasts demonstrated widespread changes in gene ex
113 ed significant amounts of HbF (up to 20%) in erythroblasts derived from adult CD34(+) cells without a
114 luated the effects of DZNep in human primary erythroblasts derived from cord blood CD34-positive cell
115 nserved in maturing primitive and definitive erythroblasts despite their respective intravascular and
117 ly, all stages of Hb Null-derived definitive erythroblasts develop normally in vivo in chimeric mice,
119 poietin receptor-HM allele, major defects in erythroblast development occurred selectively at stage E
121 nt with TRbeta agonists stimulated premature erythroblast differentiation in vivo and alleviated anem
122 found that Stat5 protein levels decline with erythroblast differentiation, governing the transition f
123 o revealed a critical activating function in erythroblast differentiation, in addition to its known i
126 Unlike the Stat5 protein, EpoR expression in erythroblasts does not limit the Stat5 signaling respons
129 m (unable to bind STAT-5) on erythropoiesis, erythroblast (EB) expansion cultures of mononuclear cell
130 d cell cycle regulatory pathways, whereas in erythroblasts EKLF is associated with repression of thes
132 These macrophages make physical contact with erythroblasts, enabling signaling and the transfer of gr
134 s, FLKO mice show significant enhancement of erythroblast enucleation during definitive erythropoiesi
137 , Konstantinidis et al provide evidence that erythroblast enucleation is a more complex and multistep
138 of structural and signaling requirements of erythroblast enucleation with the cytokinesis process ha
140 te common cytoskeletal mechanisms underlying erythroblast enucleation, notwithstanding the morphologi
141 skeleton and membrane signaling molecules in erythroblast enucleation, we developed a novel analysis
150 ry cultured megakaryocytes (MEG) and primary erythroblasts (ERY) from murine fetal liver hematopoieti
152 was established in extensively self-renewing erythroblasts (ESREs), a well-characterized, nontransfor
157 he human beta-globin locus, like human fetal erythroblasts, express predominately human gamma-, low b
159 assessed by quantitative proteomics, mutant erythroblasts expressed higher levels of proteins involv
161 ession of Lamin isoforms, with primary mouse erythroblasts expressing only Lamin B and primary human
162 rm switching and protein 4.1R-null primitive erythroblasts fail to establish normal membrane stabilit
163 ipolar microtubule spindle in orthochromatic erythroblasts, followed by Rac-directed formation of a c
164 oblasts:basophilic:polychromatic:orthromatic erythroblasts follows the expected 1:2:4:8 ratio, reflec
168 ages on the proliferation and enucleation of erythroblasts from healthy individuals and patients with
169 lysis of clonally derived JAK2V617F-positive erythroblasts from MPN patients also demonstrated impair
170 oblasts, clonally derived JAK2V617F-positive erythroblasts from MPN patients displayed increased ROS
171 immunofluorescence analysis of intermediate erythroblasts from patients with CDA-1 reveals abnormal
172 intra-S checkpoint response was impaired in erythroblasts from polycythemia vera (PV) patients, but
174 an ActRIIA ligand, was increased in splenic erythroblasts from thalassemic mice and in erythroblasts
176 ernative approach, immortalizing early adult erythroblasts generating a stable line, which provides a
177 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-
182 ns in mitosis and cytokinesis, as induced in erythroblasts in an E2F-2-dependent manner, and we found
185 (ERFE) is a glycoprotein hormone secreted by erythroblasts in response to stimulation by erythropoiet
186 ) macrophages markedly reduced the number of erythroblasts in the bone marrow but did not result in o
188 ied DNA methylation in differentiating mouse erythroblasts in vivo by using genomic-scale reduced rep
189 s defective terminal maturation of nucleated erythroblasts in vivo Here, we found that these defects
190 ous hepcidin decreased FPN1 expression in BM erythroblasts in vivo, whereas iron depletion and associ
191 e polychromatophilic and orthochromatophilic erythroblasts, in concert with extensive cellular remode
192 b1 to the beta-globin promoter in GATA1 null erythroblasts, in which the beta-globin locus is relaxed
193 id cell lines and primary CD71(+) Lyn(up/up) erythroblasts, including significant alterations to the
195 gamma-globin promoter in primary adult human erythroblasts increases gamma-globin promoter-LCR contac
196 or (PlGF), released at high levels by sickle erythroblasts, induced PAI-1 expression in primary human
199 s, using exogenous Stat5, we converted later erythroblasts into high-intensity graded signal transduc
201 ized by abnormal chromatin ultrastructure in erythroblasts, is caused by abnormalities in codanin-1,
204 ediated actin remodeling may be required for erythroblast-macrophage adhesion, coordination of cell c
205 tream of cytokine signaling, and in terminal erythroblast maturation and enucleation, as master regul
208 ify 1109 polyadenylated lncRNAs expressed in erythroblasts, megakaryocytes, and megakaryocyte-erythro
210 a8--whose expression was increased in mutant erythroblasts, monocytes and macrophages--is functionall
211 ng at the cell surface constriction in mouse erythroblasts, nor at the membrane protein-sorting bound
213 uring enucleation, whereas human bone marrow erythroblast nuclei unexpectedly retain their spherical
215 uction of moderate iron deficiency increases erythroblasts number, reduces apoptosis, and enhances er
217 dy of gene expression alterations in primary erythroblasts obtained from cyclin E(T74A T393A) knock-i
221 tment exhibited reduced Ter119/CD71 positive erythroblasts, peripheral blood RBCs and hemoglobin leve
222 licing program in terminally differentiating erythroblasts plays a major role in regulating gene expr
223 flow-imaging analysis, colchicine inhibited erythroblast polarization, implicating microtubules duri
224 cause of 4.1R deficiency, the ratio of these erythroblast populations remains the same as that of wil
226 deficient spleen and bone marrow, BFU-Es and erythroblast populations were increased compared with WT
228 transporters, primitive, but not definitive, erythroblasts preferentially accumulate reactive oxygen
229 e migrated into the cytoplasm of normal late erythroblasts prior to and during enucleation, but not i
232 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
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
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
245 sized that placenta growth factor (PlGF), an erythroblast-secreted factor that is elevated in SCD, me
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
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
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
263 e reviewed in four functional contexts: (pro)erythroblast survival mechanisms, new candidate EPO/EPOR
265 EPO affects significantly more than standard erythroblast survival pathways, the development of novel
266 CFU-Es and actively proliferating definitive erythroblasts that clustered around central macrophages,
267 D31, CD34, C-kit, CXCR4, Runx1, and VEGFR2), erythroblasts that expressed embryonic hemoglobin (Hb-ep
269 roleukemia, with an accumulation of immature erythroblasts that infiltrated the bone marrow, spleen,
271 em (ES) cells and ES-derived fibroblasts and erythroblasts the folding of 10-160-megabase pair engine
273 th beta-thalassemia, by expanding late-stage erythroblasts through a mechanism distinct from erythrop
276 regulates HbF levels and causes adult human erythroblasts to differentiate with a more fetal-like ph
277 rom high-intensity graded signaling in early erythroblasts to low-intensity binary signaling in later
279 hare similar copy number, mutational status, erythroblast transformation specific (ETS) rearrangement
280 1 ALL-related ETV6 variants clustered in the erythroblast transformation specific domain and were pre
281 200c expression by physically binding to the erythroblast transformation-specific (ETS) motif within
282 protease, serine 2, gene (TMPRSS2) with the erythroblast transformation-specific (ETS)-related gene
283 on differences in the frequency of oncogenic erythroblast transformation-specific family of transcrip
284 protease, serine 2, gene (TMPRSS2) with the erythroblast transformation-specific-related gene (ERG),
286 lenced embryonic globin gene in adult murine erythroblasts triggers its transcriptional reactivation.
288 d into induced endothelial cells and induced erythroblasts using lineage-specific growth factors.
289 t, by ultrastructural examination of primary erythroblasts, we observed an accumulation of vacuoles i
290 on, maturation, and enucleation of primitive erythroblasts were also impaired by Vegfc deletion.
292 ellular pools decreased in the polychromatic erythroblast, whereas surface expression increased and w
293 e membrane protein-sorting boundary in human erythroblasts, which do not have a constriction, arguing
294 tant restores terminal maturation of beta-TM erythroblasts, which may provide a rationale for new tar
295 sition of the membrane skeleton in primitive erythroblasts, which progressively mature while circulat
296 endogenous alpha globin locus in developing erythroblasts will provide important mechanistic insight
297 uent enucleation were not affected in murine erythroblasts with genetic deletion of Rac1 and Rac2 GTP
298 To test this hypothesis, we treated primary erythroblasts with inhibitors of cytokinesis, including
299 EPOR-Spi2A serpin-cathepsin axis in maturing erythroblasts, with lysosomal cathepsins as novel therap
300 cle trafficking block enucleation of primary erythroblasts without affecting differentiation, cell di
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