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1 is a context-dependent GATA-1 corepressor in erythroid cells.
2 the production of terminally differentiated erythroid cells.
3 d genes expression in K562 and primary human erythroid cells.
4 or1 and the transcription repressor Gfi1b in erythroid cells.
5 re low, GPI expression is near normal in IGD erythroid cells.
6 sence enhances hemoglobinization in cultured erythroid cells.
7 enic endothelial cells capable of generating erythroid cells.
8 e fine regulation of hemoglobin synthesis in erythroid cells.
9 s and heme synthesis in vivo and in cultured erythroid cells.
10 roteins are abundantly expressed in maturing erythroid cells.
11 expression in terminally differentiating BM erythroid cells.
12 ma-globin expression and fetal hemoglobin in erythroid cells.
13 the GATA-1/Foxo3-dependent transcriptome in erythroid cells.
14 ng, enhances HbF production in primary human erythroid cells.
15 rs and heme biosynthetic enzymes in immature erythroid cells.
16 ible for increased protein turnover in human erythroid cells.
17 34(+) progenitor-derived human primary adult erythroid cells.
18 1, NF-E2, KLF1, and SCL, using primary human erythroid cells.
19 naling pathway increase HbF in primary human erythroid cells.
20 central macrophage surrounded by developing erythroid cells.
21 HbF post-transcriptionally in human primary erythroid cells.
22 aintain HbF silencing in primary human adult erythroid cells.
23 y increase fetal hemoglobin in primary human erythroid cells.
24 or in various solid tumours, is expressed in erythroid cells.
25 iron uptake by the intestine and developing erythroid cells.
26 tart site (TSS) of genes highly expressed in erythroid cells.
27 el PU.1 binding site by quantitative ChIP in erythroid cells.
28 on, leading to increased cation transport in erythroid cells.
29 globin promoter complexes in fetal and adult erythroid cells.
30 y increase fetal hemoglobin in primary human erythroid cells.
31 n erythrocytes and to a lesser extent in non-erythroid cells.
32 cell line and primary human fetal and adult erythroid cells.
33 idation state controls NOS signalling in non-erythroid cells.
34 nt for the maturation of primary fetal liver erythroid cells.
35 and optimal activity of the EKLF protein in erythroid cells.
36 al erythroid cells but is repressed in adult erythroid cells.
37 and resulting in decreased apoptosis of DBA erythroid cells.
38 proteolysis to degrade free alpha-globin in erythroid cells.
39 f this lncRNA can inhibit apoptosis in mouse erythroid cells.
40 ultipotent hematopoietic progenitor cells to erythroid cells.
41 inct functions during the differentiation of erythroid cells.
42 or mitochondrial iron delivery in developing erythroid cells.
43 n and fetal gamma-globin genes in definitive erythroid cells.
44 tokine-dependent mast cells, thymocytes, and erythroid cells.
45 opmental transcriptional silencing in normal erythroid cells.
46 nformation of the beta-globin locus in human erythroid cells.
47 omoter, directing expression specifically to erythroid cells.
48 within this region in the chromatin of adult erythroid cells.
49 ssion programs during the differentiation of erythroid cells.
50 ression in adults prevents the maturation of erythroid cells.
51 and molecular identity of maturing primitive erythroid cells.
52 d impairing transferrin-bound iron uptake by erythroid cells.
53 vated cell sorting for SB-Tn-transduced K562 erythroid cells.
54 D117(hi)) cells inhibited the development of erythroid cells.
55 e a role in the generation of SPH and S1P in erythroid cells.
56 s complex in human CD34+ cell-derived normal erythroid cells.
57 atients with DBA and differentiate them into erythroid cells.
58 the potential of MPPS to differentiate into erythroid cells.
59 bin gene expressed specifically in primitive erythroid cells.
60 do not express NR4A1 primarily develop into erythroid cells.
61 the silenced PU.1 promoter in differentiated erythroid cells.
62 and impair the growth and differentiation of erythroid cells.
63 A1, TAL1, LMO2, LDB1 and Pol II at least, in erythroid cells.
64 shown to facilitate direct iron transfer in erythroid cells.
65 f relevant cell surface markers in Eklf(-/-) erythroid cells.
66 of the strongest putative super-enhancers in erythroid cells.
67 d associates with erythropoietin receptor in erythroid cells.
68 ation of ULK1 and inhibition of autophagy in erythroid cells.
69 poietic activity by sequestering lefty1 from erythroid cells.
71 enhancers regulates gene expression in human erythroid cells, a highly specialized cell type evolved
73 bryos exhibit a profound loss of myeloid and erythroid cells along with cardiovascular abnormalities
75 Our results uncover in chorea-acanthocytosis erythroid cells an association between accumulation of a
76 entiation, and there was also a depletion of erythroid cells and a defect in erythroid progenitor fun
77 ibits nuclease hypersensitivity in primitive erythroid cells and acts as an enhancer in gain-of-funct
78 in vivo associated with prominent defects in erythroid cells and an expansion of megakaryocyte progen
79 ed one such complex, MBD2-NuRD, from primary erythroid cells and have shown it contributes to embryon
81 containing biotin-tagged TR2/TR4 from adult erythroid cells and identified DNMT1, NuRD, and LSD1/CoR
82 he minor PABP isoform PABPC4 is expressed in erythroid cells and impacts the steady-state expression
83 tly, we demonstrate that Hfe is expressed in erythroid cells and impairs iron uptake, whereas its abs
84 ssed mainly in hepatocytes and in developing erythroid cells and is an important focal point in syste
86 Finally, by comparing GATA1 occupancy in erythroid cells and megakaryocytes, we find that the pre
91 e that HPIP is a target of GATA1 and CTCF in erythroid cells and plays an important role in erythroid
92 and stability of JAK2-associated EpoR in UT7 erythroid cells and primary CD71+ erythroid progenitors.
93 a signaling component in the development of erythroid cells and rationalize the use of sotatercept i
94 least in part, by activation of p38 MAPK in erythroid cells and rescued by inhibition of TNF-alpha o
95 nd deacetylation (NuRD) complex from primary erythroid cells and showed that MBD2 contributes to DNA
96 We have demonstrated that HO-1 is present in erythroid cells and that its expression is upregulated d
97 e-5'-monophosphate dehydrogenase activity in erythroid cells and that this is a likely mechanism of a
98 ngs explain intact PIGM transcription in IGD erythroid cells and the lack of clinically significant i
99 pression pattern characteristic of primitive erythroid cells, and (4) promoted the generation of a TP
100 mast cells, eosinophils, megakaryocytes and erythroid cells, and a pathway lacking expression of tha
101 induce a differentiation defect in wild-type erythroid cells, and genetic inactivation of S100a8 expr
102 kably selective transcriptional activator in erythroid cells, and its perturbation might offer new op
103 Pu.1 itself directly regulate Pu.1 levels in erythroid cells, and loss of both factors is critical fo
105 for beta-like globin expression in primitive erythroid cells, and that it defines a novel class of en
106 We found that cyclin E protein levels in BM erythroid cells are dynamically regulated in a CPD-depen
107 ation of iron, showing that arhgef3-depleted erythroid cells are fully capable of hemoglobinization.
109 he HLH proteins expressed in differentiating erythroid cells are the ubiquitous proteins Myc, USF1, U
111 cyclin E expression, p53 is activated in BM erythroid cells as part of a DNA damage response-type pa
112 s occurs endogenously in primary neurons and erythroid cells as well as neuroblastoma cells overexpre
115 tive, fetal definitive, and adult definitive erythroid cells at morphologically equivalent stages of
119 , a dramatic and persistent loss of immature erythroid cells, B and T lymphocytes, and neutrophils wa
120 te enhancer that drives globin expression in erythroid cells, before the divergence of jawless and ja
121 equired for repression of HbF in adult-stage erythroid cells but are dispensable in non-erythroid cel
122 etal gamma-globin gene is expressed in fetal erythroid cells but is repressed in adult erythroid cell
123 f PlGF is abolished in EKLF-deficient murine erythroid cells but rescued by conditional expression of
125 control region (LCR) and gene in adult mouse erythroid cells, but whether this complex mediates chrom
127 hondrial protein that is highly expressed in erythroid cells, can homodimerize and assemble [2Fe-2S]
128 ctively abolishes the expression of ACKR1 in erythroid cells, causing a Duffy-negative phenotype.
131 erythroid differentiation, and used a human erythroid cell culture system to explore this concept.
133 ed beta-globin gene activity and location in erythroid cells derived from mice with deletions of indi
134 erythroid-related factor 2 (Nrf2)/kelch-like erythroid cell-derived protein 1 (Keap1) pathway is dysr
135 ]-related factor 2 [Nrf2])-Keap1 (Kelch-like erythroid cell-derived protein with CNC homology [ECH]-a
136 ndogenous inhibitor protein, Kelch-like ECH (erythroid cell-derived protein with CNC homology)-associ
138 d cells will allow a better understanding of erythroid cell development, differentiation, structure,
139 To explore the effects of LIN28B in human erythroid cell development, lentiviral transduction was
141 In human hematopoiesis, megakaryocytes and erythroid cells differentiate from a shared precursor, t
142 lete correction of globin chain imbalance in erythroid cells differentiated from the corrected iPS ce
144 ological manipulations of iron metabolism or erythroid cell differentiation and survival have been sh
145 oietin response to anemia, and inhibition of erythroid cell differentiation by inflammatory mediators
146 ted B-cell development but repressed myeloid-erythroid cell differentiation in KA/KA BM B cells.
152 n essential role of TH during terminal human erythroid cell differentiation; specific depletion of TH
153 entadactyl DNA-binding protein that in human erythroid cells directly activates only a single gene, t
156 consequences of cyclin E dysregulation in BM erythroid cells during terminal maturation in vivo.
158 odel system enables the role played by Hb in erythroid cell enucleation, cytoskeleton maturation, and
161 a new EPO/EPOR target and regulator of human erythroid cell expansion that additionally acts to suppo
162 uman pluripotent stem cells allowed enhanced erythroid cell expansion with preserved differentiation.
163 om patients are confounded by poor levels of erythroid cell expansion, aberrant or incomplete erythro
165 ence of avascular blood islands of primitive erythroid cells expressing hemangioblast markers (Flk1,
167 r results demonstrate that the hematopoietic/erythroid cell fate is suppressed via Nkx2-5 during meso
171 mutations in the transcription factor GATA1 Erythroid cells from patients with DBA have not been wel
172 pomalidomide induces HbF in differentiating erythroid cells from people with sickle cell disease and
174 ncrease the production of mature, enucleated erythroid cells from umbilical cord blood derived CD34(+
177 al continuum dictates the absolute number of erythroid cells generated from each transit-amplifying p
178 s mediating establishment/maintenance of the erythroid cell genetic network, and provides a biologica
180 null/wild-type mice revealed that suppressed erythroid cell growth by N-RasE12 was restored only by p
181 We have previously identified 2 in vitro erythroid cell growth phenotypes for primary CD34(+) cel
184 iting autophagy on mitochondrial function in erythroid cells harboring mtDNA mutations in vivo, we de
185 e high-level expression of GATA1 in maturing erythroid cells have been studied extensively, the initi
186 ve in reducing the globin chain imbalance in erythroid cells hence improving the clinical outcome of
188 hat FOG1 is SUMOylated and phosphorylated in erythroid cells in a differentiation-dependent manner.
189 e show that physiologically enriched CD71(+) erythroid cells in neonatal mice and human cord blood ha
190 Tfr2(BMKO) mice, the proportion of nucleated erythroid cells in the bone marrow is higher and the apo
195 largely mediate enhancer-promoter looping in erythroid cells independent of mediator and cohesin.
197 tor (PlGF), an angiogenic factor produced by erythroid cells, induces hypoxia-independent expression
198 globin protein in terminally differentiating erythroid cells is critically dependent on the high stab
199 eporter specifically in developing embryonic erythroid cells is enhanced by addition of the gata1 3'U
201 , shRNAmiR-mediated suppression of BCL11A in erythroid cells led to stable long-term engraftment of g
204 R/Cas9 gene editing in an immortalised human erythroid cell line (BEL-A2) abolishes MAM expression.
205 non-F cells (A cells) from the human HUDEP2 erythroid cell line and primary human erythroid cultures
206 In this study we generate an immortalised erythroid cell line from peripheral blood stem cells of
207 n this process, we have exploited the K1-ERp erythroid cell line, in which KLF1 translocates rapidly
211 Treatment with deferiprone of UROS-deficient erythroid cell lines and peripheral blood CD34+-derived
212 in Epo signaling were observed in Lyn(+/up) erythroid cell lines and primary CD71(+) Lyn(up/up) eryt
213 ells, suggesting that large-scale culture of erythroid cell lines and their differentiation to reticu
215 found that, in undifferentiated murine adult erythroid cells, many of these corepressors associate wi
216 results establish SetD8 as a determinant of erythroid cell maturation and provide a framework for un
217 pendent cyclin E regulation impairs terminal erythroid cell maturation at a discrete stage before enu
223 f X-chromosome inactivation (Lyonisation) in erythroid cells, may have low G6PD activity in the major
226 FAM38A transcripts were identified in human erythroid cell mRNA, and discovery proteomics identified
227 nes are autonomously silenced in adult-stage erythroid cells, mutations lying both within and outside
230 d that RNF41 expression decreased in primary erythroid cells of lenalidomide-responding patients, sug
231 e oxidase inhibitor tranylcypromine in human erythroid cells or beta-type globin-transgenic mice enha
232 thylase 1 (LSD1) inhibition by RNAi in human erythroid cells or by the monoamine oxidase inhibitor tr
233 did not disrupt the generation of primitive erythroid cells or erythro-myeloid progenitors (EMPs) in
234 studies on heme regulation have been done in erythroid cells or hepatocytes; however, much less is kn
235 forced expression of TR2/TR4 in murine adult erythroid cells paradoxically enhanced fetal gamma-globi
238 and adhesion based functions in myeloid and erythroid cells predominantly under conditions of stress
239 ropoiesis, increasing the absolute number of erythroid cells produced from normal CD34(+) cells and f
240 pecific knockdown of Hipk2 inhibits terminal erythroid cell proliferation (explained in part by impai
241 EPO mutant is less effective at stimulating erythroid cell proliferation and differentiation, even a
243 at PML4, a specific PML isoform expressed in erythroid cells, promotes endogenous erythroid genes exp
247 served loss of both lymphocytes and immature erythroid cells/reticulocytes from the BM and peripheral
248 , in confirmatory studies using human marrow erythroid cells, ribosomal protein transcripts and prote
249 llowing Setd8 knockdown demonstrated that in erythroid cells, Setd8 functions primarily as a represso
250 the myeloid lineage regulator C/EBPalpha in erythroid cells shifts binding of SMAD1 to sites newly o
251 When tested in differentiating primary human erythroid cells, simvastatin induced HbF alone and addit
252 ciated with lower promoter accessibility, in erythroid cells, Sp1 activates PIGM transcription by bin
253 demonstrate that the Scl +40 enhancer is an erythroid cell-specific enhancer that regulates the expr
259 expressed at significantly higher levels in erythroid cells than any other cell or tissue type, sugg
261 matin interaction changes in differentiating erythroid cells that are thought to be important for pro
262 in methylcellulose culture large colonies of erythroid cells that consist of "bursts" of smaller eryt
263 e complex controls the massive production of erythroid cells that ensures organismal survival in home
264 gene repression in definitive (adult)-stage erythroid cells (the TR2/TR4 heterodimer, MYB, KLFs, BCL
265 ta2 repression in terminally differentiating erythroid cells, the -2.8 kb site was not required to in
266 ironically, has been poorly investigated in erythroid cells, the largest pool of heme-containing cel
271 e molecular mechanism of URE inactivation in erythroid cells through loss of TF binding represents a
273 and GATA-2 present in low abundance in adult erythroid cells to assemble an LTR/RNA polymerase II com
274 tor, it also exerts specialized functions in erythroid cells to control GATA-1-independent, cell-type
275 y differentiating murine fetal liver-derived erythroid cells to identify regulators of heme metabolis
276 oprecipitation (ChIP) we show that, in adult erythroid cells, TR2/TR4 bind to the embryonic beta-type
282 rmally in vivo in chimeric mice, and Hb Null erythroid cells undergo enucleation to form reticulocyte
284 mma-globin expression in primary human adult erythroid cells was achieved by combining EHMT1/2 inhibi
285 oporphyrin IX synthesis in TMEM14C-deficient erythroid cells was blocked, leading to an accumulation
287 genetic complementation assay in GATA-1-null erythroid cells, we demonstrate that Med1 and another Me
289 ing obese EpoR mice with EPO-R restricted to erythroid cells, we demonstrated an anti-inflammatory ro
290 n edited CD34+ cells are differentiated into erythroid cells, we observe the expected reduction in al
293 asize the importance of evaluating Ter119(-) erythroid cells when studying erythroid marrow failure i
294 oduction of megakaryocytic cells relative to erythroid cells, whereas inhibition of miR-145 or overex
295 in is, however, expressed on mouse primitive erythroid cells, which supply oxygen to the embryo durin
296 ssive accumulation of lymphoid, myeloid, and erythroid cells, which was not due to enhanced hematopoi
298 f terminally differentiated bone marrow (BM) erythroid cells with components of their structural and
299 show that depletion of DOCK4 levels leads to erythroid cells with dysplastic morphology both in vivo
300 ineage-specific BCL11A shRNAmiR gave rise to erythroid cells with up to 90% reduction of BCL11A prote