ライフサイエンスコーパス: erythroid cell

1 roteins are abundantly expressed in maturing erythroid cells.

2 expression in terminally differentiating BM erythroid cells.

3 the GATA-1/Foxo3-dependent transcriptome in erythroid cells.

4 ng, enhances HbF production in primary human erythroid cells.

5 rs and heme biosynthetic enzymes in immature erythroid cells.

6 ible for increased protein turnover in human erythroid cells.

7 34(+) progenitor-derived human primary adult erythroid cells.

8 1, NF-E2, KLF1, and SCL, using primary human erythroid cells.

9 naling pathway increase HbF in primary human erythroid cells.

10 central macrophage surrounded by developing erythroid cells.

11 HbF post-transcriptionally in human primary erythroid cells.

12 aintain HbF silencing in primary human adult erythroid cells.

13 y increase fetal hemoglobin in primary human erythroid cells.

14 iron uptake by the intestine and developing erythroid cells.

15 tart site (TSS) of genes highly expressed in erythroid cells.

16 el PU.1 binding site by quantitative ChIP in erythroid cells.

17 do not express NR4A1 primarily develop into erythroid cells.

18 on, leading to increased cation transport in erythroid cells.

19 globin promoter complexes in fetal and adult erythroid cells.

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

21 y increase fetal hemoglobin in primary human erythroid cells.

22 n erythrocytes and to a lesser extent in non-erythroid cells.

23 cell line and primary human fetal and adult erythroid cells.

24 idation state controls NOS signalling in non-erythroid cells.

25 nt for the maturation of primary fetal liver erythroid cells.

26 and optimal activity of the EKLF protein in erythroid cells.

27 al erythroid cells but is repressed in adult erythroid cells.

28 proteolysis to degrade free alpha-globin in erythroid cells.

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

30 f this lncRNA can inhibit apoptosis in mouse erythroid cells.

31 ultipotent hematopoietic progenitor cells to erythroid cells.

32 inct functions during the differentiation of erythroid cells.

33 or mitochondrial iron delivery in developing erythroid cells.

34 n and fetal gamma-globin genes in definitive erythroid cells.

35 tokine-dependent mast cells, thymocytes, and erythroid cells.

36 opmental transcriptional silencing in normal erythroid cells.

37 nformation of the beta-globin locus in human erythroid cells.

38 omoter, directing expression specifically to erythroid cells.

39 within this region in the chromatin of adult erythroid cells.

40 ssion programs during the differentiation of erythroid cells.

41 and molecular identity of maturing primitive erythroid cells.

42 d impairing transferrin-bound iron uptake by erythroid cells.

43 vated cell sorting for SB-Tn-transduced K562 erythroid cells.

44 D117(hi)) cells inhibited the development of erythroid cells.

45 e a role in the generation of SPH and S1P in erythroid cells.

46 s complex in human CD34+ cell-derived normal erythroid cells.

47 2 regulate distinct target-gene ensembles in erythroid cells.

48 globin predominantly restricted to primitive erythroid cells.

49 lly increased proportions of Ter119-positive erythroid cells.

50 etal hemoglobin transcripts in primary human erythroid cells.

51 the ankyrin gene promoter that is active in erythroid cells.

52 r ability to generate lymphoid, myeloid, and erythroid cells.

53 d promoter is a barrier insulator in vivo in erythroid cells.

54 gamma-globin expression in mouse definitive erythroid cells.

55 nce showing that USF interacts with NF-E2 in erythroid cells.

56 shown to facilitate direct iron transfer in erythroid cells.

57 4 mouse, improving the number and quality of erythroid cells.

58 elements in the EKLF and Tal-1 gene loci in erythroid cells.

59 be involved in controlling proliferation of erythroid cells.

60 e GATA-1 and GATA-2 occupancy genome-wide in erythroid cells.

61 d by Scl in megakaryocytic cells, but not in erythroid cells.

62 e therapeutic levels of genetically modified erythroid cells.

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

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

65 d associates with erythropoietin receptor in erythroid cells.

66 atients with DBA and differentiate them into erythroid cells.

67 ation of ULK1 and inhibition of autophagy in erythroid cells.

68 poietic activity by sequestering lefty1 from erythroid cells.

69 is a context-dependent GATA-1 corepressor in erythroid cells.

70 the production of terminally differentiated erythroid cells.

71 the potential of MPPS to differentiate into erythroid cells.

72 d genes expression in K562 and primary human erythroid cells.

73 or1 and the transcription repressor Gfi1b in erythroid cells.

74 re low, GPI expression is near normal in IGD erythroid cells.

75 sence enhances hemoglobinization in cultured erythroid cells.

76 bin gene expressed specifically in primitive erythroid cells.

77 e fine regulation of hemoglobin synthesis in erythroid cells.

78 s and heme synthesis in vivo and in cultured erythroid cells.

79 enhancers regulates gene expression in human erythroid cells, a highly specialized cell type evolved

80 In mature erythroid cells, a strong upsurge in Rcor3 and a sharp d

81 bryos exhibit a profound loss of myeloid and erythroid cells along with cardiovascular abnormalities

82 In Escherichia coli and erythroid cells, alpha globin K99E stability is rescued

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

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

85 entiation, and there was also a depletion of erythroid cells and a defect in erythroid progenitor fun

86 ibits nuclease hypersensitivity in primitive erythroid cells and acts as an enhancer in gain-of-funct

87 in vivo associated with prominent defects in erythroid cells and an expansion of megakaryocyte progen

88 this study, we performed GATA-1 ChIP-seq in erythroid cells and compared it to GATA-1-induced gene e

89 s mechanism, overexpression of 14-3-3zeta in erythroid cells and fibroblasts inhibits nuclear localiz

90 ed one such complex, MBD2-NuRD, from primary erythroid cells and have shown it contributes to embryon

91 In human erythroid cells and hematopoietic organs, LIN28B and its

92 containing biotin-tagged TR2/TR4 from adult erythroid cells and identified DNMT1, NuRD, and LSD1/CoR

93 he minor PABP isoform PABPC4 is expressed in erythroid cells and impacts the steady-state expression

94 tly, we demonstrate that Hfe is expressed in erythroid cells and impairs iron uptake, whereas its abs

95 Gene expression analysis in primary mutant erythroid cells and megakaryocytes (MKs) revealed an ess

96 Erythroid cells and megakaryocytes are derived from a co

97 Finally, by comparing GATA1 occupancy in erythroid cells and megakaryocytes, we find that the pre

98 put and in the subsequent differentiation of erythroid cells and megakaryocytes.

99 Normal FOG1 function in late-stage erythroid cells and MK requires interaction with the chr

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

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

102 e that HPIP is a target of GATA1 and CTCF in erythroid cells and plays an important role in erythroid

103 and stability of JAK2-associated EpoR in UT7 erythroid cells and primary CD71+ erythroid progenitors.

104 a signaling component in the development of erythroid cells and rationalize the use of sotatercept i

105 a-globin gene is expressed at high levels in erythroid cells and regulated by proximal and distal cis

106 least in part, by activation of p38 MAPK in erythroid cells and rescued by inhibition of TNF-alpha o

107 nd deacetylation (NuRD) complex from primary erythroid cells and showed that MBD2 contributes to DNA

108 We have demonstrated that HO-1 is present in erythroid cells and that its expression is upregulated d

109 e-5'-monophosphate dehydrogenase activity in erythroid cells and that this is a likely mechanism of a

110 ngs explain intact PIGM transcription in IGD erythroid cells and the lack of clinically significant i

111 pression pattern characteristic of primitive erythroid cells, and (4) promoted the generation of a TP

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

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

114 for beta-like globin expression in primitive erythroid cells, and that it defines a novel class of en

115 We found that cyclin E protein levels in BM erythroid cells are dynamically regulated in a CPD-depen

116 ation of iron, showing that arhgef3-depleted erythroid cells are fully capable of hemoglobinization.

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

118 myeloid cells are remarkably proliferating, erythroid cells are rather decreased and anemia is commo

119 he HLH proteins expressed in differentiating erythroid cells are the ubiquitous proteins Myc, USF1, U

120 Using differentiation of primary erythroid cells as a model, we show that the sequence-sp

121 cyclin E expression, p53 is activated in BM erythroid cells as part of a DNA damage response-type pa

122 s occurs endogenously in primary neurons and erythroid cells as well as neuroblastoma cells overexpre

123 selection occurred in myeloid, lymphoid, and erythroid cells as well as platelets.

124 However, the presence of immature erythroid cells associated with impaired maturation of t

125 tive, fetal definitive, and adult definitive erythroid cells at morphologically equivalent stages of

126 HESCs and erythroid cells at three developmental stages: ESER (emb

127 onstrated that anemia was associated with an erythroid cell- autonomous defect.

128 ic globin gene regulation is at least partly erythroid cell-autonomous.

129 , a dramatic and persistent loss of immature erythroid cells, B and T lymphocytes, and neutrophils wa

130 etal gamma-globin gene is expressed in fetal erythroid cells but is repressed in adult erythroid cell

131 f PlGF is abolished in EKLF-deficient murine erythroid cells but rescued by conditional expression of

132 control region (LCR) and gene in adult mouse erythroid cells, but whether this complex mediates chrom

133 he interacting partner proteins of BCL11A in erythroid cells by a proteomic screen.

134 hondrial protein that is highly expressed in erythroid cells, can homodimerize and assemble [2Fe-2S]

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

136 egulators, of the formation of developing BM erythroid cell cohorts.

137 erythroid differentiation, and used a human erythroid cell culture system to explore this concept.

138 ed beta-globin gene activity and location in erythroid cells derived from mice with deletions of indi

139 ]-related factor 2 [Nrf2])-Keap1 (Kelch-like erythroid cell-derived protein with CNC homology [ECH]-a

140 ndogenous inhibitor protein, Kelch-like ECH (erythroid cell-derived protein with CNC homology)-associ

141 genes, which include candidate regulators of erythroid cell development and function.

142 echanisms, new candidate EPO/EPOR effects on erythroid cell development and new EPOR responses, EPOR

143 d cells will allow a better understanding of erythroid cell development, differentiation, structure,

144 To explore the effects of LIN28B in human erythroid cell development, lentiviral transduction was

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

146 lete correction of globin chain imbalance in erythroid cells differentiated from the corrected iPS ce

147 ted B-cell development but repressed myeloid-erythroid cell differentiation in KA/KA BM B cells.

148 New studies also suggest that limited erythroid cell differentiation plays a role in the devel

149 RNA-Seq data we collected for ex vivo human erythroid cell differentiation.

150 genitor cell expansion and megakaryocyte and erythroid cell differentiation.

151 ant of Hsp70 protects GATA-1 and rescues MDS erythroid cell differentiation.

152 adult betamajor-globin gene promoter during erythroid cell differentiation.

153 and PDZK1IP1) that are potential drivers of erythroid cell differentiation.

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

155 omplex set of events that occur at the final erythroid cell divisions and accentuates terminal differ

156 In the absence of Myc, circulating erythroid cells do not show the normal increase in alpha

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

158 consequences of cyclin E dysregulation in BM erythroid cells during terminal maturation in vivo.

159 Erythroid cell dysplasia observed in early myelodysplast

160 odel system enables the role played by Hb in erythroid cell enucleation, cytoskeleton maturation, and

161 Differentiating erythroid cells execute a unique gene expression program

162 Mfrn1(+/gt);Irp1(-/-) erythroid cells exhibit a significant increase in protop

163 ORF factor designated as regulator of human erythroid cell expansion (RHEX).

164 a new EPO/EPOR target and regulator of human erythroid cell expansion that additionally acts to suppo

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

166 Erythroid cells express only one integrin, alpha4beta1,

167 In murine and human erythroid cells, expression of erythroid Kruppel-like fa

168 r results demonstrate that the hematopoietic/erythroid cell fate is suppressed via Nkx2-5 during meso

169 In erythroid cells, ferrous iron is imported into the mitoc

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

171 Definitive erythroid cells from mutant mice arrest at the transitio

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

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

174 Analysis of RNA and protein in primary erythroid cells from these individuals provided evidence

175 ers were also enriched near genes with known erythroid cell function or phenotype.

176 In contrast to erythroid cells, GATA-2 occupied a unique target gene en

177 Therefore, erythroid cells generated ex vivo may be suitable for tr

178 s mediating establishment/maintenance of the erythroid cell genetic network, and provides a biologica

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

180 null/wild-type mice revealed that suppressed erythroid cell growth by N-RasE12 was restored only by p

181 The mature erythroid cells had an increased beta-globin to gamma-gl

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

183 iting autophagy on mitochondrial function in erythroid cells harboring mtDNA mutations in vivo, we de

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

185 Overexpression of HO-1 in erythroid cells impairs hemoglobin synthesis, whereas HO

186 hat FOG1 is SUMOylated and phosphorylated in erythroid cells in a differentiation-dependent manner.

187 e show that physiologically enriched CD71(+) erythroid cells in neonatal mice and human cord blood ha

188 ors may limit the overproduction of immature erythroid cells in thalassemia, with the potential of re

189 Tfr2(BMKO) mice, the proportion of nucleated erythroid cells in the bone marrow is higher and the apo

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

191 ogenitors, which did not give rise to mature erythroid cells in vitro or in vivo.

192 al hemoglobin (HbF) levels in cultured human erythroid cells in vitro.

193 genes and human gamma-globin genes in adult erythroid cells in vivo.

194 ed translational repression were observed in erythroid cells in which GLRX5 expression had been downr

195 acenta growth factor (PlGF), elaborated from erythroid cells, increased the mRNA expression of 5-lipo

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

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

198 tor (PlGF), an angiogenic factor produced by erythroid cells, induces hypoxia-independent expression

199 globin protein in terminally differentiating erythroid cells is critically dependent on the high stab

200 eporter specifically in developing embryonic erythroid cells is enhanced by addition of the gata1 3'U

201 Differentiation of erythroid cells is regulated by cell signaling pathways

202 that is required for growth and expansion of erythroid cells, is one target of miR-126.

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

204 Specifically, inactivation of Rb in erythroid cells led to stressed DNA replication, increas

205 In erythroid cells, lim domain binding 1 (LDB1) protein is

206 n this process, we have exploited the K1-ERp erythroid cell line, in which KLF1 translocates rapidly

207 Using a GATA1-dependent committed erythroid cell line, select MC genes were found to be oc

208 ing the method to GATA1 restoration in mouse erythroid cell line, we detected many new GATA1-binding

209 Using a promoter-reporter assay in an erythroid cell line, we show that Ppm1b superactivates E

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

211 in Epo signaling were observed in Lyn(+/up) erythroid cell lines and primary CD71(+) Lyn(up/up) eryt

212 Using human erythroid cell lines and primary cells and transgenic mi

213 ells, suggesting that large-scale culture of erythroid cell lines and their differentiation to reticu

214 ciated with elevated fetal gamma-globin into erythroid cell lines.

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

218 ression but, interestingly, have accelerated erythroid cell maturation between E9.5 and E11.5.

219 Normal human erythroid cell maturation requests the transcription fac

220 At this stage of erythroid cell maturation, CPD phosphorylation of cyclin

221 in primary erythroid precursor cells induced erythroid cell maturation.

222 of ARHGEF3 in regulation of iron uptake and erythroid cell maturation.

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

224 In non-erythroid cells, Mfrn2 is an iron transporter in the mit

225 phenotype and ability to differentiate into erythroid cells, monocytes, and endothelial cells.

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

228 ferentiated granulocytic, megakaryocytic, or erythroid cells obtained from all patients.

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

230 e oxidase inhibitor tranylcypromine in human erythroid cells or beta-type globin-transgenic mice enha

231 thylase 1 (LSD1) inhibition by RNAi in human erythroid cells or by the monoamine oxidase inhibitor tr

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

233 studies on heme regulation have been done in erythroid cells or hepatocytes; however, much less is kn

234 forced expression of TR2/TR4 in murine adult erythroid cells paradoxically enhanced fetal gamma-globi

235 and adhesion based functions in myeloid and erythroid cells predominantly under conditions of stress

236 ropoiesis, increasing the absolute number of erythroid cells produced from normal CD34(+) cells and f

237 pecific knockdown of Hipk2 inhibits terminal erythroid cell proliferation (explained in part by impai

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

239 Amassing of PPIX in erythroid cells promotes erythropoietic protoporphyria (

240 at PML4, a specific PML isoform expressed in erythroid cells, promotes endogenous erythroid genes exp

241 Several B- and myeloid-erythroid-cell regulators, including Pax5, were deregula

242 Comparison of ES and erythroid cells replication patterns revealed that these

243 2 and GATA-1 in hematopoietic precursors and erythroid cells, respectively.

244 served loss of both lymphocytes and immature erythroid cells/reticulocytes from the BM and peripheral

245 llowing Setd8 knockdown demonstrated that in erythroid cells, Setd8 functions primarily as a represso

246 the myeloid lineage regulator C/EBPalpha in erythroid cells shifts binding of SMAD1 to sites newly o

247 When tested in differentiating primary human erythroid cells, simvastatin induced HbF alone and addit

248 ciated with lower promoter accessibility, in erythroid cells, Sp1 activates PIGM transcription by bin

249 demonstrate that the Scl +40 enhancer is an erythroid cell-specific enhancer that regulates the expr

250 A-USF reduces the expression of several key erythroid cell-specific transcription factors, including

251 or tissue type, suggesting that Setd8 has an erythroid-cell-specific function.

252 ation from the earliest into the most mature erythroid cell stages.

253 duced during human erythropoiesis, conferred erythroid cell survival.

254 n of the gamma- to-beta-globin switch, adult erythroid cells synthesize low levels of HbF.

255 stimulation of MLL1 catalytic activity, and erythroid cell terminal differentiation.

256 expressed at significantly higher levels in erythroid cells than any other cell or tissue type, sugg

257 rming unit-erythroid (CFU-E) progenitors and erythroid cells that are generated.

258 matin interaction changes in differentiating erythroid cells that are thought to be important for pro

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

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

261 gene repression in definitive (adult)-stage erythroid cells (the TR2/TR4 heterodimer, MYB, KLFs, BCL

262 ta2 repression in terminally differentiating erythroid cells, the -2.8 kb site was not required to in

263 ironically, has been poorly investigated in erythroid cells, the largest pool of heme-containing cel

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

265 In TAL1-expressing erythroid cells, the locus adopts a looping "hub" which

266 In erythroid cells, the locus control region (LCR) and beta

267 In erythroid cells, the locus control region (LCR) contacts

268 3 being a regulator of transferrin uptake in erythroid cells, through activation of RHOA.

269 and GATA-2 present in low abundance in adult erythroid cells to assemble an LTR/RNA polymerase II com

270 tor, it also exerts specialized functions in erythroid cells to control GATA-1-independent, cell-type

271 y differentiating murine fetal liver-derived erythroid cells to identify regulators of heme metabolis

272 oprecipitation (ChIP) we show that, in adult erythroid cells, TR2/TR4 bind to the embryonic beta-type

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

274 These data demonstrate that late-stage erythroid cells, transduced with a tissue-specific LV, c

275 IHK-beta-globin mRNA was found in non-erythroid cell types, similar to native beta-globin mRNA

276 In primary human adult erythroid cells, UNC0638 and EHMT1 or EHMT2 short hairpi

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

278 Differentiating erythroid cells undergo dramatic changes in morphology,

279 rmally in vivo in chimeric mice, and Hb Null erythroid cells undergo enucleation to form reticulocyte

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

281 mma-globin expression in primary human adult erythroid cells was achieved by combining EHMT1/2 inhibi

282 oporphyrin IX synthesis in TMEM14C-deficient erythroid cells was blocked, leading to an accumulation

283 erythropoiesis, expression profiling of E9.5 erythroid cells was performed.

284 genetic complementation assay in GATA-1-null erythroid cells, we demonstrate that Med1 and another Me

285 By examining human and mouse primary erythroid cells, we demonstrate that the CCND3 gene prod

286 ing obese EpoR mice with EPO-R restricted to erythroid cells, we demonstrated an anti-inflammatory ro

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

288 previously to be differentially expressed in erythroid cells were annotated.

289 Results from erythroid cells were compared with those in neural and m

290 Extravascular zeta-globin(+) primitive erythroid cells were found in placental villi between 5-

291 asize the importance of evaluating Ter119(-) erythroid cells when studying erythroid marrow failure i

292 n activating transcription factor complex in erythroid cells where it also makes physical contact wit

293 ylated domain over these genes in definitive erythroid cells, where they are otherwise inactive.

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

297 Identification of enhancers in human erythroid cells will allow a better understanding of ery

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