ライフサイエンスコーパス: reticulocyte

1 show for infecting immature red blood cells (reticulocytes).

2 the proerythroblast stage to the enucleated reticulocyte.

3 scicularis) normocytes with a preference for reticulocytes.

4 pathway to orthochromatic erythroblasts and reticulocytes.

5 human cells that generates normal enucleated reticulocytes.

6 P. vivax and P. ovale, which develop inside reticulocytes.

7 ding to infectious mature gametocytes within reticulocytes.

8 that normally spans 24 hours for uninfected reticulocytes.

9 blood mononuclear cells and were shown to be reticulocytes.

10 e-stage nucleated erythroblasts to anucleate reticulocytes.

11 ed labeling of in vitro-differentiated human reticulocytes.

12 roblasts differentiate to produce enucleated reticulocytes.

13 egulate the co-ordinated daily production of reticulocytes.

14 erythroid cells undergo enucleation to form reticulocytes.

15 s red blood cell (RBC) volume, especially in reticulocytes.

16 mouse and human cells, with higher levels in reticulocytes.

17 owest in the orthochromatic erythroblast and reticulocytes.

18 mediate erythroblasts and reduced release of reticulocytes.

19 not essential for mitochondrial clearance in reticulocytes.

20 teins distribute between extruded nuclei and reticulocytes.

21 natal life, with transient production of HbF reticulocytes.

22 ndogenous lectin, has been pinpointed in rat reticulocytes.

23 are involved in mitochondrial clearance from reticulocytes.

24 r than a cause of autophagosome formation in reticulocytes.

25 n, did not impact invasive susceptibility of reticulocytes.

26 aged erythrocytes, P. vivax is restricted to reticulocytes.

27 ythropoiesis elevated hemoglobin using fewer reticulocytes.

28 concentration, number of RBCs and number of reticulocytes.

29 could explain the preference of P vivax for reticulocytes.

30 al hemoglobin, with decreased leukocytes and reticulocytes.

31 es malaria in humans and exclusively infects reticulocytes.

32 ion remains why P. vivax selectively invades reticulocytes?

33 1 fL and otherwise normal blood cell counts; reticulocytes, 0.98%; stable creatinine, 1.1 mg/dL; calc

34 oximately 74000 small molecules in search of reticulocyte 15-hLO-1 selective inhibitors.

35 actions of three human LOs (platelet 12-hLO, reticulocyte 15-hLO-1, and epithelial 15-hLO-2) with ara

36 ralogs, platelet-type 12-human lipoxygenase, reticulocyte 15-human lipoxygenase type-1, and epithelia

37 Human reticulocyte 15-lipoxygenase (15-hLO-1) and epithelial 1

38 Human reticulocyte 15-lipoxygenase-1 (15-hLO-1) and human plat

39 Human reticulocyte 15-lipoxygenase-1 (15-hLO-1), which catalyz

40 ge of dense RBCs (-2.41 vs -0.08, P < .001); reticulocytes (-4.12 vs -0.46, P < .001); lactate dehydr

41 sis of the catalytic action of RTA on rabbit reticulocyte 80S ribosomes establishes a catalytic effic

42 Plasmodium vivax merozoites only invade reticulocytes, a minor though heterogeneous population o

43 o exosomes may be the mechanism by which the reticulocyte adapts to environmental changes during its

44 We have shown previously that young sickle reticulocytes adhere to resting endothelial cells throug

45 well-described rapid decrease in circulating reticulocytes after birth suggests that they may have a

46 actile actomyosin ring (CAR) between nascent reticulocyte and nucleus, in a population of enucleating

47 ring and coalescence of lipid rafts between reticulocyte and pyrenocyte, steps which reiterate the c

48 ring, and coalescence of lipid rafts between reticulocyte and pyrenocyte.

49 During 5-fluorouracil-induced anemia, both reticulocyte and red cell formation in DYRK3-/- mice wer

50 x invasion, a narrow preference for immature reticulocytes and a rapid remodeling of the host cell, p

51 t increase the frequencies of micronucleated reticulocytes and erythrocytes in the bone marrow and bl

52 fferentiation, we conducted RNA-seq in human reticulocytes and identified nuclear receptor coactivato

53 s not revealed any differences between these reticulocytes and in vitro-cultured adult reticulocytes

54 These mutants only complete development in reticulocytes and mature into both schizonts and gametoc

55 allel increases in circulating CD71-positive reticulocytes and other markers of young RBCs.

56 asonal pattern of counts of red blood cells, reticulocytes and platelets.

57 rther evidenced by the presence of primitive reticulocytes and pyrenocytes (ejected RBC nuclei) in th

58 ls and mature erythrocytes, as well as fewer reticulocytes and sickle cells, in the peripheral blood

59 for the altered membrane function of normal reticulocytes and sickle red cells.

60 lly lost during in vitro maturation of mouse reticulocytes and that it is associated with exosomes, r

61 s in our understanding of these processes in reticulocytes and the role of these processes in erythro

62 associated with reduced NRF2 levels in HbSS reticulocytes and with decreased glutathione regeneratio

63 od revealed a modest neutrophilia, a loss of reticulocytes, and a massive lymphopenia.

64 mitogen-activated T and B cells, circulating reticulocytes, and all cell lines that we have studied.

65 ist of MIR122 increased blood levels of EPO, reticulocytes, and hemoglobin.

66 on between the extruding nucleus and nascent reticulocyte are critical steps in erythroblast enucleat

67 The autophagic vesicles found on reticulocytes are identical to those observed on red cel

68 ts low abundance cell types such as immature reticulocytes as well as high abundance cell types such

69 on width) and quantify similar parameters of reticulocytes as well.

70 he membrane-skeletal junctions are weaker in reticulocytes, as is the attachment of transmembrane pro

71 acteria, human cells and plasmodium-infected reticulocytes, as well as a viral RNA genome.

72 s of the erythrocyte binding antigens (EBA), reticulocyte binding homologues (RH), surface associated

73 locyte-binding domains efficaciously blocked reticulocyte binding of native PvRBPs, suggesting that t

74 The reticulocyte binding protein 2-P1 (RBP2-P1) of Plasmodiu

75 BP2-P1) of Plasmodium vivax, a member of the reticulocyte binding protein family, has recently been s

76 We recently showed that P. falciparum reticulocyte binding protein homolog 5 (PfRH5), a merozo

77 human primates against Plasmodium falciparum reticulocyte binding protein homolog 5 (PfRH5).

78 P. falciparum reticulocyte binding protein homologues (PfRhs) are expr

79 Previously we identified that P. falciparum reticulocyte binding protein-like homologue 4 (PfRh4) bi

80 muno-precipitation experiments with P. vivax Reticulocyte Binding Proteins showed no evidence of comp

81 parasite interactions, with an enrichment in reticulocyte binding proteins, merozoite surface protein

82 yte binding antigen family and P. falciparum reticulocyte binding-like families.

83 al component of a ternary complex, including Reticulocyte binding-like Homologous protein 5 (PfRH5) a

84 icate process in which Plasmodium falciparum reticulocyte binding-like homologous protein 5 (PfRH5) i

85 by the erythrocyte binding antigen (eba) and reticulocyte binding-like homologue (Rh) gene families.

86 Members of the P. falciparum reticulocyte binding-like protein homolog (PfRh) family

87 y, naturally acquired antibodies against the reticulocyte-binding domains efficaciously blocked retic

88 Reticulocyte-binding domains of PvRBP2c/PvRBP1a are targ

89 cyte-binding specificity, and their specific reticulocyte-binding domains were mapped within their N-

90 nvasion can be mediated by the P. falciparum reticulocyte-binding homologue protein 4 (PfRh4) on the

91 -based analysis was performed of the PvRBP reticulocyte-binding properties and binding-inhibitory a

92 y, the Duffy-binding protein (PvDBP) and the reticulocyte-binding protein (PvRBP) families.

93 human malaria parasite Plasmodium falciparum reticulocyte-binding protein homolog 5 (PfRH5) as a targ

94 The Plasmodium falciparum reticulocyte-binding protein homolog 5 (PfRH5) has recen

95 For instance, Plasmodium falciparum reticulocyte-binding protein homolog 5 (PfRH5) is essent

96 The Plasmodium falciparum reticulocyte-binding protein homolog 5 (PfRH5) is the le

97 ood cells involves malaria proteins, such as reticulocyte-binding protein homolog 5 (RH5), RH5 intera

98 the contribution of the recently discovered Reticulocyte-binding protein Homolog 5 (RH5)-Basigin (BS

99 cies, are two parasite protein families, the reticulocyte-binding protein homologue (RH) and erythroc

100 Plasmodium falciparum reticulocyte-binding protein homologue 2b (PfRh2b) is an

101 Plasmodium falciparum reticulocyte-binding protein homologue 5 (PfRH5) is a bl

102 We show that the full-length P. falciparum reticulocyte-binding protein homologue 5 (PfRH5) is high

103 s, we resurrected the ancestral introgressed reticulocyte-binding protein homologue 5 (RH5) sequence

104 Members of the reticulocyte-binding protein-like (RBL) family of invasi

105 ticulocytes that is mediated by the P. vivax reticulocyte-binding proteins (PvRBPs) specifically PvRB

106 PvRBP2c and PvRBP1a displayed a distinct reticulocyte-binding specificity, and their specific ret

107 ifted our understanding of the P. falciparum reticulocyte-binding-like family to the level of individ

108 wn to invade and develop in erythrocytes and reticulocytes, but little is known about their infection

109 Surprisingly, it was the immature reticulocytes (CD71(+)) that are generally restricted to

110 t were preferentially invaded, whereas older reticulocytes (CD71(-)), principally found in the periph

111 Our results show that the immature reticulocytes (CD71+) targeted by P. vivax invasion are

112 ulate PRF to levels as high as 58% in rabbit reticulocyte cell-free translations and 81% during virus

113 modium vivax parasites preferentially invade reticulocyte cells in a multistep process that is still

114 Red cell and reticulocyte cellular indices are widely used in the dia

115 Successful invasion of reticulocytes complemented with a truncated mutant exclu

116 the initially biomechanically rigid CD71(+) reticulocytes convert into a highly deformable CD71(-) i

117 resents a newly described mechanism by which reticulocytes could adapt to environmental modifications

118 n of DBP with a small population of immature reticulocytes could explain the preference of P vivax fo

119 Reversion, predicted by baseline reticulocyte count >/=400 x 10(9)/L (P< .001), occurred

120 Abnormal reticulocyte count (P<0.001, c-statistic 0.623) and hemo

121 al red cell indices, in particular increased reticulocyte count and decreased hemoglobin concentratio

122 nd-Stage Liver Disease (MELD) to incorporate reticulocyte count and hemoglobin concentration (MELD-re

123 Mean absolute reticulocyte count peaked at day 11 or 15 in each group

124 Abnormal reticulocyte count was also found to predict mortality i

125 versus normal RBC, but the correlation with reticulocyte count was poor, with inter-individual varia

126 ilar in both msk(-/-) and msk(+/+) mice, but reticulocyte count was significantly increased in msk(-/

127 Serum erythropoietin concentration, absolute reticulocyte count, and adverse events.

128 Host ABO blood group, reticulocyte count, and parasitemia were not correlated

129 nin/piperaquine and determined the Hb level, reticulocyte count, G6PD genotype, and Hb type.

130 lobin is lowest in patients with the highest reticulocyte counts and concomitantly shortened RBC life

131 hrocyte and hemoglobin levels with increased reticulocyte counts and elevated plasma erythropoietin c

132 e antioxidant, tempol, resulted in decreased reticulocyte counts and improved erythrocyte survival.

133 y lower erythrocyte and significantly higher reticulocyte counts compared to patients with low biliru

134 Reticulocyte counts decreased from days 1 to 3, peaking

135 Peak reticulocyte counts increased from a median of 10x10(9)

136 nia, lympocytosis, hyperglycemia, and higher reticulocyte counts, along with the activation of pro-in

137 m a significant decrease in serum bilirubin, reticulocyte counts, and serum erythropoietin following

138 al hemoglobin and higher white blood cell or reticulocyte counts, reinforcing the need for early diag

139 blood cells and hemoglobin and a decrease in reticulocyte counts.

140 arge amounts of undigested Hb remains in the reticulocyte cytoplasm and in vesicles in the parasite.

141 Furthermore, iron uptake studies in hem6 reticulocytes demonstrate defective incorporation of iro

142 These data establish the use of reticulocytes derived from immortalized erythroblasts as

143 Here we report that reticulocytes derived through in vitro differentiation o

144 Here, using a rabbit-reticulocyte-derived in vitro translation system, we fou

145 ticular, ribosome elimination, a hallmark of reticulocyte differentiation, was defective in Ube2o(-/-

146 n, which normally partition predominantly to reticulocytes, distribute to both nuclei and reticulocyt

147 ata1-DYRK3 mice, in contrast, produced fewer reticulocytes during hemolytic anemia, and pA2gata1-DYRK

148 CD71/RNA double staining of reticulocytes enriched from adult peripheral blood revea

149 In addition, reticulocyte-enriched chorea-acanthocytosis red cell fra

150 in vitro, in humans, they are restricted to reticulocytes expressing both transferrin receptor 1 (Tr

151 phosphatidylserine-exposing erythrocytes are reticulocytes expressing high levels of CD47, a "do-not-

152 ce of increased levels of circulating mature reticulocytes expressing inside-out PS-exposed autophagi

153 sucrose gradients, following synthesis in a reticulocyte extract or as purified proteins.

154 mitochondria and ribosomes, which occurs in reticulocytes following nuclear extrusion, depends on au

155 ith elevations of plasma EPO and circulating reticulocytes following single oral dose administration,

156 Invasion assays based on the CD71(+) reticulocyte fraction revealed substantial postinvasion

157 We measured micronuclei frequency in reticulocytes from peripheral blood and bone marrow and

158 quantities of functional mature human adult reticulocytes from peripheral blood CD34(+) cells.

159 oth lymphocytes and immature erythroid cells/reticulocytes from the BM and peripheral blood.

160 ron incorporation into heme was unaltered in reticulocytes from UCP2-deficient mice.

161 se reticulocytes and in vitro-cultured adult reticulocytes functionally or at the molecular level, an

162 proving the preferential infection of young reticulocytes (generally restricted to the bone marrow),

163 RECENT FINDINGS: Functional human reticulocytes have been generated from adult peripheral

164 Functional adult reticulocytes have been made in culture and shown to sur

165 on >11 g/dL, mean corpuscular volume >70 fL, reticulocyte hemoglobin equivalent >25 pg, serum ferriti

166 rrin saturation, transferrin receptor level, reticulocyte hemoglobin level, and mean cell volume) and

167 We found a higher percentage of reticulocytes in adult Klf1(wt/ko) mice and a mild compe

168 reticulocytes, distribute to both nuclei and reticulocytes in an ankyrin-1-deficient murine model of

169 e elimination, remain polarized in Atg7(-/-) reticulocytes in culture.

170 es (BIAbs) also inhibit P. vivax invasion of reticulocytes in vitro.

171 ound that mAbs inhibited P. vivax entry into reticulocytes in vitro.

172 of hepcidin, non-transferrin-bound iron, and reticulocyte indexes is being explored in research setti

173 me also is detected in HeLa cells and rabbit reticulocytes, indicating that it exists in vivo.

174 f spleen cells are immature CD71(-)Ter119(+) reticulocytes, indicating that massive erythropoiesis oc

175 Reticulocyte infection is facilitated by P vivax Duffy b

176 evelopment of a protocol that allows sorting reticulocytes into defined developmental stages and a ro

177 The transition of reticulocytes into erythrocytes is accompanied by extens

178 ts in the release of 2 million new enucleate reticulocytes into your circulation and mine each second

179 aps in our understanding of Plasmodium vivax reticulocyte invasion and protective immunity have hampe

180 lly modified to express PvDBP and to prevent reticulocyte invasion by multiple clinical isolates of P

181 DBPII-DARC interaction and inhibit P. vivax reticulocyte invasion, and Ab levels correlate with prot

182 targeting PvDBP, the key ligand involved in reticulocyte invasion.

183 Plasmodium vivax invasion into human reticulocytes is a complex process.

184 Thus, a constant supply of reticulocytes is considered critical for continuous P. v

185 bsence of Atg7, mitochondrial clearance from reticulocytes is diminished but not completely blocked.

186 In human reticulocytes, KCC3a mRNA levels were consistently the h

187 There was a short-term increase in reticulocyte levels at the start of treatment, which dro

188 haematocrit, red blood cell (RBC) counts and reticulocyte levels in high-risk patients with T2DM rece

189 ted human malaria parasite, is restricted to reticulocytes, limiting its asexual proliferation.

190 AQP-1 in young reticulocytes localizes to the plasma membrane and also

191 d prey proteins (probes) in cell-free rabbit reticulocyte lysate (RRL) systems.

192 expressed in a mammalian cell lysate, rabbit reticulocyte lysate (RRL), was able to assemble into cap

193 ent in mock and Ric-8A-immunodepleted rabbit reticulocyte lysate (RRL).

194 ver, it did not affect translation in rabbit reticulocyte lysate (RRL).

195 e dimer is dependent upon factors present in reticulocyte lysate and other cytosols.

196 o assay combining a ribosome-depleted rabbit reticulocyte lysate and ribosomes prepared from HeLa or

197 order Q70E/Q162E>Q162E> Q70E=WT betaB2 using reticulocyte lysate as the source of degradation machine

198 , by the endogenous ubiquitinating system in reticulocyte lysate fraction II, and by intact HEK293 ce

199 thase by the native ubiquitinating system of reticulocyte lysate is dependent upon both Hsp70 and the

200 The apo-nNOS activating activity of reticulocyte lysate is retained in a pool of fractions c

201 Furthermore, translation activity in rabbit reticulocyte lysate is strongly inhibited by RNAs exceed

202 pitation of proteins in vitro expressed in a reticulocyte lysate system showed an interaction between

203 lenocysteines can be reconstituted in rabbit reticulocyte lysate translation reactions.

204 tion substrates in fraction II of the rabbit reticulocyte lysate with an efficiency parallel to their

205 70, RPS3, and NF45) were expressed in rabbit reticulocyte lysate, bacteria, and MCF-7 cells.

206 ssa in vitro translation system or in rabbit reticulocyte lysate.

207 e potent inhibitors of translation in rabbit reticulocyte lysate.

208 h the RNA subunit hTR in two systems (rabbit reticulocyte lysates and human cell lines) with respect

209 of translational repression, we used rabbit reticulocyte lysates as an in vitro translation system t

210 vitro degradation of a target mRNA in rabbit reticulocyte lysates containing in vitro-translated Vhs.

211 accumulation of heavy polymeric ribosomes in reticulocyte lysates in vitro.

212 0-2 AGG interruptions, both in vitro (rabbit reticulocyte lysates) and in cell culture (HEK-293 cells

213 bition of eRF1 enhanced PRF in yeast, rabbit reticulocyte lysates, and mammalian cells.

214 fused to glutathione S-transferase in rabbit reticulocyte lysates, suggesting a role for the pU(L)34/

215 degrees C than 30 degrees C, when tested in reticulocyte lysates.

216 d from budding yeast, wheat germ, and rabbit reticulocyte lysates.

217 lation of this mRNA both in cells and rabbit reticulocyte lysates.

218 ranscription, translation and prenylation in reticulocyte lysates.

219 porter gene and assayed their translation in reticulocyte lysates.

220 Although genetic ablation of Rip3 normalizes reticulocyte maturation and prevents anemia, ROS accumul

221 Secretion of exosomes during reticulocyte maturation is an integral part of the red c

222 o the loss of all the internal compartments, reticulocyte maturation is characterized by an extensive

223 Early reticulocyte maturation is characterized by the selectiv

224 We show that the final stage of reticulocyte maturation occurs by a previously undescrib

225 restingly, the total DARC protein throughout reticulocyte maturation was constant.

226 erminal erythroid differentiation and during reticulocyte maturation was discerned.

227 onstrating that VPS4A is critical for normal reticulocyte maturation.

228 kle erythrocytes to a physiological event in reticulocyte maturation.

229 nistic basis of crucial changes accompanying reticulocyte maturation.

230 and their interactions change during murine reticulocyte maturation.

231 n the constitutive expression of DARC during reticulocyte maturation.

232 owever, studies of the process whereby human reticulocytes mature to erythrocytes have been hampered

233 Haematocrit, RBC and reticulocyte measurements were conducted during this stu

234 During maturation to an erythrocyte, a reticulocyte must eliminate any residual organelles and

235 e found that although glycophorin C sorts to reticulocytes normally, it distributes to nuclei in 4.1R

236 ice leads to severe anemia despite increased reticulocyte numbers.

237 After this uptake, P. vivax-infected reticulocytes obtained from patients show specific adhes

238 atures of P. vivax, particularly invasion of reticulocytes, occurrence of dormant liver forms of the

239 What do reticulocytes offer to P. vivax that is not present in m

240 ment rate and preference of the parasite for reticulocytes on four key outcome measures assessing ane

241 erse reactions, bind, or deplete circulating reticulocytes or reduce BBB-expressed endogenous TfR1 in

242 nd of the merozoite, and preferentially bind reticulocytes over normocytes.

243 Reticulocyte parameters such as Hb content (CHr or ret-H

244 was significantly higher compared with other reticulocyte populations and erythrocytes.

245 om adult peripheral blood reveals 4 distinct reticulocyte populations: CD71(high)/RNA(high) ( approxi

246 nce of strains able to invade Duffy-negative reticulocytes poses a major public health threat.

247 In this article, we analyze the reticulocyte preference of a large number of Indian P. v

248 zonts in circulation correlating with a high reticulocyte preference.

249 solates significantly vary in their level of reticulocyte preference.

250 ature erythrocytes (normocytes), rather than reticulocytes, preferentially form rosetting complexes,

251 globin levels (r = 0.241; P = 0.022) and the reticulocyte production index (RPI) (r = 0.280; P = 0.02

252 ed by further stimulating erythropoiesis and reticulocyte production.

253 umption of haptoglobin (haemolysis) and poor reticulocyte production.

254 g a cell-free translation system from rabbit reticulocytes programmed with mRNAs containing different

255 led to absence of lipid raft assembly in the reticulocyte-pyrenocyte border.

256 by increased hematocrit from 23% to 34% and reticulocyte reduction from 61% to 18%, indicating a sig

257 Plasmodium vivax invasion of reticulocytes relies on distinct receptor-ligand interac

258 vax for transferrin receptor (CD71)-positive reticulocytes remained unexplained, given the constituti

259 Reticulocyte remodeling has emerged as an important mode

260 We assess the effect of varying the reticulocyte replacement rate and preference of the para

261 reased parasitemia in mice infected with the reticulocyte-restricted parasite Plasmodium berghei NK65

262 We demonstrate that PvDBP plays no role in reticulocyte restriction but can alter the macaque/human

263 This screen revealed that reticulocytes show high levels of phosphorylated ribosom

264 obin increased by 1.2-1.9 g/dL (P = 0.01) as reticulocytes simultaneously decreased; that is, better

265 ace a large arc in red blood cells (RBCs) by reticulocyte space as compared to surviving mice.

266 ll hemoglobin occupy a small area of RBCs by reticulocyte space, suggesting this approach can be used

267 Erythroid and reticulocyte-specific signatures were markedly decreased

268 protein-10/CXCL10 negatively correlated with reticulocyte-specific signatures.

269 Several members of the PvRBP family bind reticulocytes, specifically suggesting a role in mediati

270 n also be expanded and differentiated to the reticulocyte stage.

271 proteome undergoes a rapid transition at the reticulocyte stage; however, the mechanisms driving prog

272 sophilic, polychromatic, orthochromatic, and reticulocyte stages to mature erythrocytes.

273 m underlying the preferential infection of a reticulocyte subset by P vivax.

274 e indirect bilirubin level and percentage of reticulocytes than the placebo group.

275 ic alterations in P cynomolgi-infected human reticulocytes that are strikingly similar to those obser

276 rentiate efficiently into mature, functional reticulocytes that can be isolated by filtration.

277 ard expression of the WT allele in mRNA from reticulocytes that could be recapitulated in primary ery

278 P. vivax exclusively invades reticulocytes that is mediated by the P. vivax reticuloc

279 Thus, in reticulocytes, the induction of ubiquitinating factors m

280 In reticulocytes, this includes enucleation and the elimina

281 nd dramatic decrease from proerythroblast to reticulocyte; this enabled us to devise a new strategy f

282 at malaria parasite, a strict preference for reticulocytes thwarts efforts to maintain it in vitro.

283 5'-monoribonucleotides during maturation of reticulocytes to erythrocytes.

284 Adhesion of sickle reticulocytes to HC-treated endothelial cells was decrea

285 Saporin-L1 inhibition of rabbit reticulocyte translation was protected by these inhibito

286 Recombinant 4E-BP1 inhibits capped mRNA reticulocyte translation, which is partially reversed by

287 During maturation of murine reticulocytes, tubulin and cytosolic actin were lost, wh

288 First, we observed that P. vivax invasion of reticulocytes was consistently reduced when CR1 surface

289 and recombinant DBP to CD71(high)/RNA(high) reticulocytes was significantly higher compared with oth

290 For a given level of parasite preference for reticulocytes we uncover an optimal erythropoietic respo

291 rd with this, erythroid progenitor cells and reticulocytes were substantially reduced in number in mi

292 In reticulocytes, where UBE2O is highly up-regulated, unass

293 Plasmodium vivax preferentially invades reticulocytes, which are immature red blood cells.

294 er switching leads to a surge of E-Tmod41 in reticulocytes, which degrades quickly in the cytosol.

295 the preferential binding of DBP to immature reticulocytes, which is the potential mechanism underlyi

296 from the elevated phosphorylation of 4.1R in reticulocytes, which leads to a decrease in shear resist

297 but poorly understood biologic process, and reticulocytes, which undergo programmed mitochondrial cl

298 roid cell lines and their differentiation to reticulocytes will be possible.

299 Survival in reticulocytes with reduced or absent Hb digestion may im

300 markedly increased proliferation and higher reticulocyte yields, suggesting an important regulatory