ライフサイエンスコーパス: EPO

1 EPO and erythroferrone reduced liver Smad1/5 phosphoryla

2 EPO enhanced verbal recall (P=0.02) and recognition (P=0

3 EPO induction was submaximal, as hypoxia or pharmacologi

4 EPO is a glycoprotein hormone that is essential for norm

5 EPO may provide a therapeutic option for patients with m

6 EPO treatment also reduced weight gain in ovariectomized

7 EPO treatment reduced diet-induced weight gain from 9.6

8 EPO treatment reduced expansion of human naive CD4(+) T

9 EPO-associated memory improvement in TRD and BD may be m

10 Plasma (n = 204) and CSF (n = 147) EPO levels at admission were measured by radioimmunoassa

11 IL-4, TSLP, IL-17A, EPO activity, total cell count and specific IgE and IgG1

12 Here we targeted the PHD/HIF-2/EPO axis in FOXD1 stroma-derived renal interstitial cell

13 tudy to evaluate the impact of epoetin alfa (EPO) on tumor outcomes when used to treat anemia in pati

14 Epoetin alfa (EPO) robustly induced bone marrow erythroferrone (Fam132

15 ated T cells expressed CD131, an alternative EPO receptor, addition of a specific CD131 agonist pepti

16 Although EPO treatment increased hematocrit and improved glucose

17 issue-protective EPO receptor, comprising an EPO receptor subunit (EPOR) and the common beta-chain (C

18 hat the probability that a male will sire an EPO in an available brood is the primary source of genet

19 ire EPO, the male's probability of siring an EPO in an available brood and the number of offspring in

20 Serum and renal IGF-1 and EPO were significantly increased in UPI/OIR compared to

21 ating EPC and levels of VEGF, HIF-1alpha and EPO were significantly higher after exercise (P < 0.05).

22 Cotreatment with ACE-536 and EPO produced a synergistic erythropoietic response.

23 on and thus regulation of HIF-2 activity and EPO production under hypoxia or conditions of pharmacolo

24 We found that both cibinetide and EPO ameliorated the clinical course of experimental coli

25 l studies implicate erythropoietin (EPO) and EPO receptor (EPOR) signaling in angiogenesis.

26 t modulators of EPO and EPOR expression, and EPO's biological effects.

27 ationship between blood levels of MIR122 and EPO in mice with acute pancreatitis or steatohepatitis,

28 weight control and glucose sensitivity, and EPO receptor gene expression was reduced in wild-type fe

29 acetate switch controls HIF-2 signaling and EPO induction during pathophysiological states marked by

30 hematocrit levels and BP as substantially as EPO.

31 To investigate the relationship between EPO/ERFE and matriptase-2, we show that EPO injection in

32 xpression of dominant-negative Egr-1 blocked EPO promoter activation by Ang II.

33 uction of EPO levels in the host or blocking EPO-EPOR signaling may be an effective strategy to impro

34 converting enzyme inhibitors regulated blood EPO levels.

35 Local expression of both EPO and its receptor is upregulated upon injury or stres

36 latory effects on eosinophils as assessed by EPO and IL-8 release and eosinophil chemotaxis toward SE

37 KO mice counteracts hepcidin suppression by EPO, we generated double KO Bmp6-Tmprss6 KO mice.

38 eptor and CD131 on antigen-presenting cells, EPO induced the secretion of active TGFbeta by antigen-p

39 inocrit expressed the least Neu5Gc, and CIGB-EPO showed the greatest variety of high-mannose-phosphat

40 and a development product, called here CIGB-EPO, were compared to the originator product, Eprex.

41 The circulating EPO level was also constitutively higher in mice lacking

42 table changes in body weight or composition, EPO treatment reduced M1-like Msmall ef, Cyrillic and in

43 Studies using EPO-deficient mice confirm EPO serves as a major enzymatic source for protein carba

44 Hypoxia-inducible factor 2 (HIF-2) controls EPO synthesis in the kidney and liver and is regulated b

45 Conversely, EPO-initiated signals facilitated Treg proliferation by

46 Plasma and CSF EPO levels also correlated positively with coma duration

47 Plasma and CSF EPO levels did not differ in children with vs those with

48 ogenous plasma and cerebrospinal fluid (CSF) EPO levels with mortality and acute and long-term neurol

49 ha acetylation and efficient HIF-2-dependent EPO induction during hypoxia.

50 armacologic downregulation of kidney-derived EPO prevented spontaneous Treg generation.

51 armacologic downregulation of kidney-derived EPO reduced the expression of TGFbeta mRNA and abrogated

52 nd to be driven, at least in part, by direct EPO-R response in Msmall ef, Cyrillic via Stat3 activati

53 Blocking this pathway diverts EPO-stimulated HSCs to differentiate into myelomonocytic

54 se data define an active role for endogenous EPO in breast cancer progression and breast TIC self-ren

55 ted an anti-inflammatory role for endogenous EPO.

56 As a mimetic of endogenous EPO (eEPO), rHuEPO augments the oxygen carrying capacity

57 demonstrated that high levels of endogenous EPO gene expression correlated with shortened relapse-fr

58 e and analyze EMAs, in particular endogenous EPO and the recombinant forms EPOzeta, darbepoetin alfa,

59 Our engineered EPO molecule was mutated to weaken its affinity for EPO-

60 evidence that blocking erythropoietin (EPO)-EPO receptor (R) signaling promotes homing to BM and ear

61 Besides promoting erythropoiesis, EPO is also known to modulate retinal vascular integrity

62 Erythropoietin (EPO) and its receptor are expressed in a wide variety of

63 Erythropoietin (EPO) and its receptor are highly expressed in the develo

64 Erythropoietin (EPO) has neurotrophic actions and aids neurocognitive fu

65 Erythropoietin (EPO) increases neuroplasticity and reduces cognitive dif

66 Erythropoietin (EPO) is a hormone that induces red blood cell production

67 Erythropoietin (EPO) is one of the main therapeutics used to treat anemi

68 Erythropoietin (EPO) is the cytokine that regulates red blood cell produ

69 Erythropoietin (EPO) is the primary regulator of red blood cell developm

70 Erythropoietin (EPO) may be a beneficial tissue-protective cytokine.

71 Erythropoietin (EPO) stimulates proliferation of early-stage erythrocyte

72 Erythropoietin (EPO), a glycoprotein hormone indispensable for erythropo

73 ial growth factor (VEGF) and erythropoietin (EPO) expression were increased during hypoxic exposure a

74 and kidney VEGF, IGF-1, and erythropoietin (EPO) were determined.

75 tor 1-alpha (HIF-1alpha) and erythropoietin (EPO) were measured as potential mechanisms for exercise-

76 thropoiesis due to augmented erythropoietin (EPO) sensitivity.

77 ovide evidence that blocking erythropoietin (EPO)-EPO receptor (R) signaling promotes homing to BM an

78 Blood erythropoietin (EPO) increases primarily to hypoxia.

79 sis is acutely stimulated by erythropoietin (EPO) to favor iron supply to maturing erythroblasts.

80 n response to stimulation by erythropoietin (EPO).

81 -ligand system, the cytokine Erythropoietin (EPO) and its receptor (EpoR), to dimerize EpoR ectodomai

82 tion (R150Q) in the cytokine erythropoietin (EPO).

83 h in vivo to the anemia drug erythropoietin (EPO), to direct its activity to EPO receptors (EPO-Rs) o

84 emia, splenomegaly, elevated erythropoietin (EPO) levels, and extramedullary erythropoiesis in a proc

85 trends in hemoglobin (Hgb), erythropoietin (EPO) dose, intravenous (IV) iron dose, ferritin, transfe

86 The hormone erythropoietin (EPO), which is synthesized in the kidney or liver of adu

87 and animal studies implicate erythropoietin (EPO) and EPO receptor (EPOR) signaling in angiogenesis.

88 hd(1/2/3)hKO) promoted liver erythropoietin (EPO) expression 1246-fold, whereas renal EPO was down-re

89 We found that expression of erythropoietin (EPO) in a HEK293S N-acetylglucosaminyltransferase I (GnT

90 Ligation of erythropoietin (EPO) receptor (EPOR) JAK2 kinase complexes propagates si

91 t the topical application of erythropoietin (EPO) to cutaneous wounds in rats and mice with experimen

92 is and is the main source of erythropoietin (EPO), an oxygen-sensitive glycoprotein that is essential

93 they are the main source of erythropoietin (EPO).

94 (HIF)-mediated induction of erythropoietin (EPO).

95 had increased phosphorylated erythropoietin (EPO) receptor and phosphorylated STAT-5 relative to matc

96 Elevated endogenous plasma erythropoietin (EPO) levels have been associated with protection from ac

97 tors of red cell production, erythropoietin (EPO) and its cell surface receptor (EPO receptor [EPOR])

98 Recombinant erythropoietin (EPO) analogs [erythropoiesis-stimulating agents (ESA)] a

99 udies have demonstrated that erythropoietin (EPO) has extensive nonhematopoietic biological functions

100 d human models, we show that erythropoietin (EPO) signaling, together with the GATA1 transcriptional

101 te the cellular responses to erythropoietin (EPO) in different tissues.

102 revealed hypersensitivity to erythropoietin (EPO).

103 eceptor subtype (LPA3) under erythropoietin (EPO) induction.

104 Correction of anemia with erythropoietin (EPO) is associated with improved kidney transplant outco

105 the developing nervous system, and exogenous EPO therapy is potentially neuroprotective, however the

106 , an effect that was overcome with exogenous EPO administration.

107 nting that CD4(+) and CD8(+) T cells express EPO receptor (EPO-R) on their surfaces.

108 In the eye, EPO is involved in both physiological and pathological a

109 ecule was mutated to weaken its affinity for EPO-R, but its avidity for RBC precursors was rescued vi

110 These data support a role for EPO in regulating the survival, proliferation, and diffe

111 In its recombinant form, EPO is the one of most prescribed drugs to treat anemia,

112 Furthermore, EPO directly inhibited conventional T cell proliferation

113 ed the renal expression of the heterodimeric EPO receptor/CD131 complex, which is required for the ti

114 ly elevated hepcidin in the presence of high EPO levels, a role is suggested for matriptase-2 in EPO-

115 findings of this exploratory study highlight EPO as an interesting compound for treatment-resistant d

116 However, little is known about how EPO regulates bone formation, although several studies s

117 However, EPO improved BDI (P=0.02) and WHOQOL-BREF (P=0.01), and

118 However, EPO increased the expression of Nfatc1 and ephrinB2 but

119 tudies, clinical trials of recombinant human EPO (rHuEPO) have been started in children with CM.

120 tion or local injection of recombinant human EPO has demonstrated encouraging results in several mode

121 y was to determine whether recombinant human EPO improves mood and memory in treatment-resistant depr

122 activities and survival effects of identical EPO and CEPO doses in rat models of clinically relevant

123 Collectively, our findings identify EPO-R signaling as a novel regulator of WAT inflammation

124 trial start revealed ameliorated HDRS-17 in EPO (N=14) vs saline groups (N=17), which was sustained

125 els, a role is suggested for matriptase-2 in EPO-mediated hepcidin repression.

126 In human Hep3B hepatoma cells and in EPO-generating organs of hypoxic or acutely anemic mice,

127 ale mice, we observed a gender difference in EPO effects in weight control.

128 stone H3 lysine 4 dimethylation (H3K4me2) in EPO treated and control fetal neural progenitor cells, i

129 e analysis demonstrated a 2-fold increase in EPO expression in all S-HB, while 4/5 showed either Hypo

130 Moreover, systemic reduction in EPO levels by hyperbaric oxygen (HBO) used in a preclini

131 rated and resulted in transient reduction in EPO with encouraging engraftment rates and kinetics.

132 phB4 signaling may play an important role in EPO-mediated bone formation.

133 ar cells but paradoxically further increases EPO.

134 se models, acetate supplementation increases EPO expression and the resting hematocrit.

135 nvestigate this apparent hypoxia-independent EPO regulation, we assessed two sickle cell disease (SCD

136 current study, we found that Ang II induced EPO expression in situ in murine kidney slices and in 78

137 In UT7epo cells, knockdown of RHEX inhibited EPO-dependent growth.

138 phB4 knockdown through EphB4 shRNA inhibited EPO-mediated osteoblastic phenotypes.

139 We investigated EPO receptor (EPO-R) expression in WAT and characterized

140 fects in late-stage erythropoiesis, which is EPO independent.

141 n-induced AKI superimposed on CKD (5000 U/kg EPO or CEPO; three subcutaneous injections) and ischemia

142 ls and male versus female animals (1000 U/kg EPO or CEPO; three subcutaneous injections).

143 to data from a previous report, mice lacking EPO receptor (EPOR) expression on nonerythroid cells (EP

144 Our findings link EPO-R signaling on T cells to inhibition of T-cell immun

145 r hepatic PHD2 and PHD3 (Phd(2/3)hKO), liver EPO increase and renal EPO loss both occurred but were m

146 ccomplished by sensitized induction of liver EPO expression.

147 n-induced retinopathy, suggesting that local EPO may be more important than hepatic and/or renal EPO

148 Mean EPO and vitamin D dose and serum PTH levels remained hig

149 lined from 11.5 to 11.0 g/dl (P<0.001), mean EPO dose declined from 20,506 to 14,777 U/wk (P<0.001),

150 nsive in vivo and in vitro analyses in mice, EPO treatment inhibited WAT inflammation, normalized ins

151 r cytokines and growth factors that modulate EPO's actions, and a comparison of the effects of full-l

152 RHEX therefore comprises a new EPO/EPOR target and regulator of human erythroid cell ex

153 l, can potentiate the accelerating action of EPO on the healing of the burn injury.

154 ess understood is the nonerythroid action of EPO, including metabolic regulation of fat accumulation

155 pressed Ang II transcriptional activation of EPO.

156 enewal and reveal a potential application of EPO pathway inhibition in breast cancer therapy.

157 Furthermore, mice with targeted deletion of EPO receptor in white adipose tissue exhibited sex-diffe

158 However, high doses of EPO are associate with adverse effects, including thromb

159 proach may allow higher restorative doses of EPO without platelet-mediated side effects, and also may

160 ic and transcriptional changes downstream of EPO signaling in neural cells are not well understood.

161 sting a role for REST and NRF1 downstream of EPO signaling.

162 d explain the observed protective effects of EPO in kidney transplant recipients.

163 We examined the effects of EPO on human T-cell alloimmunity by first documenting th

164 n this study, we investigated the effects of EPO on the communication between osteoclasts and osteobl

165 AF, and remission rates showed no effects of EPO over saline at week 9 (P-value >/= 0.09).

166 l role in mediating the metabolic effects of EPO.

167 ant DNA technology allowed the expression of EPO-encoding genes in several eukaryotic hosts to produc

168 cts of full-length versus truncated forms of EPO.

169 us core-fucosylated Man5GlcNAc2 glycoform of EPO in the FUT8-overexpressed HEK293S GnT I(-/-) cell li

170 Here, we investigated the impact of EPO modulation on tumorigenesis.

171 ms for hypoxia-inducible factor induction of EPO expression, and within erythroid progenitors EPOR en

172 the EPO enhancer and efficient induction of EPO gene expression.

173 tor 2-mediated (HIF-2-mediated) induction of EPO in peritubular interstitial fibroblast-like cells, w

174 The expression level of EPO mRNA was elevated in the kidney and liver but not in

175 tagonist of MIR122 increased blood levels of EPO, reticulocytes, and hemoglobin.

176 the contribution of AQP3 to the mechanism of EPO action on the healing of burn wounds in the skin of

177 including previously identified mediators of EPO signaling (STAT5, STAT3), and novel factors such as

178 ncover new clinically relevant modulators of EPO and EPOR expression, and EPO's biological effects.

179 associated with a reduction in the number of EPO-producing renal interstitial cells.

180 s delineate the protolerogenic properties of EPO in inhibiting conventional T cells while simultaneou

181 Such a systemic reduction of EPO in the host enhanced myeloid differentiation and imp

182 studies indicate that systemic reduction of EPO levels in the host or blocking EPO-EPOR signaling ma

183 ed, the mechanism(s) for basal regulation of EPO are not well understood.

184 Although hypoxic regulation of EPO has been extensively studied, the mechanism(s) for b

185 signaling mechanism of Ang II regulation of EPO in 786-O cells.

186 types also contributes to the regulation of EPO production.

187 tify a novel pathway for basal regulation of EPO via AT1R-mediated Egr-1 activation by p21Ras-mitogen

188 e cells, which serve as the cellular site of EPO synthesis in the kidney.

189 gnal transduction factors, 32 new targets of EPO-modulated tyrosine phosphorylation were defined.

190 However, several types of EPO-resistant anemia are characterized by defects in lat

191 A full understanding of EPO's effects on various cell types and their potential

192 a-pair reproduction if extra-pair offspring (EPO) inherit high value for EPRS from their successful e

193 DSS-exposed mice treated with cibinetide or EPO displayed preserved tissue integrity due to reduced

194 d eosinophil activation (CD11b expression or EPO/IL-8 release), mCD48 (flow cytometry), sCD48 (ELISA)

195 increase in mice subjected to hemorrhage or EPO therapy, that ERFE acts on hepatocytes to suppress h

196 We use this assay to show that blood loss or EPO administration increases serum ERFE concentrations i

197 ts; data were thus analyzed for 69 patients (EPO: n = 35, saline: n = 34).

198 Here we show eosinophil peroxidase (EPO), an abundant granule protein released by activated

199 operoxidase (MPO) and eosinophil peroxidase (EPO).

200 Plasma EPO levels correlated positively with markers of endothe

201 High endogenous plasma EPO levels are associated with prolonged coma duration a

202 ll anaemia (homozygous HBBE6V; HbSS), plasma EPO is elevated due to hemolytic anaemia-related hypoxia

203 in level, a 1-natural-log increase in plasma EPO level was associated with a 1.74-fold increase in mo

204 llele of SNP rs60684937 and increased plasma EPO (n = 567, combined P = 5.5 x 10 - 8 adjusted for hae

205 atological changes with elevations of plasma EPO and circulating reticulocytes following single oral

206 In conclusion, we demonstrate that plasma EPO elevation with hydroxyurea in SCD is independent of

207 cohorts for genetic associations with plasma EPO, by prioritizing 237,079 quantitative trait loci for

208 -functional antibody fusion exhibited potent EPO and GCSF agonist activities.

209 e in allogeneic CD4(+) T-cell proliferation (EPO 1000 U/ml: 44.6%+/-22.9% of vehicle, P<0.05; 2000 U/

210 ffects than JAK2 R1063H and caused prolonged EPO-induced phosphorylation of JAK2/STAT5 via EPOR.

211 aling via ephrinB2-Fc significantly promoted EPO-mediated osteoblastic differentiation in ST2 cells.

212 selectively activates the tissue-protective EPO receptor, comprising an EPO receptor subunit (EPOR)

213 nanomolar concentrations, STS-E412 provided EPO-like cytoprotective effects in primary neuronal cell

214 In mixed lymphocyte reactions, EPO induced a dose-dependent decrease in allogeneic CD4(

215 We investigated EPO receptor (EPO-R) expression in WAT and characterized the role of i

216 (+) and CD8(+) T cells express EPO receptor (EPO-R) on their surfaces.

217 poietin (EPO) and its cell surface receptor (EPO receptor [EPOR]) have been intensely studied.

218 O), to direct its activity to EPO receptors (EPO-Rs) on red blood cell (RBC) precursors and prevent i

219 tional murine transplant models, recombinant EPO administration prolonged heart allograft survival, w

220 te variants in key hematopoiesis regulators (EPO, TFR2, HBB, TUBB1 and SH2B3) associated with blood c

221 (Phd(2/3)hKO), liver EPO increase and renal EPO loss both occurred but were much less dramatic than

222 PHDs in REPC pool size regulation and renal EPO output.

223 and the role of the PHD/HIF-2 axis in renal EPO-producing cell (REPC) plasticity is unclear.

224 erstitial cellular crosstalk modulates renal EPO production under conditions of epithelial HIF activa

225 Moreover, suppression of renal EPO production was associated with increased glucose upt

226 be more important than hepatic and/or renal EPO in mediating protective effects in the retina.

227 in (EPO) expression 1246-fold, whereas renal EPO was down-regulated to 6.7% of normal levels.

228 Compared with saline, EPO was associated with mood-independent memory improvem

229 es not result in discernible change in serum EPO or hemoglobin (n = 60).

230 Using a combination of studies we now show EPO uses plasma levels of the pseudohalide thiocyanate (

231 of broods available to a focal male to sire EPO, the male's probability of siring an EPO in an avail

232 established, mice were treated with solvent, EPO or the selective IRR agonist cibinetide.

233 underscore the potential for gender specific EPO action beyond erythropoiesis.

234 ntrolled, prospective cohort clinical study, EPO administration at doses used to correct anemia augme

235 In summary, EPO-mediated protein carbamylation is promoted during al

236 nvestigate whether the ability to synthesize EPO is a general functional feature of pericytes, we use

237 rmore suggest that the ability to synthesize EPO may represent a functional feature of pericytes in t

238 ound that pericytes in the brain synthesized EPO in mice with genetic HIF activation and were capable

239 The terminal plasma half-life of targeted EPO was approximately 28.3 h in transgenic mice vs. appr

240 huGYPA transgenic mice dosed with targeted EPO exhibited elevated RBC levels, with only minimal pla

241 s may be erythropoiesis-independent and that EPO exhibits immunosuppressive properties.

242 re, in vivo assays clearly demonstrated that EPO efficiently induces new bone formation in the alveol

243 We determined that EPO was induced by hypoxia in breast cancer cell lines,

244 Furthermore, we found that EPO is detectable in cyst fluid from S-HB (n = 14), whil

245 mouse models of breast cancer, we found that EPO promoted tumorigenesis by activating JAK/STAT signal

246 We found that EPO slightly promotes osteoblastic differentiation with

247 Herein we test the hypothesis that EPO, a hormone predominantly produced by the adult kidne

248 Mechanistic studies revealed that EPO prevented IL-2-induced proliferation by uncoupling I

249 ween EPO/ERFE and matriptase-2, we show that EPO injection induces Erfe messenger RNA expression but

250 analysis in the complete cohort showed that EPO reduced depression composite at weeks 9 and 14 (P-va

251 ion, although several studies suggested that EPO can affect bone homeostasis.

252 The EPO mutant is less effective at stimulating erythroid ce

253 ased phosphorylation of EPOR, CD131, and the EPO-associated signaling molecules JAK2 and AKT in HEK29

254 cutoff (1,337 deaths) was 17.2 months in the EPO and 17.4 months in the best standard of care group (

255 ol arm (median not reached) and 63.1% in the EPO arm (median, 90 days) (P < .001).

256 ion requirements decreased (P < .001) in the EPO arm, but not during the first month in the nonmyeloa

257 induction, and suggest that manipulating the EPO/EPO receptor signaling axis could be exploited to pr

258 ignaling only in the specific context of the EPO receptor (EPOR).

259 In vitro, in a manner dependent on the EPO receptor and CD131 on antigen-presenting cells, EPO

260 Surprisingly, the EPO R150Q mutant shows only a mild reduction in affinity

261 We found that the EPO produced from the FUT8 knockdown cell line was the p

262 red signals transmitted directly through the EPO-R expressed on T cells, resulting in diminished Th1

263 formation, CBP-HIF-2alpha recruitment to the EPO enhancer and efficient induction of EPO gene express

264 While the EPO mutant can stimulate effectors such as STAT5 to a si

265 poxia sensing and EPOR mutations exert their EPO hypersensitivity.

266 thropoietin (EPO), to direct its activity to EPO receptors (EPO-Rs) on red blood cell (RBC) precursor

267 tic breast cancer, were randomly assigned to EPO 40,000 IU subcutaneously once a week or best standar

268 ays and gene expression profiles compared to EPO.

269 ariation at SNP rs60684937 may contribute to EPO regulation through a cAMP-dependent protein kinase A

270 Exposure of UCB CD34(+) HSPC to EPO inhibits their migration and enhances erythroid diff

271 erythroid progenitors were hypersensitive to EPO.

272 evidence for a sex-differential response to EPO in weight control in mice and underscore the potenti

273 esting that the sex-differential response to EPO was associated with estrogen.

274 mice do not suppress hepcidin in response to EPO.

275 nt, fail to suppress hepcidin in response to EPO.

276 ors, improves the hepcidin responsiveness to EPO in Tmprss6 KO mice.

277 Thus, CEPO therapy may be superior to EPO in improving outcomes in common forms of clinical AK

278 We found that topical EPO treatment of the burns accelerated their healing thr

279 ial constituent of the ECM, into the topical EPO-containing gel, can potentiate the accelerating acti

280 In randomized trials, EPO administration to cancer patients has been associate

281 STS-E412 triggered EPO receptor phosphorylation in human neuronal cells.

282 Unlike EPO, RAP-536 promoted maturation of late-stage erythroid

283 was rapidly PY-phosphorylated >20-fold upon EPO exposure, and coimmunoprecipitated with the EPOR.

284 Studies using EPO-deficient mice confirm EPO serves as a major enzymat

285 The first HIF target gene characterized was EPO, which encodes erythropoietin-a glycoprotein hormone

286 n vivo selectivity depended on the weakening EPO mutation, fusion to the RBC-specific antibody, and e

287 arm) or erythropoietin at 500 U/kg per week (EPO arm).

288 artial remission were randomized to 8 weekly EPO (40,000 IU) or saline infusions in a double-blind, p

289 score >/= 17 were randomized to eight weekly EPO (Eprex; 40,000 IU) or saline infusions in a double-b

290 all ef, Cyrillic via Stat3 activation, where EPO effects on M2 but not M1 Msmall ef, Cyrillic require

291 delineate epigenetic changes associated with EPO signaling, we compared histone H3 lysine 4 dimethyla

292 Renal interstitial cells with EPO-producing capacity are poorly characterized, and the

293 Renal interstitial cells with EPO-producing capacity were entirely derived from FOXD1-

294 Compared with EPO therapy in the other AKI groups, CEPO therapy induce

295 Compared with EPO therapy, CEPO therapy induced greater improvements i

296 g with PBS treatment and 3.3 +/- 2.1 g with EPO treatment).

297 s oxygen sensors and respond to hypoxia with EPO synthesis.

298 RBC) precursors and prevent interaction with EPO-Rs on nonerythroid cells, such as platelets.

299 ocitrulline is shown to be co-localized with EPO within human asthmatic airways.

300 Using obese EpoR mice with EPO-R restricted to erythroid cells, we demonstrated an

301 expression was not detected in patients with EPO receptor (EPOR) gain-of-function, suggesting distinc