The most recent information on EPO is here. Click here for the function of EPO. Edit this page in Wiki Genes - EPO or see Wiki Gene. In addition, CIS was activated by Epo but not SCF. Paper-8406308. EPO also slightly enhanced expression of GPIIb/IIIa. Paper-6226898. Human hematopoietic progenitors express erythropoietin. Paper-1439719. EPO treatment was without influence on AVP plasma levels. Paper-8488. This therapy may also enhance the hematopoietic effects of EPO. Paper-9311970. There was no competition between TPO and EPO for binding to EPO receptor. Paper-1546278. EPO also enhanced the CA1 level of brain-derived neurotrophic factor. Paper-11821239. On the other hand, Epo had no effect on number and affinity of GM-CSF receptors. Paper-7388892. STAT3 upregulates expression of HIF-1 induced EPO. Paper-13318385. The improvement in EPO responsiveness may be caused by the effect of statins on CRP. Paper-9940047. Does parathyroid hormone affect erythropoietin therapy in dialysis patients? Paper-12375440. Epo binding induces the stimulation of Jak2 tyrosine kinase. Paper-1646591. Thus, erythroid development of M-TAT cells is promoted by EPO and suppressed by GM-CSF. Paper-137135. IFN-gamma produced significant increases in medium levels of Epo and nitrite. Paper-988470. CONCLUSIONS: Urine characteristics clearly affect the detectability of an EPO profile. Paper-12495111. Erythrocytosis caused by an erythropoietin- producing hepatocellular carcinoma. Paper-8608254. IL-6 dependent pathways could be involved in mediating elevated EPO levels in CLD patients. Paper-10354359. These studies suggest that SHP-1 and Jak2 are constitutively associated in UT-7/ EPO cells. Paper-8459741. Finally, Epo- induced signal transduction was also inhibited in cells lacking Btk. Paper-10428208. The cytokines IL-1 beta and TNF prevented this hypoxia- induced increase in Epo mRNA levels. Paper-145384. Both the production and the action of EPO may fall under the control of IL-1 and IFN-gamma. Paper-1141470. TGF-beta also inhibited hypoxia- induced Epo production, but only by as much as 56%. Paper-7211427. CONCLUSIONS: Epo and EpoR were expressed in NB but did not modify tumor cell proliferation. Paper-12500631. Interleukin 2 and erythropoietin activate STAT5/ MGF via distinct pathways. Paper-259794. However, DFO, EPO and DFO- EPO treatment had no effect on the loss of MBP staining. Paper-13598482. IL-4 alone neither supports nor suppresses the erythropoietin (Epo)-dependent colony formation. Paper-6667046. Indeed, Epo induced the transient tyrosine phosphorylation of GAB1 in UT-7 cells. Paper-1812483. However, BFU-E responses to SCF and erythropoietin were suppressed in STAT(-/-) mice. Paper-8388675. (c) SPTB remains unmethylated in human DNA from UT-7/ EPO cells and from cultured erythroblasts. Paper-11494708. With this regard, we analyzed a patient with EPO- producing clear-cell RCC and polycythemia. Paper-12681312. Significantly, Liar affected Epo- activated signaling molecules including Erk2, STAT5, Akt and Lyn. Paper-13524856. Expression of HIF-1alpha and its target genes EPO, VEGF and p21 was also upregulated. Paper-12128895. Overexpression of CYP2C8 in Hep3B induced EPO and VEGF under hypoxia. Paper-13012255. EPA potentiated the effect of Epo on this progenitor only in experiments performed at unicellular level. Paper-6264065. In UT-7 cells, both GM-CSF and EPO induced the activation of Stat1 alpha, Stat3 and Stat5. Paper-1424448. A protective effect of erythropoietin against Fas- induced BAP31 cleavage and apoptosis was observed. Paper-13034992. Stem cell factor ( SCF) stimulates proliferation of UT-7/ Epo only transiently, for three to five days. Paper-8406308. In this study, we examined the roles of Stat1alpha and Stat3 in EPO- induced erythroid differentiation. Paper-1501349. Furthermore, perfusion with EPO resulted in a 50% increase in the phosphorylated MAP kinases p42/ p44. Paper-11431267. In contrast, erythropoietin starvation induces the nuclear export of Hsp70 and the cleavage of GATA-1. Paper-12393190. Recombinant murine interleukin 9 enhances the erythropoietin-dependent colony formation of human BFU-E. Paper-7391985. Neurogenin 1 mediates erythropoietin enhanced differentiation of adult neural progenitor cells. Paper-11399930. Erythropoietin induces tyrosine phosphorylation of the beta chain of the GM-CSF receptor. Paper-189182. The role of interleukin 1, erythropoietin and red cell bound immunoglobulins in the anaemia of rheumatoid arthritis. Paper-7072458. Increased levels of C-reactive protein ( CRP) have been associated with relative EPO resistance in dialysis patients. Paper-9940047. Furthermore, IL-1 beta (10 U/ml) proved to block Epo formation in isolated serum-free perfused rat kidneys. Paper-7518582. Incubation with EPO (10(-13)-10(-10) M) stimulated mitogen-activated protein kinase activity in PC12 cells. Paper-1861280. Protective effect of erythropoietin on beta-amyloid- induced PC12 cell death through antioxidant mechanisms. Paper-12961766. Taken together, these results show that PtdIns 3-kinase controls Epo- induced GPI hydrolysis through PLC-gamma2. Paper-9315543. Further, the mRNAs of Akt, eNOS and EPO receptor were significantly enhanced in MI- EPO hearts (n = 7, P < 0.05). Paper-13773603. UT-7/ EPO cells expressing c-Mpl changed their morphology and the other characteristics similar to the UT-7/ TPO cells. Paper-1926699. Erythropoietin- producing renal cell carcinoma arising from autosomal dominant polycystic kidney disease. Paper-11230719. Conversely, IL-6- induced enhancement was blocked by the anti- IL-6 antibody but not by the anti- Epo antibody. Paper-7104146. Hypoxia-inducible factor-1 ( HIF-1) regulates the expression of neuroprotective genes such as erythropoietin ( EPO). Paper-12854007. Treatment of PC12 cells with PI3K inhibitors LY294002 abolished the protective effects of EPO. Paper-13761536. It was concluded that erythropoietin- induced protection from apoptosis involved JAK2, but not MAP kinases or c-jun. Paper-11783989. Incubation with thapsigargin resulted in decreased EPO synthesis (P < 0.05) but stimulated VEGF secretion (P < 0.05). Paper-1920627. CONCLUSIONS: We show that upon extended exposure, EPO induces NOS activity but does not affect ET-1 release. Paper-8493313. Erythropoietin ( EPO) induces endothelin expression in endothelial cells (EC) and has angiogenic effects. Paper-779582. Concomitant measurements of the production of alpha-fetoprotein indicated that the observed effects were specific for Epo. Paper-6955028. Thus, EPO may protect the kidneys against ischemia reperfusion injury by activating HIF-1alpha. Paper-13253497. Excessive level of parathyroid hormone may induce the reduction of recombinant human erythropoietin effect on renal anemia. Paper-376547. This preliminary study shows that EPO may inhibit GH secretion from the pituitary gland and IGF-1 production. Paper-11619869. Hepatic release of erythropoietin induced by transarterial chemoembolization in patients with hepatocellular carcinoma. Paper-280555. Juvenile hemochromatosis associated with B-thalassemia treated by phlebotomy and recombinant human erythropoietin. Paper-8591328. Neuroprotective effect of erythropoietin after experimental cold injury- induced vasogenic brain edema in rats. Paper-12769177. Erythropoietin protects CA1 neurons against global cerebral ischemia in rat: Potential signaling mechanisms. Paper-11821239. Amniotic fluid erythropoietin showed an independent effect on cord serum CRP in multiple regression analysis. Paper-10441256. Antioxidant effect of erythropoietin on 1-methyl-4-phenylpyridinium-induced neurotoxicity in PC12 cells. Paper-13234035. These motifs are also found on cytokine, erythropoietin and growth hormone receptors and provide docking sites for JAK kinases. Paper-1937152. In contrast, GM-CSF and IL-3 both induced GM colonies and sustained the formation of erythroid bursts in the presence of Ep. Paper-5799792. While HIF-1 and HIF-2 activate the EPO gene, HIF-3, GATA-2 and NFkappaB are likely inhibitors of EPO gene transcription. Paper-10561481. Treatment of the cells with antisense-vav and -p85 abrogated Epo- induced cell proliferation and PI3-kinase activity. Paper-1038443. Interleukin-10 inhibits erythropoietin-independent growth of erythroid bursts in patients with polycythemia vera. Paper-1567810. The levels of carbonic anhydrase I in K562 cells induced by erythropoietin and in other blood cells were determined. Paper-6545898. This study attempts to investigate the effect of bcl-xL overexpression on q of rCHO cells producing erythropoietin ( EPO). Paper-13628340. Taken together, these results suggest that Epo enhances plasma cell responses by a different mechanism than does IL-6. Paper-7104146. Recombinant human erythropoietin induces a delayed increase in reticulocytosis and in soluble transferrin receptor levels. Paper-9891725. Northern blot analysis of CA-I mRNA using a cloned genomic DNA as a probe showed that mRNA of CA-I was induced by EP. Paper-7135716. In addition, we have shown that EPO stimulates the formation of a ternary complex consisting of Ship1, Shc, and Grb2. Paper-2129008. Erythropoietin and hypoxia stimulate erythropoietin receptor and nitric oxide production by endothelial cells. Paper-10559611. Recombinant human erythropoietin stimulates vascular endothelial growth factor release by glomerular endothelial cells. Paper-1941060. Our results demonstrate that PKB/Akt is activated by Epo and SCF, but not by IGF-1 in human primary erythroid progenitors. Paper-8430288. Recently, the erythropoietin ( Epo) has been found to be upregulated in renal and other tumors associated with VHL disease. Paper-12159825. The gp130 receptor-ligand complexes are contrasted with the complex formed by erythropoietin ( Epo) and its receptor, EpoR. Paper-9996440. Coexpression of TRPC6 or C3/C6 chimeras with TRPC3 and Epo-R inhibited the Epo-stimulated increase in [Ca(2+)](i). Paper-13606795. Expression of EPO mRNA was always associated with activation of HIF, which could involve HIF-1alpha and/or HIF-2alpha. Paper-12512194. Stimulation of GATA-2 as a mechanism of hydrogen peroxide suppression in hypoxia- induced erythropoietin gene expression. Paper-8674799. Wortmannin, another PtdIns 3-kinase inhibitor, also suppressed Epo- induced PLC-gamma2 tyrosine phosphorylation. Paper-9315543. The objective of the present study was to investigate the role of heme oxygenase (HO)-1 in the antiapoptotic effects of EPO. Paper-13560387. Activation of the Akt/ FKHRL1 pathway mediates the antiapoptotic effects of erythropoietin in primary human erythroid progenitors. Paper-8430288. Furthermore, the inhibition of JNK using small interference RNA (siRNA) suppressed EPO-enhanced proliferation of AR42J cells. Paper-12963825. EPO treatment of MoDCs was also associated with an increase in surface expression of CD80 and CD86 as well as that of HLA-DR. Paper-13093623. RESULTS: EPO induced a 5.0-fold+/-0.4-fold increase in STAT5 transactivation, which could be further enhanced by SCF. Paper-9766422. OBJECTIVE: Current data suggest that erythropoietin protects the brain and the spinal cord from ischemic and traumatic injury. Paper-12021675. CONCLUSION: Treatment with EPO significantly inhibits the LPS- induced secretion of midkine and TNF-alpha regardless of the dosage. Paper-12866425. On the contrary, EPO activates neither JAK2 nor STAT5 in other cell lines that failed to respond to EPO ( ERT cells). Paper-259794. A case of erythrocytosis caused by a hepatocellular carcinoma ( HCC) that produced erythropoietin ( Epo) is described. Paper-8608254. Prostaglandin-E2 enhances EPO- mediated STAT5 transcriptional activity by serine phosphorylation of CREB. Paper-9498698. Thus, activation of AT1 with angiotensin II enhances erythropoietin-stimulated erythroid proliferation in vitro. Paper-1248131. High blood soluble receptor p80 for tumour necrosis factor-alpha is associated with erythropoietin resistance in haemodialysis patients. Paper-8938030. Immunoreactive serum erythropoietin concentrations were measured in 35 patients with anaemia associated with active rheumatoid arthritis. Paper-6710643. A role for heme oxygenase-1 in the antioxidant and antiapoptotic effects of erythropoietin: the start of a good news/bad news story? Paper-12042807. Role of heme oxygenase-1 in the cardioprotective effects of erythropoietin during myocardial ischemia and reperfusion. Paper-13560387. Among these growth factors, erythropoietin ( EPO) and granulocyte colony- stimulating growth factor ( G-CSF) are the most prominent. Paper-12820602. These findings suggest a suppressed serum EPO response ot anemia and the effectiveness of r- EPO in treating anemia associated with RA. Paper-6729630. Recombinant human erythropoietin inhibits iNOS activity and reverts vascular dysfunction in splanchnic artery occlusion shock. Paper-2010345. Erythropoietin reduces lipopolysaccharide- induced cell Damage and midkine secretion in U937 human histiocytic lymphoma cells. Paper-12866425. Interestingly, not only was this increase not seen with IL-3, but IL-3 prevented the Ep- induced appearance of beta-globin message. Paper-147270. Recombinant human erythropoietin stimulates production of interleukin 2 by whole blood cell cultures of hemodialysis patients. Paper-10568163. Recombinant human erythropoietin stimulates production of interleukin 2 by whole blood cell cultures of hemodialysis patients. Paper-2054580. STAT3 was significantly associated with EPO and EPOR in all the cancers (r=0.2370, p=0.039 and r=0.3336, p=0.003, respectively). Paper-13318385. Erythropoietin mediates hepcidin expression in hepatocytes through EPOR signaling and regulation of C/EBPalpha. Paper-12826285. Lack of influence of recombinant human erythropoietin on parathyroid function in hemodialysis patients with secondary hyperparathyroidism. Paper-360348. In mechanistic study, EPO induced time-dependent phosphorylation of phosphatidylinositol 3-kinase ( PI3K) substrate Akt. Paper-13761536. Furthermore, our data show that Gab1 is the primary IRS-related protein activated by erythropoietin in primary erythroid progenitor cells. Paper-1990473. CONCLUSION: SCF enhances the EPO- mediated STAT5 transactivation by triggering a PKA/ CREB-dependent pathway. Paper-9766422. By using nonadherent mononuclear cells from peripheral blood, Epo-dependent colony formation was enhanced by IL-3 and GM-CSF in PV patients. Paper-6232808. Epo gene expression has been previously shown to be down-regulated through a GATA binding site at its promoter region. Paper-8674799. Human recombinant erythropoietin (rHuEPO) was produced from Chinese hamster ovary (CHO) cells transfected with the human EPO gene. Paper-12004696. In contrast, TGFbeta blocks EPO signaling downstream of c-myc induction through a Smad3-dependent mechanism. Paper-12531062. The restoring effect of EPO in the RAW264.7 cells was associated with the increased of c-Fos and c-Jun expression as well as AP-1 activation. Paper-11389386. Using this cell line, we examined the effect of a truncated human EPO receptor ( EPOR-T) on EPO- induced erythroid differentiation. Paper-1749577. However, markers of an underlying inflammatory state and of secondary hyperparathyroidism were associated with decreased response to erythropoietin. Paper-8674874. Biochemical analysis of EPO mediated signaling in the BM-DCs showed activation of the AKT, MAPK and NF-kappaB pathways. Paper-13587764. Our results suggest that the Src kinase Lyn is involved in PLC-gamma 2 phosphorylation and PI 3-kinase activation induced by Epo. Paper-9684969. In vitro kinase assay using histone H2B and glucose synthase kinase as substrates demonstrated that Akt was actually activated by EPO. Paper-8364491. These results suggest that EPOR-T is a negative regulator of EPO- induced anti-apoptosis and EPO- induced erythroid differentiation. Paper-1749577. These findings suggest that pp60c-src plays crucial roles in the proliferation and EPO- induced erythroid differentiation of K562 cells. Paper-8223764. We recently found that erythropoietin produced by erythroid progenitors stimulates erythropoiesis via gp130 and c-kit signals. Paper-8540730. Epo was also able to activate p21ras as measured by exchange of guanosine diphosphate for guanosine triphosphate. Paper-63263. Our results strongly support a role for the common beta chain CD131 in the protective effect of EPO derivatives on motoneuron degeneration. Paper-12305474. The differential stimulation of neovascularization by EPO was associated with increased EPO-receptor and VEGF expression in ischemic hearts only. Paper-13084446. We report a case of EPO- producing RCC associated with ADPKD in a 66-year-old woman, and discuss the clinical and radiological findings. Paper-11230719. Hypoxia-induced transcription from the Epo promoter was specifically enhanced by ectopic p300 and inhibited by E1A binding to p300/ CBP. Paper-781896. Moreover, it was found that EPO- induced downregulation of EPOR mRNA level was preceded by a transient downregulation of GATA-1 mRNA. Paper-905785. Erythropoietin stimulates growth and STAT5 phosphorylation in human prostate epithelial and prostate cancer cells. Paper-10842001. Recombinant human erythropoietin enhances superoxide production by FMLP-stimulated polymorphonuclear leukocytes in hemodialysis patients. Paper-1221482. This study examined whether EPO can protect against neuronal death in the CA1 region of the rat hippocampus following global cerebral ischemia. Paper-11821239. Epo- induced tyrosine phosphorylation of GAB1 was also observed in normal human erythroid progenitors isolated from cord blood. Paper-1812483. In murine models, NF-E2 overexpression increases proliferation and promotes cellular viability in the absence of erythropoietin ( EPO). Paper-13885413. In this study, we tested the hypothesis that endothelial NO synthase ( eNOS) plays a key role in the vascular protective effect of EPO. Paper-13187720. CONCLUSIONS: The EPO- induced STAT3 serine 727 phosphorylation is mediated by a pathway involving MEK, ERK, and MSK1. Paper-9660261. Erythropoietin receptor mutations associated with familial erythrocytosis cause hypersensitivity to erythropoietin in the heterozygous state. Paper-2024259. The loss of VHL function may result in the accumulation of HIF-1alpha and overproduction of HIF-1 downstream target genes including Epo. Paper-9661944. The PI3-kinase/ AKT signaling pathway is identified as a mediator of Epo- induced phosphorylation of GATA-1. Paper-10815635. Erythropoietin protects PC12 cells from beta-amyloid(25-35)- induced apoptosis via PI3K/Akt signaling pathway. Paper-13761536. In contrast, R103A homodimer induces proliferation and transduces signal at concentrations similar to that of wild-type Epo monomer and homodimer. Paper-1425057. The effect of erythropoietin, with or without transferrin-iron is blocked by pre-incubation of the erythropoietin with rabbit anti erythropoietin serum. Paper-3789706. It was previously shown that HNF-4 functions as a tissue-specific and hypoxia- activated transcription factor for the erythropoietin ( Epo) gene. Paper-9597035. Differentiating CD34(+) cells that are stimulated with recombinant human EPO in serum-free liquid cultures express both EPO and EPO receptor ( EPOR). Paper-1439719. The addition of IL-1 alpha, IL-1 beta, or TNF-alpha resulted in a dose-dependent inhibition of hypoxia- induced Epo production by as much as 89%. Paper-7211427. EPO binds to an erythroid progenitor cell surface receptor that includes a p66 chain, and, when activated, the p66 protein becomes dimerized. Paper-9776170. Male gender, diabetes as cause of ESRD, older age, higher transferrin saturation and higher albumin concentrations were associated with lower Epo/Hb index. Paper-9719204. Recombinant Human Erythropoietin Protects Against Experimental Spinal Cord Trauma Injury by Regulating Expression of the Proteins MKP-1 and p-ERK. Paper-13729173. Stimulation with either TPO or EPO induced rapid increases in adhesion of M07ER cells to fibronectin without apparent change of expression of integrins. Paper-1290176. This unliganded EPOR dimer is formed from self-association of the same key binding site residues that interact with EPO-mimetic peptide and EPO ligands. Paper-1745948. EPO upregulated expression of phosphorylated Ser1177- eNOS and normalized the vasodilator response to acetylcholine (P<0.05). Paper-13187720. The majority of clear cell RCC displays a strong activation of the transcription factor regulating EPO, the Hypoxia-inducible Factor ( HIF). Paper-12512194. Tyrosine 343 in the erythropoietin receptor positively regulates erythropoietin- induced cell proliferation and Stat5 activation. Paper-439006. Erythropoietin stimulates phosphorylation and activation of GATA-1 via the PI3-kinase/ AKT signaling pathway. Paper-10815635. It is concluded that cobalt stimulates a signal cascade with cytochrome b as receptor and H2O2 as second messenger for regulating erythropoietin production. Paper-126312. The results indicated that Epo potently protected against lung I/R injury by inhibiting systemic and local expression of TNF-alpha and MMP-9. Paper-13570412. In summary, these studies demonstrate that PGE2 enhancement of EPO- induced STAT5 transactivation is mediated by the cAMP/PKA/ CREB pathway. Paper-9498698. Interleukin-1 ( IL-1) and tumor necrosis factor-alpha ( TNF-alpha) have been reported to inhibit the synthesis of erythropoietin ( EPO) in vitro. Paper-1181075. In this report, we demonstrate that insulin receptor substrate-2 ( IRS-2) is phosphorylated on tyrosine following treatment of UT-7 cells with erythropoietin. Paper-1206734. Flow cytometric analysis showed that incubation of K562 cells with EP as well as hemin induced CA-I at the 3rd h, while alpha-globin was detected at the 8th h. Paper-7135716. We used alanine substitution of EBP residues that contact EMP1 in the crystal structure to investigate the function of these residues in both EMP1 and EPO binding. Paper-1866584. Epo production was inhibited by MS from patients compared to controls both before and after stimulation with LPS (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS) Paper-7927997. Antisense src RNA expression in K562 cells inhibited the erythropoietin- induced activation of PI3-kinase and its association with erythropoietin receptor. Paper-9024942. Active PKC appeared essential for Epo- induced phosphorylation of the Epo receptor itself, STAT5, Gab1, Erk1/2, AKT, and other downstream targets. Paper-8606389. Epo activates specific signaling pathways and leads to activation of key transcription factors such as GATA-1, in order to ensure erythroid differentiation. Paper-13713754. Evaluating patients receiving recombinant epeoetin therapy who experience a sudden loss of epoetin efficacy for the possibility of antibody- mediated PRCA is crucial. Paper-10753697. However, Epo gene expression is also regulated by transcription factor GATA-2, which binds to the GATA binding site of the Epo promoter. Paper-9903776. Treatment with erythropoietin inhibited the expression of iNOS mRNA and nitrite production resulting from proinflammatory stimulation by IFN-gamma and LPS. Paper-11345194. We describe here that EPO activates hTERT gene transcription in in vitro-expanded primary erythroid precursors as well as in UT7 erythroleukemia cells. Paper-12531062. Activation of Raf/ ERK1/2 MAP kinase pathway is involved in GM-CSF- induced proliferation and survival but not in erythropoietin-induced differentiation of TF-1 cells. Paper-9046912. From these findings, it was concluded that EPOR was expressed in NIT-1 cells and EPO could protect NIT-1 cells from apoptosis induced by cytokines. Paper-12745296. CONCLUSION: Our data suggest that correction of anaemia with EPO therapy is associated with a significant decrease in TF, TFPI and SOX in diabetic CAPD patients. Paper-13424852. Our data suggest that up-regulation of SOCS2 in neuronal progenitor cells derived from the adult SVZ may regulate EPO enhanced neuronal differentiation. Paper-10455819. Previously, we demonstrated that FKHRL1 functions downstream of Akt in erythropoietin ( EPO) signaling and that it is directly phosphorylated by activated Akt. Paper-12630908. Separation of cytosol from resting or erythropoietin- stimulated UT-7 cells by anion-exchange chromatography revealed two peaks of myelin basic protein kinase activity. Paper-443232. When applied in vitro, EPO increased the percentage of peripheral blood DCs and monocyte-derived DCs (MoDCs) expressing the costimulatory molecules CD80 and CD86. Paper-13093623. To determine whether EPO is also produced by hematopoietic cells, we analyzed the expression of EPO in normal human hematopoietic progenitors and in their progeny. Paper-1439719. However, the enhancing effect of Epo is different from that of IL-4 or IL-6, since Epo effect was not blocked by anti- IL-4 antibody or anti-IL-6 antibody. Paper-7164431. In contrast, erythropoietin (EPO)- stimulated UT-7 cells (UT-7/ EPO) did not express PAI-1 mRNA after stimulation with TPO because they do not have endogenous c-Mpl. Paper-1926699. CsA induced the apoptosis of ECFCs in the presence of EPO or IFN-gamma, but at different magnitudes. Paper-10734540. IL1 alpha added to Epo alone had no effect on the growth of BFU-E whereas it potentiated the combined action of IL3 and GM-CSF on the primitive BFU-E. Paper-6264065. Hypoxia-induced erythropoietin ( Epo) production in vitro is suppressed by interleukin 1 beta ( IL-1 beta), tumor necrosis factor alpha ( TNF) and phorbol esters. Paper-145384. Activation of extracellular signal-regulated kinases ERK1 and ERK2 induces Bcl-xL up-regulation via inhibition of caspase activities in erythropoietin signaling. Paper-9676138. Erythropoietin promotes survival of primary human endothelial cells through PI3K-dependent, NF-kappaB-independent upregulation of Bcl-xL. Paper-13227226. Male gender, older age, diabetes, higher Hct, and increasing weight, urea reduction ration, and transferrin saturation were associated with lower EPO doses (all P < 0.01). Paper-9437409. To evaluate the acute effect of human erythropoietin (r-HuEPO) on basal and stimulated prolactin ( PRL) secretion, 18 normal subjects (12 females, 6 males) were studied. Paper-7796200. We show that VHL disease- associated renal clear cell carcinomas (RCC) consistently coexpress erythropoietin ( Epo) and Epo receptor (EpoR). Paper-10772509. Erythropoietin inhibits basal and stimulated corticotropin-releasing hormone release from the rat hypothalamus via a nontranscriptional mechanism. Paper-12497771. Involvement of erythropoietin- induced cytosolic free calcium mobilization in activation of mitogen-activated protein kinase and DNA synthesis in vascular smooth muscle cells. Paper-8697984. This EPO- induced protection was sensitive to a phosphatidylinositol 3-kinase ( PI3K) inhibitor, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one ( LY294002), in sham. Paper-11368522. In HEK 293T cells heterologously expressing TRPC and erythropoietin receptor ( Epo-R), Epo stimulated an increase in [Ca(2+)](i) through TRPC3 but not TRPC6. Paper-13606795. TPO also stimulates the proliferation of megakaryocytic progenitor cells and augments the erythroid progenitor response to erythropoietin and other early-acting cytokines. Paper-534267. Brain effects of erythropoietin ( Epo) are proposed to involve a heteromeric receptor comprising the classical Epo receptor (Epo-R) and the common beta chain (betac). Paper-13715006. Here we report that Epo prevented tau hyperphosphorylation in SH-SY5Y cells exposed to the beta-amyloid peptide and that this effect may depend on the PI3K/Akt-GSK-3beta pathway. Paper-13002030. We identified a novel erythropoietin (Epo)- induced protein ( CIP29) in lysates of human UT-7/ Epo leukemia cells using two-dimensional gel analysis and cloned its full-length cDNA. Paper-9417615. Stimulation with EPO of cells co-expressing EPO-R and either PTP1BD or PTP1B resulted in an increase or decrease respectively in phosphotyrosine EPO-R. Paper-10284157. Anti-TGF-beta augmented the proliferation of CD34(+)CD38(-)Lin(-) cells (day 21) in SCF- stimulated (6.4-fold +/- 1.5-fold) and SCF/ Epo-stimulated (2.9-fold +/- 1.2-fold) cultures. Paper-9990992. NIT-1 apoptosis was induced by cytokines and their effects on cell apoptosis and cell insulin secretion were assayed after binding of EPO to EPOR. Paper-12745296. Neither erythropoietin ( EPO) nor granulocyte macrophage-colony stimulating factor ( GM-CSF) was able to activate IEX-1 gene expression in UT7-Mpl cells. Paper-11390755. IFN-gamma and IL-1 had an additive inhibitory effect, whereas IFN-gamma and TNF-alpha acted in a synergistic fashion in inhibiting Epo production by Hep3B cells. Paper-7992170. Erythropoietin (Epo)- induced glycosylphosphatidylinositol (GPI) hydrolysis was previously described to be correlated with phospholipase C-gamma 2 ( PLC-gamma2) activation. Paper-9315543. Methods reported here permit the efficient recovery of purified EBP which quantitatively binds EPO in solution as determined by high performance size exclusion chromatography. Paper-1007127. Finally, TGF-beta1 accelerated Epo- induced terminal erythroid differentiation and resulted in a greater level of enucleation (22% +/- 6% versus 7% +/- 3%) in serum-free conditions. Paper-9990992. The biological activity was examined by the fact that hPL could stimulate erythroid maturation by the formation of hemoglobin in K-562 cells in the presence of erythropoietin. Paper-11331386. Most notably, EPO significantly increased systolic blood pressure and enhanced medial thickening of injured carotid arteries in eNOS-deficient mice (P<0.05). Paper-13187720. We further demonstrate that S100B release patterns do reflect successful neuroprotective drug treatment with recombinant human erythropoietin ( EPO) in acute stroke patients. Paper-10171427. RESULTS: The peak CK level and cumulative CK release were significantly lower in the above-median EPO group than in the below-median EPO group. Paper-10763331. In Chinese hamster ovary cells expressing EpoR, the G(i) inhibitor pertussis toxin blocked mitogen-activated protein kinase ( MAPK) Erk1/2 activation induced by Epo. Paper-9870811. In vitro assay of erythropoietin in fetal mouse liver cultures. II. Effects of human transferrin bound iron and of serum on the stimulation of incorporation of 3H-thymidine into DNA. Paper-3789706. Epo binds surface EpoR faster than NESP (k(on) = 5.0 x 10(8) m(-1) min(-1) versus 1.1 x 10(8) m(-1) min(-1)) but dissociates slower (k(off) = 0.029 min(-1) versus 0.042 min(-1)). Paper-10830112. Thrombopoietin and erythropoietin activate inside-out signaling of integrin and enhance adhesion to immobilized fibronectin in human growth-factor-dependent hematopoietic cells. Paper-1290176. AIMS AND BACKGROUND: Recombinant human erythropoietin ( Epo) and granulocyte-colony- stimulating factor ( G-CSF) are used to stimulate hematopoiesis in patients with malignant diseases. Paper-9497182. At multiple linear regression analysis, haemoglobin, BMI, albumin, CRP and serum iron levels were independently associated with the natural logarithm of the weekly EPO dose (R(2) = 0.22). Paper-11813487. The proinflammatory cytokines interleukin-1 ( IL-1) and tumor necrosis factor a ( TNF-alpha) suppress in vitro Epo gene expression and Epo protein secretion. Paper-9173344. Monocyte supernatants from patients in the anaemic PTB group had markedly elevated TNF alpha levels and significantly suppressed Epo output by HepG2 cells in vitro (p < 0.01). Paper-385849. We conclude that IL-3 enhanced the marrow erythropoiesis in most of the patients and exerted a corrective effect on the aberrant colony formation in the presence of erythropoietin. Paper-6265113. Stem cell factor enhances erythropoietin- mediated transactivation of signal transducer and activator of transcription 5 ( STAT5) via the PKA/ CREB pathway. Paper-9766422. The inability to detect EPO mediated activation of STAT5 in the BM-DCs, suggests that in DCs, STAT3 may play a more important role than STAT5 in EPO-R signaling. Paper-13587764. In FBS-supplemented cultures of unfractionated marrow cells, IL-1 induced optimal GM colony growth and increased by 50% the number of erythroid bursts that formed in the presence of Epo. Paper-6868193. An alternative approach towards the identification of an EPO-like mimetic is to target an intracellular signalling molecule such as haematopoietic cell phosphatase ( HCP), also known as SHP1. Paper-1883161. ERP binds to a different receptor site than EPO, and binding of ERP does not change the dissociation constant and maximal binding for EPO binding to the receptor. Paper-9464456. We thus suggest that PTP1B dephosphorylates EPO- stimulated EPO-R and participates in the down-regulation cascade of EPO-mediated signal transduction. Paper-10284157. In response to reduced O(2), hypoxia-inducible factor 1alpha ( HIF-1alpha) activates erythropoietin ( Epo) as well as many other target genes that counteract the effects of O(2) deficiency. Paper-12317051. We recently reported that interleukin-3, Steel factor, and erythropoietin all induce the tyrosine phosphorylation of Shc and its association with Grb2 in hemopoietic cell lines. Paper-132911. The signal transduction mediated by EPO that has a neuroprotective effect and mediated by proinflammatory cytokines that lead to brain damage shares the common JAK/ STAT pathway. Paper-13533312. Incubation of the progenitor cells with rhEPO in the presence of a neutralizing antibody against EPO abolished the effects of EPO on neuronal differentiation and expression of SOCS2. Paper-10455819. When local oxygen tension decreases, accumulated HIF binds to the key sequence of the EPO gene, the hypoxia-responsive element (HRE), and activates transcription of EPO. Paper-12637506. Studies in other VHL- associated tumors suggest that VHL gene deficiency causes coexpression of erythropoietin ( Epo) and its receptor (Epo-R), which facilitates tumor growth. Paper-11290025. Because of this mutation, Epo (R103A) is only able to bind to one of the 2 subunits of the erythropoietin receptor ( EpoR) homodimer and is thus a competitive inhibitor of Epo activity. Paper-9472182. PURPOSE: To assess the effect of erythropoietin ( EPO) plus granulocyte-colony stimulating factor ( G-CSF) treatment on survival and leukemic transformation in myelodysplastic syndrome (MDS). Paper-12934323. The inhibition likely occurred through an interaction between the two receptors because GR became associated with the EPO receptor and STAT-5 in cells stimulated with EPO and DXM. Paper-13723038. Epo (R103A) inhibits erythropoiesis of human CD34(+) hematopoietic cells and completely blocks erythroid burst-forming unit formation in normal human bone marrow colony assays. Paper-9472182. Treatment with Epo or 12-O-tetradecanoyl-phorbol-13-acetate (TPA) up-regulated expression of GATA-2 and Bcl-xL, and these elevations were inhibited by inhibitors of protein kinase C (PKC), H7 and H8. Paper-1280993. The expression of Nix and Bcl-xL proteins decreased relative to glyceraldehyde-3-phosphate dehydrogenase ( GAPDH) control on the removal of erythropoietin ( EPO) from the culture medium. Paper-9814533. Addition of rhEPO in vitro to the whole blood cell cultures of the HD patients before implementation of erythropoietin confirmed that rhEPO is able to directly stimulate IL-2 production. Paper-2054580. METHODS AND RESULTS: EPO cDNA was cloned into pPICZalphaA for expression under control of AOX1 promoter and fused, on the amino-terminal end, with a polyhistidine tag for rapid purification. Paper-13435350. Here we show that LFM-A13 efficiently inhibits erythropoietin (Epo)- induced phosphorylation of the erythropoietin receptor, Janus kinase 2 ( Jak2) and downstream signalling molecules. Paper-10428208. In addition, Epo treatment of erythroid progenitors induces phosphorylation of a member of the Forkhead family (FH) of transcription factors FKHRL1, downstream of activation of the Akt kinase. Paper-8430288. Erythropoietin induces the tyrosine phosphorylation of insulin receptor substrate-2. An alternate pathway for erythropoietin-induced phosphatidylinositol 3-kinase activation. Paper-1206734. The same progenitor cells can be induced to differentiate into other lineages when SCF is used with various lineage-specific colony- stimulating factors such as erythropoietin for erythrocytes. Paper-8210515. In Hep3B cells, clones modified to express HAF antisense RNA showed an attenuated response to hypoxia- mediated induction of both erythropoietin and vascular endothelial growth factor transcription. Paper-8356659. EPO (10(-13)-10(-10) M) increased dopamine release from PC12 cells and tyrosine hydroxylase activity; these increases were sensitive to nicardipine or anti- EPO antibody. Paper-1861280. There was no evidence of an association between birth weight SDS and pair mean log EPO, indicating that the association is entirely due to fetus-specific rather than pair-specific factors. Paper-11180458. In contrast, granulocyte-colony stimulating factor ( G-CSF), macrophage-colony stimulating factor ( M-CSF), and erythropoietin ( EPO) had no effects on the colony formation of CMK cells. Paper-6226898. Thus, inactivation of Erk1 and Erk2 kinases promoted EPO- induced erythroid differentiation and suppressed TPO-induced megakaryocytic differentiation of UT-7/GM cells. Paper-8962906. Background Preoperative epoetin-alpha administration is said to have a limited effect in patients with chronic inflammatory diseases such as rheumatoid arthritis ( RA), due to lower iron availability. Paper-12189748. Also, the dose of erythropoietin was directly associated with the CRP concentration, before (r = 0.081, P = 0.009) and after (t = 2.03, P = 0.042) adjustment for the serum albumin and iron concentrations. Paper-1577169. The response of erythroid precursors to EPO +/- TNF-alpha was assessed by detecting activated key proteins of EPO- EPO receptor signalling pathway using Western Blot and EMSA. Paper-13784978. RA patients given EPO had red blood cell (RBC) production that was enhanced by 624 +/- 137 ml (mean +/- SD) as compared with 271 +/- 174 ml (p = 0.02) for RA patients given placebo treatment. Paper-1217306. Erythropoietin stimulates the Janus kinase-2 ( JAK-2) and nuclear factor-kappaB (NF-kB) signaling pathways in neurons to prevent programmed cell death after ischemic or excitotoxic stress. Paper-10334300. FACS analysis of Epo- stimulated erythroid progenitors showed that the increased mRNA expression of KIT and CDH1 was accompanied by an induction of the corresponding proteins CD117 and E-cadherin. Paper-12220336. These findings suggest an alternative process of tumorigenesis in VHL- and MEN 2- associated pheochromocytomas and implicate Epo as a clinical biomarker to differentiate these tumors. Paper-11290025. We demonstrate that VHL disease- associated central nervous system tumors are composed of developmentally arrested angioblasts that coexpress erythropoietin ( Epo) and Epo receptor. Paper-10053830. Hypoxia-inducible factor 1 ( HIF-1) binds to cis-acting hypoxia-response elements within the erythropoietin, vascular endothelial growth factor, and other genes to activate transcription in hypoxic cells. Paper-1104611. Furthermore, Epo pretreatment reduced nuclear translocation of NF-kappaB and inhibited phosphorylation of inhibitor of kappa B (IkappaB) in TNF-alpha-stimulated cardiac myoblasts. Paper-14027823. In addition, GM-CSF inhibited EPO- induced erythroid differentiation and concomitantly activated Stat1 alpha and Stat3 in UT-7/GM cells even in the presence of EPO. Paper-1424448. These findings strongly suggest that the intranuclear translocation of active Akt kinase represents an important step in the signaling pathway that mediates erythropoietin- induced erythroid differentiation. Paper-13577456. Cotreatment of EPO with SB-202190, an inhibitor of p38 activation, blocked the EPO- mediated HO-1 expression and antiapoptotic effects, suggesting a p38-dependent mechanism. Paper-13560387. In-vivo experiments in EPO-injected mice and in transgenic mice over- expressing human EPO showed an increased splenic DC population with a higher cell surface expression of CD80 and CD86. Paper-13587764. We thus suggest that erythropoietin deficiency may be one of the endocrine abnormalities associated with APS1, and clinicians should be cognizant of the association of treatable anemia in patients with APS1. Paper-10302169. These results suggest that exposure to Epo can activate the c-kit receptor and provide further evidence for cross-talk between the Epo and c-kit receptors in human hematopoietic cell lines. Paper-1307116. Taken together, these findings point to a novel role for the PKC-alpha isoform in mediating EPO- induced erythroid differentiation of the CD34(+) progenitor cells from human bone marrow. Paper-2079999. The ectopic expression of Fli-3 in an erythroblastic cell line switches erythropoietin (Epo)- induced differentiation to Epo- induced proliferation through activation of the Ras and PI3K pathways. Paper-12500599. In each patient, erythroid and nonerythroid colonies, grown in the presence of erythropoietin and granulocyte-macrophage colony- stimulating factor ( GM-CSF), exhibited no remarkable difference in clonal constitution. Paper-125934. In this study, we investigated the possibility that AmB inhibits the transcription of the EPO gene by inactivating HIF-1, which is a known key transcription factor and regulator of EPO expression. Paper-10815592. Partially purified HIF-1 bound specifically to the wild-type HIF-1 binding site from the EPO enhancer but not to a mutant sequence that lacks hypoxia-inducible enhancer activity. Paper-155625. These results suggest that IL-3 enhances the effect of Epo on erythropoiesis, but the combination of the two growth factors does not lead to a preferential and significant enhancement of HbF production. Paper-6496595. Finally, hTERT appears to be efficiently regulated by EPO and TGFbeta in an opposite way in erythropoietic cells, arguing for a role of telomerase in red blood cell production. Paper-12531062. In the present study, we demonstrate the previously unrecognized EPO- mediated invasion by HNSCC cells through the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway. Paper-10753061. The increase of anemia after OLT and the maintenance of a defective endogenous Epo production after liver transplantation excluded an inhibitory effect of the circulating TTR V30M on the Epo-producing cells. Paper-13199295. We have also presented data showing that SCF together with phytohemagglutinin- stimulated leukocyte conditioned medium can stimulate erythroid colony growth in the presence of antibodies to erythropoietin. Paper-7354048. MGF stimulated both Epo-dependent and Epo-independent erythroid colony formation from PV peripheral blood progenitor cells in vitro at a dose similar to normal erythroid progenitor. Paper-7552994. Epo also did not bind to chimeric receptors that had the amino acids encoded by the fifth exon replaced by IL2R beta or that had the amino acids subsequent to asparagine residue 209 replaced by IL2R beta. Paper-427773. Erythropoietin ( Epo) stimulation of its receptor's downstream signaling pathways and optimum function of GATA-1 transcription factor are both essential for normal erythroid cell development. Paper-10815635. Activation of FKHRL1 Plays an Important Role in Protecting Erythroid Cells from Erythropoietin Deprivation-Induced Apoptosis in a Human Erythropoietin-Dependent Leukemia Cell Line, UT-7/ EPO. Paper-12630908. This suggests that the Epo- triggered onset of terminal maturation is intact in DBA, and the defect lies down-stream of the Epo receptor, influencing survival and/or proliferation of erythroid progenitors. Paper-11016755. RESULTS: Expression of either P190 BCR/ ABL1 or P210 BCR/ ABL1 resulted in expansion of erythroid cells and stimulated erythropoietin-independent burst-forming unit-erythroid colony formation. Paper-13616665. Although erythropoietin ( EPO) alone stimulated neither proliferation nor differentiation of HML/SE cells, it did stimulate proliferation of HML/SE cells and production of hemoglobin in the presence of SCF. Paper-1501003. Wortmannin only inhibits MAPK activation induced by EPO but not that by SCF, suggesting that SCF and EPO may activate MAPK through different pathways, which would facilitate synergy. Paper-1537623. BACKGROUND: The aims of this study were to evaluate the efficiency of EPO in the treatment of cold injury- induced brain edema, apoptosis, and inflammation and to compare its effectiveness with DSP. Paper-12769177. Erythropoietin protects primary cultures of rat cortical neurons from hypoxia- induced toxicity through attenuating both glutamate release and NMDA receptor evoked neurotoxicity pathway. Paper-13704858. Furthermore, NG-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor, significantly decreased IFN-gamma induced elevations in medium levels of Epo and nitrite as well as cGMP levels in Hep3B cells. Paper-988470. These data indicate that Epo production by hepatoma cells in vitro is inhibited by IFN-gamma, and that a complex network of interacting cytokines may regulate Epo production in response to an hypoxic stimulus. Paper-7992170. These data define the limits of EPO activity in fetal erythropoiesis to cells that express CD38 and demonstrate the potential for various cytokine interactions to be involved in regulating fetal erythropoiesis. Paper-8761372. We show that cells engineered to concomitantly express the wild-type (WT) EPOR and mutant EPORs associated with FE (FE EPORs) are hypersensitive to EPO- stimulated proliferation and activation of Jak2 and Stat5. Paper-2024259. Endothelial PAS domain protein-1 ( EPAS1) regulates transcription of the genes encoding erythropoietin and vascular endothelial growth factor, which are important for maintaining oxygen homeostasis. Paper-10463077. The hypoxia-inducible factor-1 ( HIF-1) transcriptionally up-regulates erythropoietin, transferrin, and transferrin receptor, leading to increased erythropoiesis and hematopoietic iron supply. Paper-9787335. To investigate the mechanism underlying determination of cell differentiation, we investigated the role of signal transducers and activators of transcription ( STAT) in EPO- induced erythroid differentiation. Paper-1424448. Thus EPO promotes survival of endothelial cells through PI3K-dependent Bcl-x(L)-induction and BIM regulation, as well as through a separate mechanism involving the ERK pathway. Paper-13227226. Western blot analysis and polymerase chain reaction assessment showed that NB cells express neither HNF4alpha nor the splicing variant HNF4alpha7 and thus express EPO in an HNF4alpha-independent manner. Paper-9574225. Erythropoietin (EPO)- producing renal cell carcinomas (RCC) in patients with chronic renal failure secondary to autosomal dominant polycystic kidney disease ( ADPKD) has not previously been reported. Paper-11230719. We conclude that in anemic RA patients exogenous erythropoietin induces a swift and sustained increase in the serum concentration of TfR, which probably reflects increased expression of TfR on erythroblasts. Paper-748712. These data demonstrated the suppressive effects of TNF alpha on erythropoiesis in vitro and that the suppressed erythropoiesis could be partly corrected by the addition of excess r-h- EPO to the cultures. Paper-8180591. Indirect immunofluorescence using globin chain-specific monoclonal antibodies detected fetal, but not adult hemoglobin in the uninduced cells. beta-globin was induced and gamma-globin was increased after Epo exposure. Paper-7135820. However, the Epo effect was specific since Epo- induced enhancement of Ig production and thymidine uptake was blocked by the anti- Epo antibody but not by the anti- IL-6 antibody or the control antibody. Paper-7104146. Using Ba/F3-EPOR cell lines and primary human erythroblast cultures, we found that JUNB was transcriptionally induced after erythropoietin addition and that JAK2 V617F constitutively induced JunB protein expression. Paper-13574589. It is a well recognized problem that sample derived transferrin- bound iron (Tf-Fe) interferes with radio-iron incorporation into heme in the in vitro assay of erythropoietin ( Ep) using fetal mouse liver cells (FMLC). Paper-3785555. Inhibition of the mitogen-activated protein kinase pathway by the specific inhibitors PD98059 and U0126 and of phosphatidylinositol 3-kinase by LY294002, strongly inhibited Epo- induced TIMP-1 expression and secretion. Paper-8574127. However, combination of SF with lineage-specific factors, such as erythropoietin ( Epo) or/and granulocyte colony- stimulating factor ( G-CSF) was not sufficient for the proliferation of multipotential progenitors (CFU-GEMM). Paper-11715462. In contrast, Grb2 associated efficiently with the activated erythropoietin receptor and a significant part of Grb2 was associated to a particulate subcellular fraction upon erythropoietin stimulation. Paper-443232. CONCLUSIONS: MEN 11303 and the combination of GM-CSF/ EPO are equally potent in recruiting hematopoietic progenitors into cycle, but the fusion protein is superior in promoting the expansion of committed erythroid percursors. Paper-8501268. In CD34(+) progenitor cells, Epo alone was able to induce cell cycle progression as demonstrated by upregulation of cyclin D(3), E and A leading to hyperphosphorylation of the retinoblastoma protein ( RB). Paper-12220336. IL-1 and TNF-alpha were shown to inhibit EPO mRNA levels and EPO formation in the human hepatoma cell cultures HepG2 and Hep3B, and to lower EPO formation in isolated perfused rat kidneys. Paper-8085949. The average number of hematopoietic colonies and clusters apparent from replated cultures of cord blood or bone marrow CFU-GEMM stimulated by Epo + MGF was greater than with Epo + rhuIL-3 or Epo alone. Paper-6872481. In the present study we examined the effect of pharmacological dose of human recombinant erythropoietin (rHuEpo) on the IL-1beta- induced NO and cGMP production as well as inducible nitric oxide synthase ( iNOS) in cultured rat VSMC. Paper-1840465. Monomeric Epo mutant R103A is unable to support Epo-dependent cell growth or trigger Janus kinase 2 and STAT5 activation, even at concentrations greater than 7,000 times that sufficient for wild-type Epo activity. Paper-1425057. We observed a fourfold increase in low-affinity IL-3 sites in an erythroid precursor cell line stimulated with EPO, and a threefold increase in GM-CSF high-affinity sites in a myeloid cell line stimulated with IL-3. Paper-7276362. Further studies have been carried out to clarify the role of NO in the hypoxic regulation of Epo production in Epo producing human hepatocellular carcinoma (Hep3B) cells, which produce Epo in response to physiological stimuli. Paper-988470. DBA cultures were indistinguishable from controls until the end of erythropoietin (Epo)-free phase 1, but failed to demonstrate the normal synchronized wave of erythroid expansion and terminal differentiation on exposure to Epo. Paper-11016755. OBJECTIVE: Erythropoietin interacts with vascular endothelial growth factor ( VEGF) and stimulates endothelial cell mitosis and motility; thus it may be of importance in the complex phenomenon of wound healing. Paper-11407123. Erythroid differentiation of human erythroleukemia cell line K562 induced by erythropoietin is a complex process that involves modifications at nuclear level, including nuclear translocation of phosphatidyl-inositol 3-kinase. Paper-13577456. Treatment with erythropoietin in combination with granulocyte colony- stimulating factor ( G-CSF) may synergistically improve the anemia in patients with MDS, with a concomitant decrease in the number of apoptotic bone marrow precursors. Paper-9855731. Supplementation of TNF to culture resulted in a dose-dependent suppression of granulocyte colony- stimulating factor ( G-CSF) induced granulocytic colony formation and also erythropoietin ( Epo) induced erythroid burst formation. Paper-6903445. It was concluded that impaired Epo production or reduced bone marrow Epo sensitivity might be associated with ACD but it is not certain whether these factors are causally linked with ACD or side phenomena of RA disease activity. Paper-6573927. Stepwise regression analysis for covariance revealed that phosphorus remained significantly correlated with EPO resistance after the removal of the effect of PTH while PTH lost its significance after the effect of phosphorus was removed. Paper-12252637. Treatment of cells with mitogen-activated protein/ ERK kinase ( MEK) inhibitor PD98059 or JNK inhibitor SP600125 significantly inhibited EPO-enhanced proliferation and also increased the fraction of cells in G0/ G1 phase. Paper-12963825. EPO effects were not mediated by modification of CRH gene expression, either in the absence or the presence of KCl or veratridine; in this paradigm, KCl and veratridine per se did not modify CRH gene expression. Paper-12497771. Thus, Epo protects cardiac myocyte progenitors or myoblasts against the cytotoxic effects of TNF-alpha by inhibiting NF-kappaB-mediated iNOS expression and NO production and by preventing caspase-3 activation. Paper-14027823. Furthermore, CREB-binding protein (CBP)/p300 was shown to be involved in EPO- mediated STAT5 transactivation, and a CBP mutant with increased affinity for CREB resulted in an additional enhancement of the PGE2 effect. Paper-9498698. In this study, we have shown that erythropoietin ( Epo) activates the mitogen-activated protein kinase, extracellular signal-regulated kinase ( ERK), and promotes migration in MCF-7 breast cancer cells. Paper-11118457. EPO- induced phosphorylation of Akt was completely blocked by a PI3K-specific inhibitor, LY294002, at 10 micromol/L, indicating that activation of Akt by EPO is dependent on PI3K activity. Paper-8364491. In order to explore the expression of erythropoietin receptor ( EPOR) in pancreatic cell line NIT-1 and its effect on cell apoptosis after binding with erythropoietin ( EPO), NIT-1 cells were cultured and expanded. Paper-12745296. BACKGROUND AND AIMS: Recombinant erythropoietin upregulates the expression of the vascular endothelial growth factor ( VEGF) receptors, Flt-1 ( VEGFR-1) and KDR/Flk-1 ( VEGFR-2), in endothelial cells. Paper-11152437. We examined the role of the Src kinase Lyn in phospholipase C-gamma 2 ( PLC-gamma 2) and phosphatidylinositol (PI) 3-kinase activation in erythropoietin (Epo)- stimulated FDC- P1 cells transfected with a wild type (WT) Epo-receptor (Epo-R). Paper-9684969. When we attempted to support this cross-talk model using endogenous loci, we observed that activation of the hypoxia pathway inhibited Cyp1a1 up-regulation, but that activation of the AHR actually enhanced the induction of Epo by hypoxia. Paper-1832011. Protein kinase B (c-Akt), phosphatidylinositol 3-kinase, and STAT5 are activated by erythropoietin ( EPO) in HCD57 erythroid cells but are constitutively active in an EPO-independent, apoptosis-resistant subclone (HCD57-SREI cells). Paper-1875039. In this study we confirmed the presence of the erythropoietin (EPO) receptor on both cultured cortical neurons and PC12 cells and showed that EPO can induce changes in p38, ERK, and JNK signaling molecules in these cells. Paper-11408673. In vitro, we verify that EPO protects RPE cells from light, hyperoxia, and hydrogen peroxide-induced retinal cell apoptosis, and that these stimuli increase EPO and EPOR expression in cultured RPE cells. Paper-13838941. In its autocrine-paracrine roles, EPO mediates preconditioning (ischemic tolerance) and specifically limits the destructive potential of tumor necrosis factor alpha and other proinflammatory cytokines in the brain, heart, kidney, and other tissues. Paper-12063400. Production of Epo, in contrast to KDEL- modified Epo, induced reductions in Epo binding, Epo receptor (EpoR) mRNA, and phosphorylation levels similar to those induced by the addition of exogenous Epo to the parental cell line. Paper-134718. Furthermore, EPO, but not SCF, led to activation of STAT5, whereas SCF and wortmannin had no effect on the EPO- induced STAT5 activation, suggesting that STAT5 is not involved in the synergistic action of SCF and EPO. Paper-1537623. Chromatin immunoprecipitation (ChIP) and sequential ChIP (re-ChIP) analysis showed that both Brm and Brg-1 associate with the enhancer region of the EPO gene in vivo in a hypoxia-dependent fashion and that each is present in a complex with HIF-1. Paper-10563667. Analysis of two EPO receptor ( EPOR) transfected CTLL-2 cell lines discloses that IL-2 activates JAK1 and JAK3 as well as STAT5, while EPO stimulates STAT5 and JAK2 in EPO-responsive CTLL-2 cells ( ERT/E2). Paper-259794. Erythropoietin promotes MCF-7 breast cancer cell migration by an ERK/ mitogen-activated protein kinase-dependent pathway and is primarily responsible for the increase in migration observed in hypoxia. Paper-11118457. In AS-E2 cells STAT5 is constitutively phosphorylated on Ser780 ( STAT5A) and EPO-dependently phosphorylated on Ser726/731 ( STAT5A/ STAT5B), but overexpression of STAT5 serine mutants did not affect STAT5 transactivation. Paper-9498698. The effects that IL-1 alpha, IL-1 beta, TGF-beta, TNF-alpha, and IL-6 have on hypoxia- induced Epo production may provide new insights into the signal transduction pathway by which hypoxia leads to changes in gene expression. Paper-7211427. Inhibition of MKP-1 expression using siRNA technique could enhance HIF-1alpha phosphorylation, accompanied by an increase in transcriptionally active HIF-1 as well as a rise in the levels of HIF-1- induced erythropoietin expression. Paper-10101738. The Epo- induced kinetics and dose response on phosphorylated Jak2 in anti-SHP-1 precipitates of UT-7/ Epo cell lysates were similar to those in direct anti- Jak2 precipitates, suggesting that Jak2 coprecipitated with SHP-1. Paper-8459741. Hypoxia-inducible factor 1 ( HIF-1) is a heterodimeric basic helix-loop-helix protein implicated in the transcriptional activation of genes encoding erythropoietin, glycolytic enzymes, and vascular endothelial growth factor in hypoxic mammalian cells. Paper-760628. These results indicate that activation of p38 and JNKs but not of ERKs is required for Epo- induced erythroid differentiation of SKT6 cells, whereas all of these kinases are involved in Epo- induced mitogenesis of FD- EPO cells. Paper-1567798. We did a secondary analysis of patients with chronic kidney disease enrolled in the Correction of Hemoglobin in the Outcomes in Renal Insufficiency trial to measure the potential for competing benefit and harm from achieved hemoglobin and epoetin dose trials. Paper-12979069. We designed the present study to address the question of whether recombinant human erythropoietin stimulates DNA synthesis and vascular endothelial growth factor ( VEGF) secretion in vitro using cultured bovine glomerular endothelial cells (GENs). Paper-1941060. In EPO-H hemodialysis patients, the EPO signaling pathway is attenuated as a result of dephosphorylation of STAT5 via upregulation of SHP-1 phosphatase activity, and SHP-1 may be a novel target molecule to sensitize EPO action in these patients. Paper-10616646. The addition of flt3L to a growth factor combination of IL-1 alpha + IL-3 + IL-6 + EPO resulted in a synergistic effect on progenitor cell expansion comparable to that observed with the addition of SLF to IL-1 alpha + IL-3 + IL-6 + EPO. Paper-386393. These results indicate that Stat1 alpha and Stat3 have an inhibitory effect on the EPO- induced erythroid differentiation, and more complicated combination of transcription factors may play an important role in the decision of cell differentiation. Paper-1424448. The costimulatory effect of PGE2 on EPO- mediated STAT5 transactivation was inhibited by overexpression of serine-dead CREB or protein kinase A (PKA) inhibitor (PKI), in contrast to EPO-mediated transactivation, which was PKA independent. Paper-9498698. Granulocyte-macrophage colony-stimulating factor ( GM-CSF) and erythropoietin ( EPO) induce tyrosine phosphorylation of the GM-CSF receptor beta chain and the EPO receptor, respectively, although their receptors lack the tyrosine kinase activity. Paper-189182. Taken together, our data demonstrate that Gab proteins are engaged in erythropoietin signaling to mediate downstream activation of the SHP2 and phosphatidylinositol 3'-kinase pathways and possibly participate in the generation of the erythropoietin-induced mitogenic responses. Paper-1990473. We previously reported that erythropoietin ( Epo) has a mitogenic effect on rat vascular smooth muscle cells (VSMC) and that activation of the mitogen-activated protein kinase ( MAPK) cascade is an important mediator for Epo-induced mitogenesis. Paper-9587496. The aim of this study was to investigate the relations among reactive oxygen species (ROS), hypoxia inducible factor ( HIF-1 alpha) gene expression, HIF-1 alpha target gene erythropoietin ( EPO), and vascular endothelium growth factor ( VEGF) in humans. Paper-13563016. Together, these results suggest that EPO could protect against oxidative injury- induced cell death and mitochondrial dysfunction in RPE cells through modulation of Akt1 phosphorylation, mitochondrial membrane potential, and cysteine protease activity. Paper-13700690. METHODS:: In the current meta-analysis of published literature, erythroid response (ER) rates with EPO as a single agent versus its combination with granulocyte-colony- stimulating factor ( G-CSF) or granulocyte-macrophage-colony- stimulating factor ( GM-CSF) were compared. Paper-13605811. RESULTS: Western blotting of extracts of cells exposed to various chemical inhibitors revealed that the MEK inhibitors PD98059 and U0126 abrogated the EPO- mediated STAT3 serine 727 phosphorylation without an effect on tyrosine phosphorylation. Paper-9660261. The effect of erythropoietin was mediated by the phosphatidylinositol 3-kinase ( PI3K) signaling pathway since erythropoietin failed to rescue cells from MPP(+) insult in the presence of the PI3K inhibitor, LY 294002. Paper-13234035. EPO has potent neuroprotective properties in vivo and in vitro and appears to act in a dual way by directly protecting neurones from ischaemic damage and by stimulating endothelial cells and thus supporting the angiogenic effect of VEGF in the nervous system. Paper-10495312. Interestingly, EPO inhibits the increase in iNOS, poly(ADP)ribose polymerase, and intercellular adhesion molecule 1 expression in the aorta of endotoxemic rats and attenuated the decline in the expression of both Bcl-xl and Bcl-2 caused by LPS. Paper-13716462. Data from previous studies of VHL disease- associated hemangioblastomas (HBs) and renal cell carcinomas (RCCs) have indicated that VHL gene deficiency causes coexpression of erythropoietin ( Epo) and its receptor (Epo-R), which facilitates tumor growth. Paper-10990205. Such Epo-dependent activation of FKHRL1 apparently regulates the generation of Epo-dependent antiapoptotic signals as evidenced by the induction of apoptosis of erythroid progenitors during treatment of cells with the PI3-kinase ( PI3K) inhibitor LY294002. Paper-8430288. Since GH would stimulate EPO release, the results of this study may suggest the existence of feedback mechanism operating between GH secretion and EPO production, with inhibitory effect of EPO on GH secretion, and stimulatory action of GH on EPO production. Paper-11619869. Substitution of Phe93 with alanine resulted in a dramatic decrease in EPO binding to the Escherichia coli- expressed extracellular domain of the EPOR ( EPO- binding protein or EBP) and no detectable binding to full-length mutant receptor expressed in COS cells. Paper-1866584. Intravenous high-dose EPO therapy was associated with an improvement in the clinical outcome and preclinical studies with intravenous high-dose G-CSF therapy have clearly shown that it has considerable neuroprotective potential in the acute, as well as in the chronic phase of stroke. Paper-13143834. Antiapoptotic signalling through erythropoietin ( EPO) binding to its receptor ( EPOR) is triggered by systemic or local hypoxia and may exist in the post-ischaemic brain, and a neuroprotective effect by EPO was described recently and proposed for clinical stroke treatment. Paper-11400080. SCF interacted with erythropoietin ( Epo) and granulocyte colony- stimulating factor ( G-CSF) to maintain large numbers of cells as well as to generate a twofold to threefold increase in CFC in the case of Epo, and a 10-fold increase in CFC in the case of G-CSF. Paper-7212859. These alterations in metabolism and tumorigenicity caused by the EPOR with activating point mutations are similar to those observed in erythropoietin-independent activation of the wild type EPOR by association with gp55, the Friend spleen focus-forming virus glycoprotein. Paper-6510941. Expression of a mutant EPO-R lacking all eight tyrosine residues in the cytosolic domain supported a low but detectable level of EPO- induced STAT5 activation, indicating the existence of an alternative pathway for STAT5 activation independent of any tyrosine in the EPO-R. Paper-619210. CONCLUSION: This preliminary study shows that the concomitant administration of EPO may allow a control of the neoplastic growth in advanced cancer patients progressing on IL-2 alone, reduce the subjective toxicity, prevent hemoglobin decrease and counteract IL-2-related VEGF increase. Paper-8725600. Thus, these findings indicate that EPO protects against apoptosis in PC12 cells exposed to MPP(+), through the Akt/GSK-3beta/caspase-3 signaling pathway, but the ERK pathway is not involved in the EPO-dependent survival enhancing effect in this model system. Paper-13312660. Immunohistochemistry showed that erythropoietin-treated SCI rats had a significantly lower phospho-extracellular signal- regulated kinase (p-ERK) protein expression and a significantly higher mitogen-activated protein kinase phosphatase-1 ( MKP-1) protein expression than saline-treated SCI rats. Paper-13729173. TPO has a synergistic effect with EPO or EPO + IL-3 on erythropoiesis of human BM, as the addition of TPO to EPO significantly gave rise to more erythroid bursts (p = 0.0001) and the addition of TPO to EPO + IL-3 might give rise to more erythroid bursts (p = 0.05). Paper-2116712. 2. In the present study, we investigated the angiogenic potential of recombinant human erythropoietin on cyclosporine A (CsA)- induced nephrotoxicity in the rat kidney and compared it with the effect of basic fibroblast growth factor ( bFGF), a well-known angiogenic factor. Paper-13350019. BACKGROUND AND OBJECTIVES: The anemia of low-risk myelodysplastic syndromes (MDS), refractory anemia (RA) and RA with ringed sideroblasts ( RARS), may respond to treatment with hematopoietic growth factors (GF)); erythropoietin ( Epo) +/- granulocyte colony- stimulating factor ( G-CSF). Paper-11431896. Treatment of ECFCs with wortmannin, a specific inhibitor of phosphoinositide 3-kinase ( PI3K), inhibited the antiapoptotic effect of SCF but had no effect on that of EPO, indicating that SCF but not EPO inhibits apoptosis through the PI3K pathway. Paper-8416048. The chemoattractant SDF-1 was up-regulated significantly assessed by quantitative realtime PCR and immunohistology. c-Kit(+) and CD34(+) stem cells were significantly more numerous in MI- EPO than in MIC at 24 hrs in peripheral blood (n = 7, P < 0.05) and 48 hrs in the infarcted hearts (n = 6, P < 0.001). Paper-13773603. Using our design algorithm, an unrelated protein, rat PLCdelta(1)-PH ( pleckstrin homology domain of phospholipase C-delta1), was successfully designed to bind the human erythropoietin receptor ( EPOR) after grafting the key interaction residues of human erythropoietin binding to EPOR. Paper-12476254. In several repetitive experiments, IL-4 inhibited CFU-GM colony replication by 24 to 65% in a dose-dependent fashion at concentrations ranging from 0.01 to 10 micrograms/ml when patients' cells were cultured in the presence of erythropoietin alone or with phytohemagglutinin-conditioned medium, GM-CSF, or IL-3. Paper-7570301. Total blockage of Epo secretion induced by the endoplasmic reticulum-retention amino acids Lys-Asp-Glu-Leu ( KDEL) signals in 11 lines prevented autonomous proliferation, whereas a leaky retention system, observed in 3 other lines, resulted in limited autocrine stimulation without true long-term autonomous proliferation. Paper-134718. To better understand the relationship between the expression of this fetal protein and growth, donated human erythroid progenitor cells were cultured in the presence of erythropoietin ( EPO) plus the growth- modifying cytokine stem cell factor ( SCF), and several growth-related signaling pathways were interrogated. Paper-10386566. In all patients this purified cell population showed erythroid ( burst-forming unit erythroid; BFU-E) or non-erythroid colony growth, both of which were more restricted than non-purified mononuclear cell population under stimulation with erythropoietin ( EPO) or granulocyte/macrophage colony- stimulating factor ( GM-CSF) alone. Paper-8226543. Stable overexpression of catalytically inactive SHIP decreased proliferation and resulted in prolonged activation of the extracellular signal-regulated protein kinases ERK1/2 and protein kinase B ( PKB), while wild-type SHIP did not affect EPO- mediated proliferation or phosphorylation of ERK and PKB. Paper-9083207. We hypothesize that a major mechanism for degradation of Epo in the body occurs in cells expressing the Epo receptor, through receptor-mediated endocytosis of Epo followed by degradation in lysosomes, and therefore investigated the trafficking and degradation of Epo and NESP by EpoR-expressing cells. Paper-10830112. Among the different factors with a recognized activity on blood progenitor cells, TRAIL - a member of the TNF family of cytokines - has an emerging role in the modulation of normal hematopoiesis.PKC(epsilon) levels are regulated by EPO in differentiating erythroid progenitors and control the protection against the apoptogenic effect of TRAIL. Paper-11808844. Hypoxia-inducible factor 1 ( HIF-1) is a basic helix-loop-helix transcription factor which is expressed when mammalian cells are subjected to hypoxia and which activates transcription of genes encoding erythropoietin, vascular endothelial growth factor, and other proteins that are important for maintaining oxygen homeostasis. Paper-822901. Both, in the cultured rat hepatocytes (10 U/ml for 15 minutes) and in the rat liver perfused in situ with rHu-EPO (8.9 U/ml for 15 minutes) no evidence for EPO-dependent signalling was found as indicated by missing effects of rHu-EPO on phosphorylation of JAK-2, STAT-3 and STAT-5 and on the induction of Bcl-2 mRNA. Paper-13755987. The crystal structure of erythropoietin complexed to the extracellular ligand- binding domains of the erythropoietin receptor, determined at 1.9 A from two crystal forms, shows that erythropoietin imposes a unique 120 degrees angular relationship and orientation that is responsible for optimal signalling through intracellular kinase pathways. Paper-1602681. These findings in the present study suggest that Pl3K plays a crucial role in the transducing the erythroid differentiation signal through EPOR activated by EPO- binding ib K562 cells and that the signaling pathways involved in EPO- induced erythroid differentiation differ from those involved in hemin-induced differentiation. Paper-534255. Data from this study support the hypothesis that committed HSCs ( E14 or G14) cells can still be redirected to develop into myeloid or erythroid cells when erythropoietin ( EPO) is replaced with granulocyte-colony stimulating factor ( G-CSF) under erythroid-cultured condition or G-CSF with EPO in myeloid-cultured environment, respectively. Paper-12354453. Addition of recombinant HGF significantly promoted the formation of burst-forming unit-erythroid ( BFU-E) and colony-forming unit-granulocyte erythroid macrophage (CFU-GEM) by BM mononuclear cells in the presence of erythropoietin and granulocyte-macrophage colony- stimulating factor ( GM-CSF), but the formation of CFU-GM was not modified. Paper-928638. This was confirmed by carrying out PI 3-kinase assays with anti-phosphotyrosine immunoprecipitates from erythropoietin- stimulated Y503F EpR-infected DA-3 cells and suggested that PI 3-kinase has a role in regulating erythropoietin-induced proliferation, but at a site distinct from the EpR. Paper-377086. Fetal hepatic BFU-E, unlike adult bone marrow (BM) or peripheral blood (PB) BFU-E, were capable of proliferating in response to erythropoietin in the absence of added GM colony- stimulating factor ( GM-CSF) or interleukin-3 ( IL-3), and erythropoietin ( Epo) directly stimulated the expansion of the fetal BFU-E pool in suspension culture. Paper-6226901. In the present study, we demonstrate that erythropoietin ( Epo) induces the expression and the release of tissue inhibitors of metalloproteinase-1 ( TIMP-1) in a time- and dose-dependent manner in Epo-dependent cell line UT-7 cells and in normal human erythroid progenitor cells from cord blood (CD36+) and required de novo protein synthesis. Paper-8574127. To investigate whether the formation of vascular endothelial growth factor ( VEGF) influences erythropoietin ( EPO) expression in physiological conditions, we injected into the left lateral cerebral ventricle of the Mongolian gerbil an adeno-associated virus ( AAV) vector capable of expressing the 165-amino-acid isoform of VEGF (VEGF165). Paper-12132043. Our results indicate that HIF-1alpha induces EPO gene released by astrocytes and acts as an essential mediator of neuroprotection, prove the protective role of intrinsic astrocytic-neuronal signaling pathway in hypoxic/ischemic injury and demonstrate an optimal therapeutic time-window of extrinsic rhEPO in ischemia/reperfusion injury in vitro. Paper-10846597. These in vitro results suggest that EPO enhances VEGF secretion in neural progenitor cells through activation of the PI3K/ Akt and ERK1/2 signaling pathways and that neural progenitor cells treated with rhEPO upregulate VEGFR2 expression in cerebral endothelial cells, which along with VEGF secreted by neural progenitor cells promotes angiogenesis. Paper-12849074. These synonyms are used for gene EPO (erythropoietin): MVCD2, MGC138142, Erythropoietin, EP. These accession numbers are used for gene EPO: Q549U2 (UNIPROT__AC), Q2M2L6 (UNIPROT__AC), AAF23132 (NCBI_GENBANK__AC), AAD13964 (NCBI_GENBANK__AC). EPO is a homologue of LOC100002479 (similar to Erythropoietin precursor (Erythropoietin-L2)) from Danio rerio. EPO is a homologue of EPO (erythropoietin) from Bos taurus. EPO is a homologue of EPO (erythropoietin) from Pan troglodytes. EPO is a homologue of EPO (erythropoietin) from Canis lupus familiaris. EPO is a homologue of Epo (erythropoietin) from Mus musculus. EPO is a homologue of Epo (erythropoietin) from Rattus norvegicus. EPO is a homologue of epo (erythropoietin) from Danio rerio. Important links ! iHOP - Information Hyperlinked over Proteins . Concept & Implementation by Robert Hoffmann.