ライフサイエンスコーパス: TPO

1 TPO agonist antibodies are monoclonal antibodies activat

2 TPO also controlled MEIS1 expression at mRNA levels, at

3 TPO and CXCL12 regulate beta4GalT1 in the MK lineage.

4 TPO causes megakaryocyte proliferation and increased pla

5 TPO directly affects the double-strand break (DSB) repai

6 TPO levels did not correlate with platelet count and wer

7 TPO peptide mimetics contain TPO receptor-activating pep

8 TPO was added to ROO and RSO at four different concentra

9 TPO-mediated phosphorylation of STAT5 triggers its genom

10 TPO-RAs induce platelet counts > 50 000/muL in 60%-90% o

11 n GPVI-expressive cell lines, including UT-7/TPO and CHRF288-11.

12 ced the nuclear import of HOXA9 both in UT-7/TPO cells and in primitive Sca-1(+)/c-kit(+)/Gr-1(-) hem

13 as added to a megakaryocytic cell line, UT-7/TPO, the cells ceased cell division but continued to acc

14 Both of these pathways are required for a TPO-mediated increase in DSB repair.

15 cell proliferation and megakaryopoiesis in a TPO-independent fashion, inducing LPS-like responses, su

16 Eltrombopag is a TPO nonpeptide mimetic administered orally that activate

17 Romiplostim is a TPO peptide mimetic given by subcutaneous injection that

18 in HSC expansion conditions (SFEM with added TPO, SCF, FLT3L, IL3 and IL6) in the presence of UM171 p

19 t not in CD41+-enriched cells obtained after TPO differentiation.

20 rombopag, a thrombopoietin receptor agonist (TPO-RA), on platelet function and reactivity.

21 uximab and thrombopoietin receptor agonists (TPO-RAs) as options for second-line therapy.

22 OF REVIEW: Thrombopoietin-receptor agonists (TPO-RAs) have been approved for use in immune thrombocyt

23 duction by thrombopoietin-receptor agonists (TPO-RAs) is an effective second-line treatment in immune

24 own pathological situation caused by altered TPO signaling, and found that the EDA FN is increased in

25 negative regulator of JAK2 in stem cells and TPO/Mpl/JAK2/Lnk as a major regulatory pathway in contro

26 erse relationship between platelet count and TPO levels was not observed in ALF.

27 showed similar connections with Ri, Ig, and TPO.

28 it-megakaryocytes (CFU-MK) are increased and TPO-induced expansion of primary marrow cells yielded a

29 only one that enhanced SCF, Flt3 ligand, and TPO expansion of myeloid progenitor cells ex vivo.

30 BVE-PTC tumors subcutaneously into nude and TPO-Braf(WT) mice.

31 planted tumors was observed in both nude and TPO-Braf(WT) mice.

32 telets were observed only in the spleen, and TPO levels remained unaltered.

33 9-/- as well as thrombocytopenic Thpo-/- and TPO receptor-deficient (Mpl-/-) mice.

34 had reliable connections with areas Tpt and TPO, which are sites of multisensory integration.

35 the correction of ischemia in wild-type and TPO(-/-), but not c-mpl(-/-), mice.

36 ine (FT4), thyroid peroxidase antibody (Anti-TPO), and thyroid stimulating hormone (TSH).

37 Men were less likely to be anti-TPO positive compared to women (p < 0.001).

38 in serum are 1.7 IU/mL and 6 IU/mL for anti-TPO and anti-TG, respectively.

39 ithyroid AAbs (strong evidence) and IgE-anti-TPO (weak evidence) than controls.

40 IgE levels (P < 0.0001) and higher IgG anti-TPO levels (P < 0.001).

41 anti-IgE; IgG-anti-thyroperoxidase (IgG anti-TPO); total serum IgE; and basophil reactivity (BASO) us

42 ere no differences in the prevalence of anti-TPO antibodies and AGTAs.

43 s (AGTAs), and anti-thyroid peroxidase (anti-TPO) antibodies were measured.

44 (anti-TG) and anti-thyroid peroxidase (anti-TPO) as models.

45 g with concomitant elimination of serum anti-TPO antibodies, may elucidate disease mechanisms.

46 fatigue questionnaire scores, and serum anti-TPO antibody titers at 6, 12, and 18 months.

47 Median serum anti-TPO antibody titers decreased from 2232 to 152 IU/mL, fo

48 or and CD150(+)CD9(hi)endoglin(lo) cells are TPO-responsive and that the latter population specifical

49 Area TPO in the upper bank of the superior temporal sulcus (S

50 tal, the lateral parietal cortices, and area TPO, as well as the thalamus, where projections from som

51 Three subdivisions of area TPO (TPOr, TPOi, and TPOc) were examined with cytochrome

52 as TS1-3, and from the middle sector of area TPO in the superior temporal sulcus.

53 temporo-parieto-occipital association area (TPO), PGa, and IPa], the motion complex [including media

54 Orally available, TPO nonpeptide mimetics (eltrombopag, AKR-501) bind and

55 is species specific in that it can only bind TPO-R in human and primate cells, these findings further

56 th a specific inhibitor substantially blunts TPO-induced growth of single sca-1(+)/c-kit(+)/Gr-1(-) m

57 ous signal transduction molecules induced by TPO, we found that p38 mitogen-activated protein kinase

58 hylation, which can be directly initiated by TPO.

59 Therefore, RAG2(-/-)gamma(c)(-/-) TPO-humanized mice represent a useful model to study hum

60 wer levels of MPL than normal CD34(+) cells, TPO promoted the proliferation of MF CD34(+) cells and H

61 rophiles also provided a library of P-chiral TPOs in high enantiomeric purity.

62 e expression signature indicative of chronic TPO overstimulation as the underlying causative mechanis

63 tive mechanism, despite a normal circulating TPO level.

64 Collectively, TPO modulates the function of HOXA9 by leading to its nu

65 TPO peptide mimetics contain TPO receptor-activating peptides inserted into complemen

66 Endocytic AMR controls TPO expression through Janus kinase 2 (JAK2) and the acu

67 mmunoglobuln type (domain subclass-converted TPO agonist antibodies; ie, MA01G4G344).

68 y could not unmask an immunodominant cryptic TPO epitope.

69 Thus, we hypothesized that host-derived TPO, present in the tumor microenvironment, or pharmacol

70 the epitopes recognized by the 10 different TPO-specific T cell clones.

71 l epitope repertoire recognized by different TPO-specific T cell clones.

72 ne-rescued megakaryocytes exhibit diminished TPO-dependent kinase phosphorylation and reduced platele

73 ng that KCNQ1-KCNE2 is not required for Duox/TPO-mediated I(-) organification.

74 enitors and of MKs and PLTs via dysregulated TPO turnover.

75 ocytopenia in a manner additive with earlier TPO treatment.

76 creasing MPL signaling and conferring either TPO hypersensitivity or independence to expressing cells

77 When applied to enamel, TPO-only adhesives had ~80% DC in resin, which gradually

78 failure, despite already elevated endogenous TPO levels.

79 ion of neutralizing antibodies to endogenous TPO.

80 which had no sequence homology to endogenous TPOs, studies confirmed clinical effect.

81 g pathways will provide a means of enhancing TPO-desirable effects on HSCs and improving the safety o

82 To examine TPO surface distribution in thyrocyte cell lines, we pre

83 Even after excluding TPO-Ab and low-titer GAD65-Ab, Abs strongly suggesting a

84 orylated tyrosine residues in JAK2 following TPO stimulation.

85 e TPO receptor by a mechanism different from TPO and may have an additive effect to TPO.

86 Furthermore, TPO-stimulated cellular proliferation appears to be dire

87 tion-specific differentially expressed gene, TPO, was validated at the protein level using immunohist

88 Like other glycoproteins, TPO molecules in transit to the cell surface have the po

89 Lyn-deficient MKs supported greater TPO-mediated phosphorylation and kinase activity of both

90 b, 2 (1.8%) had GAD65-Ab and VGKCc-Ab, 1 had TPO-Ab and GAD65-Ab, and 1 had anti-Hu Ab and GAD65-Ab.

91 tients included in the study, 15 (13.4%) had TPO-Ab, 14 (12.5%) had GAD65-Ab, 12 (10.7%) had VGKCc (4

92 detected in 7 patients (6.3%): 3 (2.7%) had TPO-Ab and voltage-gated potassium channel complex (VGKC

93 ortional hazard model demonstrated that high TPO levels were associated with shorter survival (P < .0

94 r adoptive transfer in immunodeficient human TPO-transgenic mice.

95 When tested in healthy humans, TPO peptide and nonpeptide mimetics produced a dose-depe

96 However, impaired TPO homeostasis in the transgene-rescued mice produces e

97 endogenous angiogenic response is blunted in TPO(-/-) and c-mpl(-/-) mice.

98 the role of specific hematopoietic cells in TPO-dependent hematopoiesis, we generated mice that expr

99 age-negative murine marrow cells cultured in TPO, Flt3 ligand, and SCF, without affecting the rate of

100 gical inhibition of TLR4 or TLR4 deletion in TPO(high) mice abrogated Mk hyperplasia, BM fibrosis, IL

101 elp identify the receptor motifs involved in TPO-induced internalization of Mpl and suggest that Mpl

102 1 staining was detected in nearly all MKs in TPO-stimulated BM cultures.

103 und that p110beta plays an essential role in TPO-mediated (i) priming of protease-activated receptor

104 RISC knockdown was associated with increased TPO-mediated JAK2 activation and protein levels, and inc

105 at SOCS1 expression is sufficient to inhibit TPO-induced STAT5 phosphorylation.

106 nts continued to grow when transplanted into TPO-Braf(V600E) mice.

107 IPCs derived from HPCs in FLT3-L/TPO cultures display blood IPC phenotype and have the ca

108 stal hematopoietic receptor domain just like TPO.

109 Many TPOs undergo considerable reduction at ambient temperatu

110 We demonstrate that JAK2 and MPL mediate TPO-induced proliferation arrest and megakaryocytic diff

111 ty and cell-surface expression, and mediates TPO-induced signal transduction.

112 in which we replaced the gene encoding mouse TPO by its human homolog.

113 ification of cancer cells to express the NIS/TPO genes.

114 10, or 20 mg), an investigational nonpeptide TPO-RA active in humans, or placebo; subjects completing

115 n, suppress this antiproliferative action of TPO.

116 loproliferation by restricting the amount of TPO available to stimulate the production of megakaryocy

117 Subsequent analysis of TPO signaling revealed enhanced Akt and ERK1/2 phosphory

118 of strategies to disrupt the association of TPO with its receptor as a means of targeting MF hematop

119 No risk was found for children of TPO-antibody-positive mothers (n=308).

120 urement of the intracellular distribution of TPO has often relied on this assumption.

121 The protective effect of TPO against the primary oxidation of these refined oils

122 2008 two new drugs that mimic the effect of TPO became available to treat thrombocytopenia.

123 istration of AdTPO showed that the effect of TPO gene transfer was systemic, not local, and it could

124 ta and p110gamma contribute to the effect of TPO on ERK1/2 phosphorylation and TxA(2) formation.

125 mpletely prevented the synergistic effect of TPO on ERK1/2 phosphorylation and TxA(2) synthesis.

126 More importantly, the synergistic effect of TPO on phosphorylation of extracellular-regulated kinase

127 isoforms involved in mediating the effect of TPO on platelet function and elucidate the underlying me

128 In conclusion, the synergistic effect of TPO on RAP1 and integrin activation is largely mediated

129 cts of beta2-M were masked by the effects of TPO in the patients with TPO levels higher than 639 pg/m

130 our studies, we investigated the effects of TPO on HOXA9 in this same cell population.

131 The efficacy of TPO in stabilizing refined olive (ROO) and sunflower (RS

132 ITP, more studies are providing evidence of TPO-RA efficacy and safety, as well as their applicabili

133 The fraction of TPO-RA-treated patients who will be treatment-free after

134 fficiency of 250microg/g and 2000microg/g of TPO, referring to 5microg/g and 40microg/g of lycopene,

135 bopoietic growth factors stimulate growth of TPO-dependent cell lines via JAK2/STAT signaling pathway

136 Homozygous humanization of TPO led to increased levels of human engraftment in the

137 at the antileukemic effect is independent of TPO-R.

138 Higher levels of TPO were associated with advanced Rai stage (P < .001),

139 AK2V617F(+) transgenic mice, whereas loss of TPO only mildly affects the disease phenotype.

140 bopag, a synthetic small molecule mimetic of TPO that interacts with c-MPL at a position distinct fro

141 inding site, contributing to perturbation of TPO-induced signaling pathways and decreased survival of

142 Thus, IFN-gamma-mediated perturbation of TPO:c-MPL complex formation and the resulting inhibition

143 actionated distinctly from internal pools of TPO (that co-fractionate with calnexin), yet surface TPO

144 We suggest that the presence of TPO in the thyroid draining lymph nodes induces the acti

145 se data suggest that SFKs modify the rate of TPO-induced proliferation and are likely to affect cell

146 s that Lyn kinase is a negative regulator of TPO signaling.

147 y, we have demonstrated that upon removal of TPO from the supernatant, Mpl promptly reappears on the

148 is increasing interest to expand the role of TPO-RAs, both in ITP as well as in other thrombocytopeni

149 tinct from the extracellular binding site of TPO, bypasses this inhibition, providing an explanation

150 emical components within the subdivisions of TPO.

151 gree of hypothyroidism nor with the titer of TPO antibodies.

152 vation, adenovirus (Ad)-mediated transfer of TPO (AdTPO) enhanced the correction of ischemia in wild-

153 The use of TPO-RAs continues to grow as more evidence of safety and

154 Use of TPO-RAs in hepatitis C has shown early success in allowi

155 The use of TPO-RAs in myelodysplastic syndrome (MDS) is questionabl

156 the development of the second generation of TPOs, which had no sequence homology to endogenous TPOs,

157 Tomato peels oleoresin, TPO, exhibited competitive free radicals scavenging acti

158 This suggests that platelets in patients on TPO-R treatment may play a role in improving Treg functi

159 ndardized uptake value and TSH (P = 0.09) or TPO antibody (P = 0.68) levels.

160 rombocytopenic, TPO-deficient (Thpo(-/-)) or TPO receptor-deficient (Mpl(-/-)) mice.

161 rates and AE incidence comparable with other TPO-RAs.

162 nd trimethylbenzoyl-diphenylphosphine oxide (TPO) as photoinitiator.

163 The reduction of tertiary phosphine oxides (TPOs) and sulfides with diisobutylaluminum hydride (DIBA

164 oxides (SPOs) and tertiary phosphine oxides (TPOs), was developed.

165 The peak TPO level did not correlate with the nadir platelet coun

166 lating hormone (TSH) and thyroid peroxidase (TPO) antibody levels using regression analysis.

167 Levels of IgG against thyroid peroxidase (TPO) are more often elevated in CSU than those of other

168 fic for the self-antigen thyroid peroxidase (TPO) is positively selected in the thymus of RAG KO mice

169 yroid hormone synthesis, thyroid peroxidase (TPO) molecules must be transported from the endoplasmic

170 for the main autoantigen thyroid peroxidase (TPO).

171 ree thyroxine [fT4], and thyroid peroxidase [TPO] antibodies) were assessed in 5,100 women.

172 uperior temporal sulcus including areas PGa, TPO, and MST, from the visuospatial parietal area PG-Opt

173 Plasma TPO and beta2-M may be useful for the prediction of clin

174 nsgene-rescued mice produces elevated plasma TPO levels, which serves as an unchecked stimulus to dri

175 s responding to either endogenously produced TPO (a microenvironment factor in hematologic malignanci

176 inase activity, particularly after prolonged TPO stimulation.

177 which is necessary and sufficient to promote TPO-increased DNA-PK activation and NHEJ DSB repair in b

178 ecruited to the TME of Braf(V600E)/Pten(-/-)/TPO-Cre thyroid tumors.

179 hanced the motility of Braf(V600E)/Pten(-/-)/TPO-Cre tumor cells in vitro In clinical specimens, we f

180 xtracellular matrix of Braf(V600E)/Pten(-/-)/TPO-Cre tumors was enriched with stromal-derived fibrill

181 BRAF and loss of Pten (Braf(V600E)/Pten(-/-)/TPO-Cre) leads to papillary thyroid cancers (PTC) that r

182 ished upon expression of recombinant rat (r) TPO in 293 cells, which were heterogeneous for surface e

183 XRD, Raman, TPO, and TEM analysis confirmed that the deactivation of

184 ines, we prepared new antibodies against rat TPO.

185 olecule, nonpeptide thrombopoietin receptor (TPO-R) agonist that has been approved recently for the t

186 ring treatment with thrombopoietin receptor (TPO-R) agonists (n = 9).

187 zing antibodies to some forms of recombinant TPO.

188 , confirming a role for ERK1/2 in regulating TPO-mediated increases in TxA(2) synthesis.

189 opoiesis, initially by negatively regulating TPO signaling and later by augmenting proplatelet produc

190 ine also exhibits almost no endo H-resistant TPO, much of the endogenous rTPO is localized to the cel

191 he thrombopoietin (TPO) mimetic romiplostim (TPO(high)).

192 A serum-free medium containing SCF, TPO, and FGF-1 or Flt3-L cannot significantly support ex

193 A serum-free culture containing SCF, TPO, FGF-1, angiopoietin-like 5, and IGFBP2 supports an

194 ured in serum-free medium together with SCF, TPO, FGF, with or without Igfbp2 and Angptl5 (STF/STFIA

195 Despite severe hepatic dysfunction, serum TPO levels were initially normal and increased during ho

196 ating the TPO receptor but modified in size [TPO minibodies; ie, VB22B sc(Fv)(2)] or immunoglobuln ty

197 t co-fractionate with calnexin), yet surface TPO molecules remained endoglycosidase H (endo H)-sensit

198 ow cells derived from Tpo(-/-) mice and that TPO induces VEGF transcripts in these primitive hematopo

199 Additional studies determined that TPO induces VEGF expression by increasing the level of i

200 Along with previous findings that TPO affects Hox transcription factors that regulate HSC

201 We found that TPO correlated strongly in a continuous manner with over

202 tion factor were not affected, we found that TPO induced the nuclear import of HOXA9 both in UT-7/TPO

203 We show here that TPO specifically triggers Erk and nuclear factor kappaB

204 Thus, we tested the hypothesis that TPO affects the autocrine production of VEGF to account

205 We hypothesized that TPO gene transfer should enhance correction of experimen

206 Mechanistic studies revealed that TPO stimulation of MKs from lyn(-/-) mice did not affect

207 Stem Cell, de Laval et al. (2013) show that TPO can also promote "healthy" hematopoietic stem cells

208 opyrimidine 1 and 2 (PP1, PP2), we show that TPO-dependent proliferation of BaF3/Mpl cells was enhanc

209 Results showed that TPO+4E adhesives reached DC similar to TPO-only counterp

210 Our data suggest that TPO controls HSC development through the regulation of m

211 These data suggest that TPO supports progenitor cell expansion, whereas chemokin

212 by other HSC growth factors, suggesting that TPO triggers a specific signal in HSCs facilitating DNA-

213 (eltrombopag, AKR-501) bind and activate the TPO receptor by a mechanism different from TPO and may h

214 by subcutaneous injection that activates the TPO receptor by binding to the distal hematopoietic rece

215 metic administered orally that activates the TPO receptor by binding to the transmembrane domain.

216 ies are monoclonal antibodies activating the TPO receptor but modified in size [TPO minibodies; ie, V

217 TIBAO selectively coordinates the TPO starting material, preventing further reduction.

218 reover, VEGF expression is important for the TPO effect on primitive hematopoietic cells because bloc

219 rotein kinase (MAPK) was responsible for the TPO-induced Hoxb4 elevation.

220 ts, even in the absence of components in the TPO-c-mpl-megakaryocyte-platelet pathway.

221 hat Hoxb4 might mediate at least part of the TPO effect on these cells.

222 his hypothesis, we dissected the role of the TPO-c-mpl-megakaryocyte-platelet pathway in the angiogen

223 tion, indicating that internalization of the TPO/Mpl complex may be essential for normal signal trans

224 re present in all immune organs, whereas the TPO-specific T(reg) are present in all lymphoid organs w

225 uce platelet production in thrombocytopenic, TPO-deficient (Thpo(-/-)) or TPO receptor-deficient (Mpl

226 Thrombopoietin (TPO) acting via its receptor, the cellular homologue of

227 Thrombopoietin (TPO) attracts much attention as an effective stimulus fo

228 Thrombopoietin (TPO) enhances platelet activation through activation of

229 Thrombopoietin (TPO) has been demonstrated as a crucial cytokine support

230 Thrombopoietin (TPO), the primary regulator of thrombopoiesis, is also a

231 s in the presence of dox and thrombopoietin (TPO) resulted in an exponential (at least 10(1)(3)-fold)

232 r was discovered in 1991 and thrombopoietin (TPO) was purified in 1994, the development of a clinical

233 ptors VEGFR1 and VEGFR2, and thrombopoietin (TPO) were measured in plasma samples of 95 patients by e

234 cently, interactions between thrombopoietin (TPO) and its receptor, the myeloproliferative leukemia (

235 thrombocytopenia by blocking thrombopoietin (TPO) signaling and therefore differentiation of stem cel

236 tion, signaling initiated by thrombopoietin (TPO) activation of its receptor, myeloproliferative leuk

237 iation process, regulated by thrombopoietin (TPO), on binding to its cognate receptor myeloproliferat

238 ng DNA damage are rescued by thrombopoietin (TPO)-mediated DNA repair.1 It has been recently demonstr

239 ion that can be initiated by thrombopoietin (TPO).

240 expansion through dampening thrombopoietin (TPO)-induced JAK2 signaling.

241 leukemia), the receptor for thrombopoietin (TPO), in T cells.

242 fied mouse MKs isolated from thrombopoietin (TPO)-treated bone marrow (BM) cultures indicated high ex

243 imately leading to increased thrombopoietin (TPO) production in the liver.

244 r stimulation by its ligand, thrombopoietin (TPO).

245 fragments (Fabs) that mimic thrombopoietin (TPO) were created.

246 led by circulating levels of thrombopoietin (TPO) functioning to activate megakaryocyte differentiati

247 d with rapid upregulation of thrombopoietin (TPO) messenger RNA.

248 nduces hepatic expression of thrombopoietin (TPO) mRNA and protein, thereby regulating platelet produ

249 prevents full engagement of thrombopoietin (TPO), a primary positive regulator of HSPC survival, to

250 trate that in the absence of thrombopoietin (TPO), tyrosine-unphosphorylated STAT5 (uSTAT5) is presen

251 o be a negative regulator of thrombopoietin (TPO)-induced proliferation.

252 gulating the plasma level of thrombopoietin (TPO).

253 kinase inhibitor, SU6656, on thrombopoietin (TPO)-induced growth and differentiation.

254 ed the association of plasma thrombopoietin (TPO) and overall survival in 127 patients with previousl

255 is leads to increased plasma thrombopoietin (TPO) levels and perturbed hematopoietic stem cells (HSCs

256 helial cells (BMECs) promote thrombopoietin (TPO)-independent platelet production.

257 upon self-renewal promoting thrombopoietin (TPO)-MPL-STAT5 signalling.

258 show that IFN-gamma reduces thrombopoietin (TPO)-mediated phosphorylation of signal transducer and a

259 associated with up-regulated thrombopoietin (TPO) signaling through mammalian target of rapamycin (mT

260 s of stem cell factor (SCF), thrombopoietin (TPO), insulin-like growth factor 2 (IGF-2), and fibrobla

261 Serum thrombopoietin (TPO) was maintained at normal levels in Pf4-Cre-positive

262 Soluble Kit-ligand (sKitL), thrombopoietin (TPO, encoded by Thpo) and, to a lesser extent, erythropo

263 studies we demonstrated that thrombopoietin (TPO) enhances levels of HOXB4 mRNA in primitive hematopo

264 e have previously shown that thrombopoietin (TPO), a critical HSC regulator, ensures HSC chromosomal

265 is study we demonstrate that thrombopoietin (TPO)-stimulated Src family kinases (SFKs) inhibit cellul

266 osis upon treatment with the thrombopoietin (TPO) mimetic romiplostim (TPO(high)).

267 ll surface expression of the thrombopoietin (TPO) receptor (c-MPL) and enhanced proliferation.

268 ere we show that loss of the thrombopoietin (TPO) receptor (MPL) significantly ameliorates MPN develo

269 9, specifically activate the thrombopoietin (TPO) receptor (MPL) to induce constitutive activation of

270 with mutations in JAK2, the thrombopoietin (TPO) receptor (MPL), and the calreticulin (CALR) genes.

271 bnormal interaction with the thrombopoietin (TPO) receptor (MPL).

272 HSCs are hyperresponsive to thrombopoietin (TPO) and display elevated levels of STAT5 phosphorylatio

273 n a medium supplemented with thrombopoietin (TPO) for 18 days.

274 ib1(-/-) mice, cultured with thrombopoietin (TPO) for 24 hours, produced more highly polyploid megaka

275 h factors (recombinant human thrombopoietin [TPO] and pegylated recombinant human megakaryocyte growt

276 covery that the recombinant thrombopoietins (TPOs) could enhance platelet production in a variety of

277 Thus, TPO signaling in megakaryocytes is dispensable for plate

278 iodide symporter (NIS) and thyroperoxidase (TPO) genes.

279 encephalitis Abs as well as thyroperoxidase (TPO) and glutamic acid decarboxylase 65 (GAD65) Abs.

280 Rat and mouse thyroid tissue TPO also shows little or no endo H resistance, although

281 from TPO and may have an additive effect to TPO.

282 b59, which was estimated to be equipotent to TPO.

283 cells expand and proliferate in response to TPO, and persist longer after adoptive transfer in immun

284 tivation of JAK2 specifically in response to TPO.

285 that TPO+4E adhesives reached DC similar to TPO-only counterparts upon completion of light irradiati

286 del of acute hindlimb ischemia of wild-type, TPO(-/-), and c-mpl(-/-) mice.

287 pho-JAK2 were rapidly K63-ubiquitinated upon TPO stimulation, and this action was augmented in cells

288 1994, the development of a clinically useful TPO was hampered by the appearance of neutralizing antib

289 to threefold reduced ability to sustain UT7-TPO cells, which require THPO for proliferation.

290 thyroid-specific expression of Braf(V600E) (TPO-Braf(V600E)) develop PTC rapidly with high levels of

291 is process, we first crossed LSL-Braf(V600E)/TPO-Cre with TshR knockout mice.

292 knock-in of oncogenic Braf (LSL-Braf(V600E)/TPO-Cre) to explore the role of endogenous expression of

293 etion of the Gsalpha gene in LSL-Braf(V600E)/TPO-Cre/Gnas-E1(fl/fl) mice also resulted in an attenuat

294 s could modulate the epitope repertoire when TPO was added exogenously and when expressed constitutiv

295 d thrombocytopenia is indeed reversible when TPO agonists are administered in the absence of selinexo

296 adually descended to ~50% in enamel, whereas TPO+4E adhesives consistently scored ~80% DC across the

297 ells, we treated human cord blood cells with TPO.

298 d by the effects of TPO in the patients with TPO levels higher than 639 pg/mL, but in the remainder,

299 emia virus ligand (c-Mpl), were treated with TPO, demethylation of the GP6 promoter was induced.

300 ced in Cib1(-/-) megakaryocytes treated with TPO.