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 causes megakaryocyte proliferation and increased pla

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

5 TPO is produced in the liver and levels are low in patie

6 TPO levels did not correlate with platelet count and wer

7 TPO levels from hospital day 2 were elevated in 43% of p

8 TPO peptide mimetics contain TPO receptor-activating pep

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

10 TPO with the CCP-like domain deleted expressed normally

11 TPO-mediated phosphorylation of STAT5 triggers its genom

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

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

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

15 ion of the gene 2- to 3-fold in EML and UT-7/TPO cells.

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

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

18 Eltrombopag is a TPO nonpeptide mimetic administered orally that activate

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

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

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

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

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

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

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 ivation is the triggering event of G-CSF and TPO receptor function.

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

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

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

31 Expression of NIS and TPO facilitated concentration of iodide in tumors.

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

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

34 9-/- as well as thrombocytopenic Thpo-/- and TPO receptor-deficient (Mpl-/-) mice.

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

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

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

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

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

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

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

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

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

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

45 he findings support the parcellation of area TPO into three subdivisions and extend findings of chemo

46 rchitecture and cortical connections of area TPO, the upper bank of the STS was sectioned tangential

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

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

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

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

51 egulate Hoxb4 expression, is also induced by TPO in a p38-dependent manner.

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

53 hylation, which can be directly initiated by TPO.

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

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

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

57 tive mechanism, despite a normal circulating TPO level.

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

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

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

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

62 y could not unmask an immunodominant cryptic TPO epitope.

63 We analyzed daily TPO levels for the first week of hospitalization in 12 p

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

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

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

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

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

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

70 ocytopenia in a manner additive with earlier TPO treatment.

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

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

73 ion of neutralizing antibodies to endogenous TPO.

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

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

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

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

78 orylated tyrosine residues in JAK2 following TPO stimulation.

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

80 This factor is distinct from TPO because it induces endomitosis in IL-3-generated meg

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

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

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

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

85 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.

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

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

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

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

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

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

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

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

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

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

96 1 staining was detected in nearly all MKs in TPO-stimulated BM cultures.

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

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

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

100 Full-length TPO is secreted at levels 10-20-fold greater than trunca

101 rleukin-3, growth hormone, or of full-length TPO.

102 stal hematopoietic receptor domain just like TPO.

103 ssion in primitive hematopoietic cell lines; TPO increased expression of the gene 2- to 3-fold in EML

104 Many TPOs undergo considerable reduction at ambient temperatu

105 with acute liver failure (ALF), we measured TPO concentrations (normal TPO range, 31 to 136 pg/mL) i

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

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

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

109 s in patients' sera, to detect these mutated TPO molecules by flow cytometry.

110 in significant tumor volume reduction in NIS/TPO-modified tumor xenografts without apparent adverse e

111 of iodide, apoptosis was seen in >95% of NIS/TPO-modified lung cancer cells.

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

113 10, or 20 mg), an investigational nonpeptide TPO-RA active in humans, or placebo; subjects completing

114 ALF), we measured TPO concentrations (normal TPO range, 31 to 136 pg/mL) in 51 patients with ALF to d

115 (*)OH addition to the aminoxyl moiety of 4-O-TPO and H-atom abstraction from the 2- or 6-methyl group

116 monstrated that (*)OH partially oxidizes 4-O-TPO to the corresponding oxoammonium cation.

117 n, suppress this antiproliferative action of TPO.

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

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

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

121 ned of the molecular and cellular biology of TPO and its receptor during the past several years, and

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

123 is not altered by optimal concentrations of TPO.

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

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

126 2008 two new drugs that mimic the effect of TPO became available to treat thrombocytopenia.

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

128 SF can compensate for the myeloid effects of TPO deficiency by expanding the pool of cells between th

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 We first analyzed the effects of TPO on Hoxb4 expression in primitive hematopoietic cell

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 We conclude that TGD enhances secretion of TPO and can additionally function as an inter-molecular

147 emical components within the subdivisions of TPO.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 Thyroid peroxidase (TPO) autoantibody epitopes are largely restricted to an

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

166 for the main autoantigen thyroid peroxidase (TPO).

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

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

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

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

171 at define the TPO IDR, as well as polyclonal TPO autoantibodies in patients' sera, to detect these mu

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

173 inase activity, particularly after prolonged TPO stimulation.

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

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

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

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

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

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

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

181 ines, we prepared new antibodies against rat TPO.

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

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

184 zing antibodies to some forms of recombinant TPO.

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

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

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

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

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

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

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

192 r survival-promoting cytokines (GM-CSF, SLF, TPO, and FL).

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

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

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

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

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

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

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

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

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

202 and ERK is provided by the observations that TPO, which activates RAS but not protein kinase C, does

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

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

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

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

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

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

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

210 The TPO extracellular region comprises a large myeloperoxida

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

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

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

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

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

216 an monoclonal autoantibodies that define the TPO IDR, as well as polyclonal TPO autoantibodies in pat

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

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

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

220 like domains as the putative location of the TPO autoantibody IDR.

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

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

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

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

228 Thrombopoietin (TPO) is the primary regulator of platelet production.

229 Thrombopoietin (TPO), the primary regulator of platelet production, also

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

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

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

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

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

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

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

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

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

249 gulating the plasma level of thrombopoietin (TPO).

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

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

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

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

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

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

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

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

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

259 The term thrombopoietin (TPO) was first coined in 1958 and used to describe the h

260 Here we show that thrombopoietin (TPO) cooperates with FLT3-L, inducing CD34+ HPCs to unde

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

262 es of evidence indicate that thrombopoietin (TPO) substantially impacts the number of hematopoietic s

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

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

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

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

267 9, specifically activate the thrombopoietin (TPO) receptor (MPL) to induce constitutive activation of

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

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

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

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

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

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

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

275 Thus, TPO signaling in megakaryocytes is dispensable for plate

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

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

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

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

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

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

282 tivation of JAK2 specifically in response to TPO.

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

284 at levels 10-20-fold greater than truncated TPO.

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

286 1994, the development of a clinically useful TPO was hampered by the appearance of neutralizing antib

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

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

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

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

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

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

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

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

295 3-generated megakaryocytes in vitro, whereas TPO does not, and its activity on megakaryocyte ploidy i

296 To determine whether TPO supports the impressive expansion of HSC observed fo

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.