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1 at from mice lacking c-Mpl (c-Mpl(-/-)), the thrombopoietin receptor.
3 ustained response off treatment (SROT) after thrombopoietin receptor agonist (TPO-RA) discontinuation
4 xamine the in vivo effects of eltrombopag, a thrombopoietin receptor agonist (TPO-RA), on platelet fu
13 RE), we aimed to assess eltrombopag, an oral thrombopoietin receptor agonist, for thrombocytopenia (g
15 Eltrombopag, an FDA-approved non-peptidyl thrombopoietin receptor agonist, is clinically used for
18 de 3-kinase activator, in combination with a thrombopoietin-receptor agonist and the pyrimidoindole d
19 P were randomly assigned to receive the oral thrombopoietin-receptor agonist eltrombopag (30, 50, or
23 immunosuppression, eltrombopag, a synthetic thrombopoietin-receptor agonist, led to clinically signi
25 underlying etiology, include growth factors, thrombopoietin-receptor agonist, stem cell boost, transf
29 has changed with the advent of rituximab and thrombopoietin receptor agonists (TPO-RAs) as options fo
30 bundant clinical trial evidence, such as the thrombopoietin receptor agonists (TPO-RAs) rituximab and
33 efficacy and safety, in particular, for the thrombopoietin receptor agonists and the occurrence of l
35 ents respond to antithymocyte globulins, and thrombopoietin receptor agonists are under investigation
37 intravenous immunoglobulin within 2 weeks or thrombopoietin receptor agonists within 4 weeks before r
38 who achieved complete response for 1 year on thrombopoietin receptor agonists, half of the patients m
40 pecific therapies including corticosteroids, thrombopoietin receptor agonists, rituximab, and splenec
41 templating pregnancy while on treatment with thrombopoietin receptor agonists, rituximab, or mycophen
44 Combining an immunosuppressant therapy with thrombopoietin-receptor agonists may be a good strategy
45 combination of immunosuppressant therapy and thrombopoietin-receptor agonists that lasted for a media
46 ies of small peptides that bind to the human thrombopoietin receptor and compete with the binding of
47 More recently, activating mutations in the thrombopoietin receptor and in JAK2 exon 12 have been id
48 wn decreased megakaryocyte expression of the thrombopoietin receptor (c-mpl) in patients with polycyt
49 Here we describe a deletion mutant of the thrombopoietin receptor (c-mpl) that has completely lost
51 dy, we show that PF4 binds and activates the thrombopoietin receptor, cellular myeloproliferative leu
53 growth factor receptor-1 (F36VFGFR1) and the thrombopoietin receptor (F36VMpl) induced a sustained ex
55 atic activating mutations in JAK2 and in the thrombopoietin receptor gene (MPL) in most patients with
58 a chemically induced dimerizer and modified thrombopoietin receptor has now allowed the expansion of
59 mutations of the erythropoietin receptor and thrombopoietin receptor have been identified in familial
60 e discovery of an activating mutation in the thrombopoietin receptor in JAK2-negative myelofibrosis a
61 lation of proteins and the expression of the thrombopoietin receptor in platelets from patients with
62 resultant mice were compared with a Mpl-/- (thrombopoietin receptor knockout) thrombocytopenic murin
63 expression of p21(Cip1), p27(Kip1), and the thrombopoietin receptor, known regulators of HSC self-re
69 e demonstrated that mutant CALR binds to the thrombopoietin receptor MPL, and that the positive elect
70 59457 (SB), a nonpeptidyl hydrazone class of thrombopoietin receptor (Mpl) agonist, revealed toxicity
71 5R/R938Q induced spontaneous growth of Ba/F3-thrombopoietin receptor (MPL) but not of Ba/F3-human rec
76 sformation requires both mutated CRT and the thrombopoietin receptor (Mpl), but the molecular mechani
77 port here that amino acid substitutions in a thrombopoietin receptor (Mpl)--containing cell growth sw
80 a marked reduction in the expression of the thrombopoietin receptor, Mpl, in polycythemia vera (PV)
82 nner in 1 of 3 genes: JAK2, CALR, or MPL The thrombopoietin receptor, MPL, is the key cytokine recept
83 telets, and their precursors all express the thrombopoietin receptor, Mpl, on their cell surface.
84 iates the binding to, and activation of, the thrombopoietin receptor myeloproliferative leukemia prot
85 en OTT-MAL and an activating mutation of the thrombopoietin receptor myeloproliferative leukemia viru
86 tor, the erythropoietin receptor (EpoR), the thrombopoietin receptor, or the granulocyte colony-stimu
88 scribed, somatic, activating mutation in the thrombopoietin receptor that is sensitive to down-stream
89 thymic stromal lymphopoietin, eotaxin-3, and thrombopoietin receptor to the RNA-induced silencing com
90 ombopag (EP) is a small-molecule, nonpeptide thrombopoietin receptor (TPO-R) agonist that has been ap
92 downstream signaling prematurely attenuating thrombopoietin receptor (TPO-R) signaling and constraini
94 Mutations in the MPL gene encoding the human thrombopoietin receptor (TpoR) drive sporadic and famili
97 an agonist antibody to a cytokine receptor, Thrombopoietin receptor (TPOR) that effectively induces
98 ns participate in the activity states of the thrombopoietin receptor (TpoR), a type 1 cytokine recept
100 l, small-molecule, nonpeptide agonist of the thrombopoietin receptor (TpoR), being developed as a tre
101 stably and specifically interacting with the Thrombopoietin Receptor (TpoR), inducing its constitutiv
102 ors, namely the erythropoietin receptor, the thrombopoietin receptor (TpoR)/myeloproliferative leukem
103 ase 2 phosphorylation, initiated through the thrombopoietin receptor (TPOR/Mpl) activation, was affec
106 ngle transmembrane domain (TMD) of the human thrombopoietin receptor (TpoR/myeloproliferative leukemi
107 omerize with several other tagged receptors (thrombopoietin receptor, transforming growth factor beta
109 this idea, the signaling domain of Mpl (the thrombopoietin receptor) was targeted to the plasma memb