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1 l cell line-derived neurotrophic factor, and FMS-like tyrosine kinase-3.
2 A 46-year-old white woman with a history of Fms-like tyrosine kinase 3 acute myeloid leukemia presen
3 verexpression have been identified including FMS-like tyrosine kinase-3 and nucleophosmin, which will
4 DC), the majority of which were derived from fms-like tyrosine kinase 3-dependent pre-DC, and CD11b(+
5 and primary patient specimens independent of Fms-like tyrosine kinase 3 expression and stromal-mediat
6 tion activating gene 1(+) lymphomyeloid, and Fms-like tyrosine kinase 3(+) fetal monocyte lineages.
7 ophage colony stimulating factor I receptor (Fms)-like tyrosine kinase 3 (Flt-3) ligand supported fur
9 in or point mutation in the kinase domain of FMS-like tyrosine kinase-3 (FLT-3) mediates ligand-indep
17 nd the ensuing expansion of T(reg) cells are Fms-like tyrosine kinase 3 (Flt3) independent, occur in
20 teosome inhibitors, antiangiogenesis agents, Fms-like tyrosine kinase 3 (FLT3) inhibitors, and apopto
29 e myeloid leukemia (AML) and determined that FMS-like tyrosine kinase 3 (FLT3) is transactivated by S
30 xclusively from pre-DCs under the control of fms-like tyrosine kinase 3 (Flt3) ligand, inhibitor of D
36 rnal tandem duplication (ITD) mutants of the Fms-like tyrosine kinase 3 (Flt3) receptor in leukemogen
37 Internal tandem duplications (ITDs) of the FMS-like tyrosine kinase 3 (FLT3) receptor tyrosine kina
39 mia (AML) harbor activating mutations in the FMS-like tyrosine kinase 3 (FLT3) receptor tyrosine kina
40 l-3-kinase (PI3K)/protein kinase B (AKT) and Fms-like tyrosine kinase 3 (FLT3) signaling are aberrant
41 on of HoxA9 and Meis1a and with mutations in FMS-like tyrosine kinase 3 (FLT3) to drive acute leukemi
44 aled that normal villus epithelium expresses Fms-like tyrosine kinase 3 (Flt3), a known regulator of
45 ation and discovered that ADP transactivates Fms-like tyrosine kinase 3 (Flt3), a receptor tyrosine k
46 cation (ITD) in the juxtamembrane portion of Fms-like tyrosine kinase 3 (FLT3), a type III receptor t
47 The ligand for the receptor tyrosine kinase fms-like tyrosine kinase 3 (flt3), also referred to as f
48 r of the type III receptor tyrosine kinases: FMS-like tyrosine kinase 3 (FLT3), platelet-derived grow
56 yrosine kinase domain (TKD) mutations of the fms-like tyrosine kinase-3 (FLT3) gene in acute myeloid
60 viously demonstrated that pretreatments with fms-like tyrosine kinase-3 (Flt3) ligand (Flt3L), a dend
62 al tandem duplication (ITD) mutations of the FMS-like tyrosine kinase-3 (FLT3) receptor found in acut
64 andem duplication (ITD) mutations within the FMS-like tyrosine kinase-3 (FLT3) render the receptor co
66 r of clinical trials testing the efficacy of FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibi
71 cluding 14 (93%) of 15 patients with mutated FMS-like tyrosine kinase-3 (FLT3; the 15th patient had c
73 ecreased in Mysm1(-/-) mice and defective in Fms-like tyrosine kinase-3(Flt3) ligand-induced, but not
74 expansion, cooperated with mutations in the FMS-like tyrosine kinase 3 gene (Flt3(ITD)) and the nucl
76 is a Janus kinase 2 (JAK2), JAK2(V617F), and Fms-like tyrosine kinase 3 inhibitor that does not inhib
81 enic tyrosine kinases, including BCR-ABL and FMS-like tyrosine kinase 3-internal tandem duplication (
82 f a juxtamembrane mutation in the FLT3 gene (FMS-like tyrosine kinase 3-internal tandem duplication [
84 treated with the hematopoietic growth factor fms-like tyrosine kinase 3 ligand (FL), which dramatical
87 observation that Langerin-CD11b- migDCs are Fms-like tyrosine kinase 3 ligand (Flt3L) dependent and
90 und that immunization of wild-type mice with FMS-like tyrosine kinase 3 ligand (Flt3L) DNA, which inc
93 ested this hypothesis by using DC-deficient, fms-like tyrosine kinase 3 ligand (Flt3L) knockout (KO)
96 Conversely, endogenous DC expansion using FMS-like tyrosine kinase 3 ligand (Flt3L) protected mice
99 d deficiency (DCML deficiency) with elevated Fms-like tyrosine kinase 3 ligand (Flt3L) was observed i
100 ge inflammatory protein-1alpha (MIP-1alpha), fms-like tyrosine kinase 3 ligand (Flt3L), and the DNA v
105 rotein 3alpha (hCCL20/hMIP-3alpha), or human fms-like tyrosine kinase 3 ligand (hFlt3-L), factors pre
106 IP-1alpha) and the DC-specific growth factor fms-like tyrosine kinase 3 ligand with the DNA vaccine r
108 nes, including caveolin-1, semaphorin E, and FMS-like tyrosine kinase 3 ligand, have putative roles i
109 ter their stimulation with stem cell factor, Fms-like tyrosine kinase 3 ligand, interleukin-3, interl
110 DC progenitors and accumulate in response to Fms-like tyrosine kinase 3 ligand, yet appear divergent
111 lls were defective in generating pDCs in the fms-like tyrosine kinase 3 ligand-based culture system a
112 DC differentiation depends on IRF-4, whereas Fms-like tyrosine kinase 3 ligand-mediated differentiati
113 freshly isolated, immunobead-purified (>90%) fms-like tyrosine kinase 3 ligand-mobilized C57BL/10 (B1
116 mon DC progenitor with conventional DCs, and Fms-like tyrosine kinase-3 ligand is essential for their
117 rsely, DC expansion induced either by Flt3L (fms-like tyrosine kinase-3 ligand) or adoptive transfer
119 endothelial cells were identified: endoglin, Fms-like tyrosine kinase-3 ligand, EGF-like repeats and
121 ion with the receptor tyrosine kinases FLT3 (Fms-like tyrosine kinase 3) or KIT-induced ligand indepe
122 ations of the receptor tyrosine kinase FLT3 (Fms-like tyrosine kinase 3) play an important role in le
124 ns leading to constitutive activation of the FMS-like tyrosine kinase 3 receptor (FLT3) occur in blas
126 ndritic cells (cDCs) requires the ligand for FMS-like tyrosine kinase 3 receptor (flt3L), but little
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