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1 by two homologous tyrosine kinase receptors, fms-like tyrosine kinase 1 (Flt-1) and kinase domain rec
3 r endothelial growth factor and its receptor fms-like tyrosine kinase 1 (Flt1) were up-regulated, and
7 e placental growth factor (PlGF) and soluble Fms-like tyrosine kinase 1 (sFlt-1) as clinical biomarke
12 s of placental growth factor (PlGF), soluble fms-like tyrosine kinase 1 (sFlt-1), and soluble endogli
13 ns of VEGF and its soluble receptor, soluble fms-like tyrosine kinase 1 (sFlt-1), were measured by en
14 data suggest that excess circulating soluble fms-like tyrosine kinase 1 (sFlt-1), which binds placent
15 levels of other angiogenic proteins [soluble fms-like tyrosine kinase 1 (sFlt1) and placental growth
16 ured plasma levels of antiangiogenic soluble fms-like tyrosine kinase 1 (sFlt1) and proangiogenic pla
19 rictor sensitivity and elevations in soluble fms-like tyrosine kinase 1 (sFLT1), a circulating antian
20 g PM, placental trophoblasts produce soluble fms-like tyrosine kinase 1 (sFlt1), also known as solubl
24 uteroplacental tissues, and elevated soluble fms-like tyrosine kinase 1 and soluble endoglin, markers
25 giogenic ligand PlGF and its target receptor fms-like tyrosine kinase 1 modulate vascular growth and
27 t tertile of the antepartum ratio of soluble fms-like tyrosine kinase 1 to placental growth factor wa
29 This locus is near the FLT1 gene encoding Fms-like tyrosine kinase 1, providing biological support
32 dothelial growth factor (VEGF) receptor-1 or Fms-like tyrosine kinase-1 (Flt-1) but not VEGF receptor
33 receptors, fetal liver kinase-1 (flk-1) and fms-like tyrosine kinase-1 (flt-1), was examined in rat
35 s, placental-like growth factor, and soluble Fms-like tyrosine kinase-1 (sFlt-1) are associated with
36 inetics of the antiangiogenic factor soluble Fms-like tyrosine kinase-1 (sFlt-1) in 136 consecutive R
37 regulation of expression of VEGF or soluble fms-like tyrosine kinase-1 (sFlt-1) in both an aortic ri
38 with increased circulating levels of soluble fms-like tyrosine kinase-1 (sFlt-1) in the third trimest
41 lampsia is associated with increased soluble fms-like tyrosine kinase-1 (sFlt-1), a circulating antag
42 nta-derived growth factor (PLGF) and soluble Fms-like tyrosine kinase-1 (sFLT-1, the soluble form of
44 rong evidence that overproduction of soluble fms-like tyrosine kinase-1 (sFLT1) in the placenta is a
45 giogenic factor and preeclampsia risk marker fms-like tyrosine kinase-1 (sFLT1) in the placenta tissu
46 ound, GYY4137, inhibited circulating soluble fms-like tyrosine kinase-1 and soluble endoglin levels a
47 rfering RNA increased the release of soluble fms-like tyrosine kinase-1 and soluble endoglin, as asse
49 giogenesis by inducing both sEng and soluble fms-like tyrosine kinase-1 secretion from human villous
51 ophage colony stimulating factor I receptor (Fms)-like tyrosine kinase 3 (Flt-3) ligand supported fur
58 nd the ensuing expansion of T(reg) cells are Fms-like tyrosine kinase 3 (Flt3) independent, occur in
61 teosome inhibitors, antiangiogenesis agents, Fms-like tyrosine kinase 3 (FLT3) inhibitors, and apopto
70 e myeloid leukemia (AML) and determined that FMS-like tyrosine kinase 3 (FLT3) is transactivated by S
71 xclusively from pre-DCs under the control of fms-like tyrosine kinase 3 (Flt3) ligand, inhibitor of D
77 rnal tandem duplication (ITD) mutants of the Fms-like tyrosine kinase 3 (Flt3) receptor in leukemogen
78 Internal tandem duplications (ITDs) of the FMS-like tyrosine kinase 3 (FLT3) receptor tyrosine kina
80 mia (AML) harbor activating mutations in the FMS-like tyrosine kinase 3 (FLT3) receptor tyrosine kina
81 l-3-kinase (PI3K)/protein kinase B (AKT) and Fms-like tyrosine kinase 3 (FLT3) signaling are aberrant
82 on of HoxA9 and Meis1a and with mutations in FMS-like tyrosine kinase 3 (FLT3) to drive acute leukemi
85 aled that normal villus epithelium expresses Fms-like tyrosine kinase 3 (Flt3), a known regulator of
86 ation and discovered that ADP transactivates Fms-like tyrosine kinase 3 (Flt3), a receptor tyrosine k
87 cation (ITD) in the juxtamembrane portion of Fms-like tyrosine kinase 3 (FLT3), a type III receptor t
88 The ligand for the receptor tyrosine kinase fms-like tyrosine kinase 3 (flt3), also referred to as f
89 r of the type III receptor tyrosine kinases: FMS-like tyrosine kinase 3 (FLT3), platelet-derived grow
97 A 46-year-old white woman with a history of Fms-like tyrosine kinase 3 acute myeloid leukemia presen
98 and primary patient specimens independent of Fms-like tyrosine kinase 3 expression and stromal-mediat
99 expansion, cooperated with mutations in the FMS-like tyrosine kinase 3 gene (Flt3(ITD)) and the nucl
101 is a Janus kinase 2 (JAK2), JAK2(V617F), and Fms-like tyrosine kinase 3 inhibitor that does not inhib
104 treated with the hematopoietic growth factor fms-like tyrosine kinase 3 ligand (FL), which dramatical
107 observation that Langerin-CD11b- migDCs are Fms-like tyrosine kinase 3 ligand (Flt3L) dependent and
110 und that immunization of wild-type mice with FMS-like tyrosine kinase 3 ligand (Flt3L) DNA, which inc
113 ested this hypothesis by using DC-deficient, fms-like tyrosine kinase 3 ligand (Flt3L) knockout (KO)
116 Conversely, endogenous DC expansion using FMS-like tyrosine kinase 3 ligand (Flt3L) protected mice
119 d deficiency (DCML deficiency) with elevated Fms-like tyrosine kinase 3 ligand (Flt3L) was observed i
120 ge inflammatory protein-1alpha (MIP-1alpha), fms-like tyrosine kinase 3 ligand (Flt3L), and the DNA v
125 rotein 3alpha (hCCL20/hMIP-3alpha), or human fms-like tyrosine kinase 3 ligand (hFlt3-L), factors pre
126 IP-1alpha) and the DC-specific growth factor fms-like tyrosine kinase 3 ligand with the DNA vaccine r
128 nes, including caveolin-1, semaphorin E, and FMS-like tyrosine kinase 3 ligand, have putative roles i
129 ter their stimulation with stem cell factor, Fms-like tyrosine kinase 3 ligand, interleukin-3, interl
130 DC progenitors and accumulate in response to Fms-like tyrosine kinase 3 ligand, yet appear divergent
131 lls were defective in generating pDCs in the fms-like tyrosine kinase 3 ligand-based culture system a
132 DC differentiation depends on IRF-4, whereas Fms-like tyrosine kinase 3 ligand-mediated differentiati
133 freshly isolated, immunobead-purified (>90%) fms-like tyrosine kinase 3 ligand-mobilized C57BL/10 (B1
136 ns leading to constitutive activation of the FMS-like tyrosine kinase 3 receptor (FLT3) occur in blas
138 ndritic cells (cDCs) requires the ligand for FMS-like tyrosine kinase 3 receptor (flt3L), but little
139 tion activating gene 1(+) lymphomyeloid, and Fms-like tyrosine kinase 3(+) fetal monocyte lineages.
140 ion with the receptor tyrosine kinases FLT3 (Fms-like tyrosine kinase 3) or KIT-induced ligand indepe
141 ations of the receptor tyrosine kinase FLT3 (Fms-like tyrosine kinase 3) play an important role in le
143 DC), the majority of which were derived from fms-like tyrosine kinase 3-dependent pre-DC, and CD11b(+
146 enic tyrosine kinases, including BCR-ABL and FMS-like tyrosine kinase 3-internal tandem duplication (
147 f a juxtamembrane mutation in the FLT3 gene (FMS-like tyrosine kinase 3-internal tandem duplication [
150 in or point mutation in the kinase domain of FMS-like tyrosine kinase-3 (FLT-3) mediates ligand-indep
151 yrosine kinase domain (TKD) mutations of the fms-like tyrosine kinase-3 (FLT3) gene in acute myeloid
155 viously demonstrated that pretreatments with fms-like tyrosine kinase-3 (Flt3) ligand (Flt3L), a dend
157 al tandem duplication (ITD) mutations of the FMS-like tyrosine kinase-3 (FLT3) receptor found in acut
159 andem duplication (ITD) mutations within the FMS-like tyrosine kinase-3 (FLT3) render the receptor co
161 r of clinical trials testing the efficacy of FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibi
166 cluding 14 (93%) of 15 patients with mutated FMS-like tyrosine kinase-3 (FLT3; the 15th patient had c
167 verexpression have been identified including FMS-like tyrosine kinase-3 and nucleophosmin, which will
169 mon DC progenitor with conventional DCs, and Fms-like tyrosine kinase-3 ligand is essential for their
170 rsely, DC expansion induced either by Flt3L (fms-like tyrosine kinase-3 ligand) or adoptive transfer
172 endothelial cells were identified: endoglin, Fms-like tyrosine kinase-3 ligand, EGF-like repeats and
174 ecreased in Mysm1(-/-) mice and defective in Fms-like tyrosine kinase-3(Flt3) ligand-induced, but not
178 eraction with two receptor tyrosine kinases, fms-like tyrosine kinase (Flt-1) or VEGF receptor 1 and
180 ain-containing receptor [KDR]), and VEGF-R1 (fms-like tyrosine kinase [Flt]) in bovine retinal endoth
182 ML) have an activating mutation in the FLT3 (fms-like tyrosine kinase) gene, which represents a targe
183 ated levels of hemopoietic cytokines such as fms-like tyrosine kinase ligand (FLT3-L, a dendritic cel
184 We tested the prediction that expression of fms-like tyrosine kinase ligand 3 (Flt3L) in the brain w
185 mpartment was associated with elevated serum fms-like tyrosine kinase ligand and reduced circulating
187 inding to the kinase domain receptor and the Fms-like tyrosine kinase receptor (Flt-1), the extracell
188 rosine kinase receptors, VEGF receptor 1 [or fms-like tyrosine kinase receptor (Flt-1)] and VEGF rece
189 PO), placental growth factor (PlGF), soluble fms-like tyrosine kinase receptor (sFlt)-1, and galectin
190 mediated by soluble VEGF receptor 1/soluble Fms-like tyrosine kinase receptor 1 and soluble endoglin
193 tion of specific DC subsets-using GM-CSF and fms-like tyrosine kinase receptor 3-ligand (Flt3-L)-on t
195 levels of brain natriuretic factor, soluble fms-like tyrosine kinase receptor-1, troponin I, and cre
196 oxidase, B-type natriuretic peptide, soluble fms-like tyrosine kinase receptor-1, troponin I, soluble
197 ically linked to the extracellular domain of Fms-like tyrosine kinase receptor-3 ligand (FLex; a DC g
199 ethymic signal through the cytokine receptor fms-like tyrosine kinase receptor-3 was required for the
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