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1 by two homologous tyrosine kinase receptors, fms-like tyrosine kinase 1 (Flt-1) and kinase domain rec
2                   Furthermore, VEGF receptor fms-like tyrosine kinase 1 (Flt-1) was elevated, whereas
3 r endothelial growth factor and its receptor fms-like tyrosine kinase 1 (Flt1) were up-regulated, and
4 enhanced expression of PGF and its receptor, FMS-like tyrosine kinase 1 (Flt1).
5 GF-induced phosphorylation of KDR but not of FMS-like tyrosine kinase 1 (FLT1)/VEGF receptor 1.
6                            Here we show that FMS-like tyrosine kinase 1 (Flt1, also known as VEGFR1)
7 e placental growth factor (PlGF) and soluble Fms-like tyrosine kinase 1 (sFlt-1) as clinical biomarke
8 or limits angiogenesis by increasing soluble fms-like tyrosine kinase 1 (sFlt-1) gene expression.
9                               Excess soluble fms-like tyrosine kinase 1 (sFlt-1) of vascular endothel
10                         The ratio of soluble fms-like tyrosine kinase 1 (sFlt-1) to placental growth
11                                      Soluble fms-like tyrosine kinase 1 (sFlt-1), an alternatively sp
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
17           Up-regulation of placental soluble fms-like tyrosine kinase 1 (sFlt1) contributes to the pa
18                                      Soluble fms-like tyrosine kinase 1 (sFlt1), a circulating antian
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
21      Here, we confirm that placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEG
22           Alterations in circulating soluble fms-like tyrosine kinase 1 (sFlt1), an antiangiogenic pr
23               The angiogenic factors soluble fms-like tyrosine kinase 1 and placental growth factor,
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
26              The antepartum ratio of soluble fms-like tyrosine kinase 1 to placental growth factor po
27 t tertile of the antepartum ratio of soluble fms-like tyrosine kinase 1 to placental growth factor wa
28 ted blood pressure, increased plasma soluble fms-like tyrosine kinase 1, and renal dysfunction.
29    This locus is near the FLT1 gene encoding Fms-like tyrosine kinase 1, providing biological support
30 -scavenging soluble VEGF receptor 1 (soluble fms-like tyrosine kinase 1; sFlt-1).
31                   Both LP plasma and soluble FMS-like tyrosine-kinase 1 (sFlt1) in NP plasma abolishe
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
34 nase (p85) is constitutively associated with FMS-like tyrosine kinase-1 (Flt-1).
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
39                                      Soluble Fms-like tyrosine kinase-1 (sFlt-1) is an antiangiogenic
40                                      Soluble fms-like tyrosine kinase-1 (sFlt-1) seems to interfere w
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
43          However, elevated levels of soluble fms-like tyrosine kinase-1 (sFLT1) in the placenta and i
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
48 nd hemin by abolishing both sEng and soluble fms-like tyrosine kinase-1 induction.
49 giogenesis by inducing both sEng and soluble fms-like tyrosine kinase-1 secretion from human villous
50                                             'FMS'-like tyrosine kinase 3 (FLT3) mutations in acute my
51 ophage colony stimulating factor I receptor (Fms)-like tyrosine kinase 3 (Flt-3) ligand supported fur
52                                 Mutations of Fms-like tyrosine kinase 3 (FLT3) are among the most fre
53                      Activating mutations in FMS-like tyrosine kinase 3 (FLT3) are common in acute my
54                      Activating mutations of FMS-like tyrosine kinase 3 (FLT3) are present in approxi
55                   Constitutive activation of FMS-like tyrosine kinase 3 (FLT3) by internal tandem dup
56         Internal tandem duplication (ITD) of fms-like tyrosine kinase 3 (FLT3) in acute myeloid leuke
57 goal of this study was to define the role of FMS-like tyrosine kinase 3 (FLT3) in the heart.
58 nd the ensuing expansion of T(reg) cells are Fms-like tyrosine kinase 3 (Flt3) independent, occur in
59                                              Fms-like tyrosine kinase 3 (FLT3) inhibition has elicite
60  seen to emerge as resistant mutations after FMS-like tyrosine kinase 3 (FLT3) inhibitor therapy.
61 teosome inhibitors, antiangiogenesis agents, Fms-like tyrosine kinase 3 (FLT3) inhibitors, and apopto
62                   Oncogenic addiction to the Fms-like tyrosine kinase 3 (FLT3) is a hallmark of acute
63                                              FMS-like tyrosine kinase 3 (FLT3) is a receptor tyrosine
64                                              Fms-like tyrosine kinase 3 (FLT3) is a receptor tyrosine
65                                              Fms-like tyrosine kinase 3 (Flt3) is a type III receptor
66                                              FMS-like tyrosine kinase 3 (FLT3) is almost universally
67                                              FMS-like tyrosine kinase 3 (FLT3) is expressed in human
68                                              FMS-like tyrosine kinase 3 (FLT3) is mutated in approxim
69                       Signal transduction of FMS-like tyrosine kinase 3 (FLT3) is regulated by protei
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
72                                              Fms-like tyrosine kinase 3 (FLT3) mutations are associat
73              Ever since the recognition that FMS-like tyrosine kinase 3 (FLT3) mutations exert a prof
74                                   Activating FMS-like tyrosine kinase 3 (FLT3) mutations have been id
75       Constitutively activating mutations of FMS-like tyrosine kinase 3 (FLT3) occur in approximately
76                  Mutations that activate the fms-like tyrosine kinase 3 (FLT3) receptor are among the
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
79                                          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
83             Secondary point mutations in the Fms-like tyrosine kinase 3 (FLT3) tyrosine kinase domain
84                                              FMS-like tyrosine kinase 3 (FLT3), a class III receptor
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
90 iated by HSC-specific genes such as CD34 and Fms-like tyrosine kinase 3 (FLT3), respectively.
91        Small molecule inhibitors that target fms-like tyrosine kinase 3 (FLT3)-activating mutations h
92                                     Multiple FMS-like tyrosine kinase 3 (FLT3)-inhibitors have been s
93       Signaling pathways regulated by mutant Fms-like tyrosine kinase 3 (FLT3)-internal tandem duplic
94           Rhesus macaques were injected with Fms-like tyrosine kinase 3 (Flt3)-ligand (FL) to expand
95                                              FMS-like tyrosine kinase 3 (FLT3)-mutant acute myeloid l
96 tion was identified in the gene encoding the Fms-like tyrosine kinase 3 (Flt3).
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
100        An internal tandem duplication in the fms-like tyrosine kinase 3 gene (FLT3/ITD) is associated
101 is a Janus kinase 2 (JAK2), JAK2(V617F), and Fms-like tyrosine kinase 3 inhibitor that does not inhib
102                                           In Fms-like tyrosine kinase 3 internal tandem duplication (
103                                           In Fms-like tyrosine kinase 3 internal tandem duplication (
104 treated with the hematopoietic growth factor fms-like tyrosine kinase 3 ligand (FL), which dramatical
105 C precursors that can be expanded in vivo by Fms-like tyrosine kinase 3 ligand (FL).
106                                              Fms-like tyrosine kinase 3 ligand (Flt3L) administration
107  observation that Langerin-CD11b- migDCs are Fms-like tyrosine kinase 3 ligand (Flt3L) dependent and
108    Here, we observe subcutaneous immunity is Fms-like tyrosine kinase 3 ligand (Flt3L) dependent.
109                    In contrast, injection of FMS-like tyrosine kinase 3 ligand (Flt3L) DNA, which exp
110 und that immunization of wild-type mice with FMS-like tyrosine kinase 3 ligand (Flt3L) DNA, which inc
111                                              Fms-like tyrosine kinase 3 ligand (Flt3L) expands dendri
112                                              Fms-like tyrosine kinase 3 ligand (Flt3L) is a hematopoi
113 ested this hypothesis by using DC-deficient, fms-like tyrosine kinase 3 ligand (Flt3L) knockout (KO)
114                 Daily treatment of mice with fms-like tyrosine kinase 3 ligand (Flt3L) leads to a sig
115                                              Fms-like tyrosine kinase 3 ligand (Flt3L) mobilizes stem
116    Conversely, endogenous DC expansion using FMS-like tyrosine kinase 3 ligand (Flt3L) protected mice
117            In this study we demonstrate that Fms-like tyrosine kinase 3 ligand (Flt3L) recruits plasm
118                                              Fms-like tyrosine kinase 3 ligand (Flt3L) reverses the f
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
121                          Multiple subsets of FMS-like tyrosine kinase 3 ligand (FLT3L)-dependent dend
122 ne liver pDCs, we expanded them in vivo with fms-like tyrosine kinase 3 ligand (Flt3L).
123 ministration of the potent DC growth factor, fms-like tyrosine kinase 3 ligand (Flt3L).
124                                 Mice lacking fms-like tyrosine kinase 3 ligand (Flt3L-/-) as the resu
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
127 SCs in normal mice in response to SCF, IL-7, fms-like tyrosine kinase 3 ligand, and IL-15.
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
134  DNA that encoded the secreted form of human fms-like tyrosine kinase 3 ligand.
135                           The protein kinase fms-like tyrosine kinase 3 receptor (Flt3) has an import
136 ns leading to constitutive activation of the FMS-like tyrosine kinase 3 receptor (FLT3) occur in blas
137                           The ligand for the FMS-like tyrosine kinase 3 receptor (Flt3L) is necessary
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
142                              Recently, Flt3 (Fms-like tyrosine kinase 3)-ligand has been identified a
143 DC), the majority of which were derived from fms-like tyrosine kinase 3-dependent pre-DC, and CD11b(+
144                                           In FMS-like tyrosine kinase 3-internal tandem duplication (
145                                              FMS-like tyrosine kinase 3-internal tandem duplication (
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 [
148             Distinct expression patterns for FMS-like tyrosine kinase 3-internal tandem duplication w
149                                 Increases in fms-like tyrosine kinase-3 (FLT-3) ligand, reflecting FL
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
152                      We examined 6 different FMS-like tyrosine kinase-3 (FLT3) inhibitors (lestaurtin
153                                              Fms-like tyrosine kinase-3 (FLT3) inhibitors have been u
154                                              Fms-like tyrosine kinase-3 (Flt3) ligand (FL) and Interl
155 viously demonstrated that pretreatments with fms-like tyrosine kinase-3 (Flt3) ligand (Flt3L), a dend
156         In a randomized trial of therapy for FMS-like tyrosine kinase-3 (FLT3) mutant acute myeloid l
157 al tandem duplication (ITD) mutations of the FMS-like tyrosine kinase-3 (FLT3) receptor found in acut
158                  Activating mutations of the FMS-like tyrosine kinase-3 (FLT3) receptor occur in appr
159 andem duplication (ITD) mutations within the FMS-like tyrosine kinase-3 (FLT3) render the receptor co
160                                              FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibi
161 r of clinical trials testing the efficacy of FMS-like tyrosine kinase-3 (FLT3) tyrosine kinase inhibi
162                                       Mutant Fms-Like Tyrosine kinase-3 (FLT3), which is expressed in
163               The clinical benefit of adding FMS-like tyrosine kinase-3 (FLT3)-directed small molecul
164                                              FMS-like tyrosine kinase-3 (FLT3)-internal tandem duplic
165 rbor a constitutively activating mutation in FMS-like tyrosine kinase-3 (FLT3).
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
168                                              Fms-like tyrosine kinase-3 ligand (Flt3L) is a hemopoiet
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
171 kin-7, interleukin-15, stem cell factor, and fms-like tyrosine kinase-3 ligand).
172 endothelial cells were identified: endoglin, Fms-like tyrosine kinase-3 ligand, EGF-like repeats and
173           Internal tandem duplication of the Fms-like tyrosine kinase-3 receptor (FLT3) internal tand
174 ecreased in Mysm1(-/-) mice and defective in Fms-like tyrosine kinase-3(Flt3) ligand-induced, but not
175 l cell line-derived neurotrophic factor, and FMS-like tyrosine kinase-3.
176 e myeloid leukaemia (AML) have a mutation in FMS-like-tyrosine-kinase-3 (FLT3).
177 ert domain-containing receptor (KDR) and the fms-like tyrosine kinase (Flt).
178 eraction with two receptor tyrosine kinases, fms-like tyrosine kinase (Flt-1) or VEGF receptor 1 and
179 ty for soluble kinase domain region (KDR) or Fms-like tyrosine kinase (FLT-1) receptors.
180 ain-containing receptor [KDR]), and VEGF-R1 (fms-like tyrosine kinase [Flt]) in bovine retinal endoth
181           Internal tandem duplication of the FMS-like tyrosine kinase (FLT3-ITD) receptor is present
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
186  containing receptor, or VEGFR-2) and Flt-1 (fms-like tyrosine kinase, or VEGFR-1).
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
191                    We studied the effects of fms-like tyrosine kinase receptor 3 ligand (Flt3-L) or G
192                                              Fms-like tyrosine kinase receptor 3-ligand (Flt3-L) and
193 tion of specific DC subsets-using GM-CSF and fms-like tyrosine kinase receptor 3-ligand (Flt3-L)-on t
194 ie2 (sTie2) and VEGF signalling with soluble Fms-like tyrosine kinase receptor-1 (sFlt1).
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
198                             We conclude that fms-like tyrosine kinase receptor-3 signaling is require
199 ethymic signal through the cytokine receptor fms-like tyrosine kinase receptor-3 was required for the
200 controlled in part by regulatory T cells and fms-like tyrosine kinase receptor-3.
201 asma angiogenic factor expression of soluble fms-like tyrosine kinase (sFlt)-1.

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