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1                                              PLGF significantly increased BBB permeability in NP plas
2                                              PLGFs elicit diverse biological effects via the activati
3 the C-terminus of placental growth factor-2 (PLGF-2) was selected to enhance the activity of IFNalpha
4                        Tumor-derived VEGF-A, PLGF-2, and VEGF-B augment pain sensitivity through sele
5 four different splice isoforms of VEGF-A and PLGF, each of which binds to different combinations of t
6                       VEGF165 homodimers and PLGF/VEGF heterodimers stimulate tyrosine phosphorylatio
7           Our findings suggest that VEGF and PLGF enhance BBB permeability through different VEGFR pa
8 nd that circulating sFlt1 prevents VEGF- and PLGF-induced BBB permeability during pregnancy.
9 acts through iron to induce pro-arteriogenic PLGF, suggesting iron supplementation as a novel potenti
10             There was no association between PLGF change and OS in arm A.
11  (SIFalpha) by fusing the positively charged PLGF-2 peptide to the C-terminus of the human IFNalpha.
12  expression of the proinflammatory cytokines PLGF (OMIM 601121), TGFbeta (OMIM 190180), END1 (OMIM +1
13 actor (VEGF)/placenta-derived growth factor (PLGF) and soluble Fms-like tyrosine kinase-1 (sFLT-1, th
14 luded, among others, Placenta Growth Factor (PLGF) and Vascular Endothelial Growth Factor (VEGF), bot
15 h factor (VEGF) and placental growth factor (PLGF) are increased in the maternal circulation during p
16 association between placental growth factor (PLGF) change and OS.
17 or (VEGF) but lower placental growth factor (PLGF) compared to controls.
18                     Placental growth factor (PLGF) has previously been reported to have angiogenic ef
19 VEGF receptor-1 and placental growth factor (PLGF) in HEECs.
20 ression of VEGF and Placental growth factor (PLGF) in TNBCs, and inhibited tumor cell migration in vi
21                     Placental growth factor (PLGF) is an important arteriogenic mediator.
22 rete high levels of placental growth factor (PLGF), LLC cells produce high levels of VEGF, but low le
23 response to VEGF or placental growth factor (PLGF).
24 B, VEGFC, VEGFD and placental growth factor (PLGF).
25 xpressed monomers of placenta growth factor (PLGF)129 and vascular endothelial growth factor (VEGF)16
26 rally occurring phospholipid growth factors (PLGFs).
27  human and primate embryonic hearts and find PLGF shows a biphasic expression pattern, as it is expre
28  (VEGF)165 can be re-folded in vitro to form PLGF/VEGF heterodimers.
29 ion of angiogenic growth factors (VEGF, HGF, PLGF), and SDF-1alpha receptor CXCR4.
30 ccurs in some women with low sFLT-1 and high PLGF levels.
31                                     However, PLGF/VEGF heterodimers display 20-50-fold less mitogenic
32 f these FAC and iron-NTA induced an increase PLGF expression.
33 ersely, induction of HO-1 activity increased PLGF.
34 reviously showed that elevated FSS increases PLGF in a reactive oxygen species (ROS)-dependent fashio
35 develop in all women with high sFLT-1 or low PLGF levels, and it also occurs in some women with low s
36  We also demonstrate the presence of natural PLGF/VEGF heterodimers in the conditioned media of vario
37     We discover that only the application of PLGF modRNA at early time points of hESC-CM differentiat
38              Conversely, genetic deletion of PLGF reduces generation of CMs, SMCs and ECs in vitro.
39 l cardiomyogenic and vasculogenic effects of PLGF during heart development.
40 e also confirm in vivo beneficial effects of PLGF modRNA for development of human heart progenitor-de
41 s was restored to LLC cells by expression of PLGF, strongly suggesting that the angiogenic phenotype
42 EGF-induced angiogenesis by the formation of PLGF/VEGF heterodimers in cells producing both factors.
43 oduce high levels of VEGF, but low levels of PLGF.
44 d Sp2-O-Ag14 cells suggests that a number of PLGF receptor subtypes remain unidentified.
45 e that pharmacologically distinct subsets of PLGF receptors exist that distinguish between cyclic-PA
46 O-1 knockdown abolished the effect of FSS on PLGF.
47 sis that HO-1 mediates the effects of FSS on PLGF.
48 ted ex vivo migration in response to VEGF or PLGF.
49 grate or activate AKT in response to VEGF or PLGF.
50                     The purified recombinant PLGF/VEGF heterodimers and VEGF homodimers have potent m
51                     These data indicate that PLGF may modulate VEGF-induced angiogenesis by the forma
52 mbilical vein endothelial cells reveals that PLGF/VEGF heterodimers and VEGF165 homodimers, but not P
53                                    All three PLGFs induced the formation of stress fibers in NIH3T3 f
54 on patterns were established among the three PLGFs by monitoring changes in intracellular Ca2+ in NIH
55 e for LPA and not activated by the other two PLGFs.
56 her, we identify the previously unrecognized PLGF-related transcriptional networks driven by EOMES an
57  To determine which HO-1 product upregulates PLGF, co-cultures were treated with a CO donor (CORM-A1)
58                          The effect of VEGF, PLGF, and VEGF-receptor (VEGFR) activation on BBB permea
59                                        While PLGF/VEGF heterodimers bind with high affinity to a solu