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1 also blocked the expression of KSHV-induced vascular endothelial growth factor C.
2 n activator receptor, and to a modest extent vascular endothelial growth factor C.
3 , insulin-like growth factor-1 receptor, and vascular endothelial growth factor-C.
4 agonist, up-regulated the mRNA expression of vascular endothelial growth factor-C, a HIF-regulated ge
6 ic-specific receptor VEGFR3 and its ligands, vascular endothelial growth factor-C and -D (VEGF-C, -D)
8 flammation resulted in reduced expression of vascular endothelial growth factor-C and decreased corne
9 hypothesis that the lymphangiogenesis factor vascular endothelial growth factor-C and its receptors,
10 of the murine cDNA, the orthologue of human vascular endothelial growth factor-C and vascular endoth
14 ganization and (2) lymphatic cell migration, vascular endothelial growth factor-C expression, and lym
15 ion of the potent pro-lymphangiogenic factor vascular endothelial growth factor C in pancreatic cance
17 crovascular endothelial cells also expressed vascular endothelial growth factor-C mRNA that was furth
18 vessel memory response did not depend on the vascular endothelial growth factor C or A pathway, indic
20 demonstrate important paracrine functions of vascular endothelial growth factor-C, produced by blood
23 gulated the expression of prolymphangiogenic vascular endothelial growth factor-C upon stimulation wi
25 tic network in the defected area, adenoviral vascular endothelial growth factor C (VEGF-C) was admini
26 eceptor 3 (VEGFR-3), with its cognate ligand vascular endothelial growth factor C (VEGF-C), is a majo
27 herefore studied the role of lymphangiogenic vascular endothelial growth factor C (VEGF-C), its recep
29 e developed transgenic mice that overexpress vascular endothelial growth factor-C (VEGF-C) and green
30 ary metastases, with a dramatic reduction of vascular endothelial growth factor-C (VEGF-C) and its co
31 and lymphangiogenic growth factors, such as vascular endothelial growth factor-C (VEGF-C) and VEGF-A
32 eport that induction of lymphangiogenesis by vascular endothelial growth factor-C (VEGF-C) at the sec
33 in delayed lymphatic repair, decreased local vascular endothelial growth factor-C (VEGF-C) expression
34 We have previously reported an increase in vascular endothelial growth factor-C (VEGF-C) expression
35 ctor domains 1 (CCBE1) interactions with the vascular endothelial growth factor-C (VEGF-C) growth fac
37 d the role of the lymphangiogenesis mediator vascular endothelial growth factor-C (VEGF-C) in human d
38 amples have shown an increased expression of vascular endothelial growth factor-C (VEGF-C) in metasta
39 erfering RNAs (siRNA) targeted against human vascular endothelial growth factor-C (VEGF-C) in PC-3 ce
40 nce was performed to determine the source of vascular endothelial growth factor-C (VEGF-C) in the tum
44 cent reports correlate the high abundance of vascular endothelial growth factor-C (VEGF-C) to the lym
45 mors expressing normal or elevated levels of vascular endothelial growth factor-C (VEGF-C), a molecul
46 hown that the lymphangiogenic growth factor, vascular endothelial growth factor-C (VEGF-C), and its r
47 reased convection of growth factors, such as vascular endothelial growth factor-C (VEGF-C), would lim
50 ession of the lymphangiogenic growth factor (vascular endothelial growth factor-C [VEGF-C]) can promo
51 sistive-pulse detection of cancer biomarker (Vascular Endothelial Growth Factor-C, VEGF-C) through th
57 arin-binding EGF-like growth factor (HBEGF), vascular endothelial growth factor C (VEGFC), betacellul
58 CCBE1 has emerged as a crucial regulator of vascular endothelial growth factor-C (VEGFC) signaling.
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