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1 herefore represents an inactive receptor for acidic fibroblast growth factor.
2 eviously that the synergistic interaction of acidic fibroblast growth factor (aFGF) and a coactivator
3 ty and treated the graft/host interface with acidic fibroblast growth factor (aFGF) and chondroitinas
8 tyric acid [GABA]-ergic) of cells expressing acidic fibroblast growth factor (aFGF), glial cell line-
9 efective in neurite outgrowth in response to acidic fibroblast growth factor (aFGF); however, its res
10 n in defined beta-hairpin turns within human acidic fibroblast growth factor, and demonstrate consist
11 kin (IL)-1beta, tumor necrosis factor alpha, acidic fibroblast growth factor, and phorbol ester (phor
12 s demonstrated that T cells expressed TSP-1, acidic fibroblast growth factor, and vascular endothelia
13 esis induced by tumor necrosis factor alpha, acidic fibroblast growth factor, basic fibroblast growth
14 The receptor variant binds specifically to acidic fibroblast growth factor but has no tyrosine kina
15 ine the extent to which autocrine effects of acidic fibroblast growth factor (FGF)-1 overexpression c
16 ymmetry within the hydrophobic core of human acidic fibroblast growth factor (FGF-1) a combination of
18 ned the expression of a fibrogenic cytokine, acidic fibroblast growth factor (FGF-1) and its high-aff
19 lomerulopathy, we examined the expression of acidic fibroblast growth factor (FGF-1) and its high-aff
26 ation calorimetry, we demonstrate that human acidic fibroblast growth factor (hFGF-1) binds to surami
28 e cells, wild type RPTPalpha interferes with acidic fibroblast growth factor-induced neurite outgrowt
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