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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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