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   1 y carboxylesterases, cytidine deaminase, and thymidine phosphorylase.                                
     2 tions, and mutations in the nuclear gene for thymidine phosphorylase.                                
     3 soDDU is completely resistant to cleavage by thymidine phosphorylase.                                
     4 ble clinical syndrome caused by mutations in thymidine phosphorylase.                                
     5 phosphorolytic activity was independent from thymidine phosphorylase.                                
     6  factor, basic fibroblast growth factor, and thymidine phosphorylase.                                
  
  
     9 several features of these patients including thymidine phosphorylase activity deficiency, elevated th
  
  
    12 s of 5-FU response: thymidylate synthase and thymidine phosphorylase activity; and p53 and mismatch r
    13 ve TYMP mutations cause severe reductions of thymidine phosphorylase activity; marked elevations of t
  
    15  the first to demonstrate a direct effect of thymidine phosphorylase and 2-deoxyribose on signaling p
  
  
  
  
    20 tes several proangiogenic factors, including thymidine phosphorylase and angiopoietin-1 both in vitro
    21 the intracellular metabolism of thymidine by thymidine phosphorylase and subsequent extracellular rel
  
  
    24 ointestinal encephalomyopathy and had severe thymidine phosphorylase deficiency in the buffy coat (<1
  
  
    27 r vascular endothelial growth factor (VEGF), thymidine phosphorylase differed from VEGF in that its e
    28 ccur from docetaxel-mediated upregulation of thymidine phosphorylase (dThdPase), an enzyme responsibl
    29    Two new crystal forms of Escherichia coli thymidine phosphorylase (EC 2.4.2.4) have been found; a 
    30 oietic stem cell transplantation can restore thymidine phosphorylase enzyme function in patients with
  
    32  Cdk5 (cyclin-dependent kinase 5) from Cdk2, thymidine phosphorylase from a bacterial homologue, and 
    33  and control brains, indicating that loss of thymidine phosphorylase function impairs the integrity o
    34 mine and deoxyribose-1-phosphate by the host thymidine phosphorylase greatly increases the sensitivit
  
  
  
    38 hanisms by which 2-deoxyribose might mediate thymidine phosphorylase-induced cell migration in vitro,
  
    40 ase caused by mutations in the gene encoding thymidine phosphorylase, leading to reduced enzymatic ac
    41 e synthase, dihydropyrimidine dehydrogenase, thymidine phosphorylase, microsatellite instability, 18q
    42 e in thymidylate synthase and an increase in thymidine phosphorylase mRNA expression as determined by
  
    44  of the transition state confirms that human thymidine phosphorylase proceeds through an S(N)2-like t
  
    46 revious studies showed that cells expressing thymidine phosphorylase stimulated endothelial cell migr
  
  
  
  
  
  
  
  
  
    56 ne kinase 1 (TK1), thymidylate synthase, and thymidine phosphorylase (TP) were analyzed by Western bl
    57 eterozygous mutations in the gene specifying thymidine phosphorylase (TP), located on chromosome 22q1
    58  with nuclease P1, alkaline phosphatase, and thymidine phosphorylase (TP), or from chlorinated nucleo
  
  
  
    62 s-of-function mutations in the gene encoding thymidine phosphorylase (TP; endothelial cell growth fac
  
  
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