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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
13 s of 5-FU response: thymidylate synthase and thymidine phosphorylase activity; and p53 and mismatch r
14 ve TYMP mutations cause severe reductions of thymidine phosphorylase activity; marked elevations of t
16 the first to demonstrate a direct effect of thymidine phosphorylase and 2-deoxyribose on signaling p
21 tes several proangiogenic factors, including thymidine phosphorylase and angiopoietin-1 both in vitro
22 the intracellular metabolism of thymidine by thymidine phosphorylase and subsequent extracellular rel
25 ointestinal encephalomyopathy and had severe thymidine phosphorylase deficiency in the buffy coat (<1
28 r vascular endothelial growth factor (VEGF), thymidine phosphorylase differed from VEGF in that its e
29 ccur from docetaxel-mediated upregulation of thymidine phosphorylase (dThdPase), an enzyme responsibl
30 Two new crystal forms of Escherichia coli thymidine phosphorylase (EC 2.4.2.4) have been found; a
31 oietic stem cell transplantation can restore thymidine phosphorylase enzyme function in patients with
33 Cdk5 (cyclin-dependent kinase 5) from Cdk2, thymidine phosphorylase from a bacterial homologue, and
34 and control brains, indicating that loss of thymidine phosphorylase function impairs the integrity o
35 mine and deoxyribose-1-phosphate by the host thymidine phosphorylase greatly increases the sensitivit
40 hanisms by which 2-deoxyribose might mediate thymidine phosphorylase-induced cell migration in vitro,
42 ase caused by mutations in the gene encoding thymidine phosphorylase, leading to reduced enzymatic ac
43 e synthase, dihydropyrimidine dehydrogenase, thymidine phosphorylase, microsatellite instability, 18q
44 e in thymidylate synthase and an increase in thymidine phosphorylase mRNA expression as determined by
46 of the transition state confirms that human thymidine phosphorylase proceeds through an S(N)2-like t
48 revious studies showed that cells expressing thymidine phosphorylase stimulated endothelial cell migr
59 ne kinase 1 (TK1), thymidylate synthase, and thymidine phosphorylase (TP) were analyzed by Western bl
60 ioned medium from Smo- mice were depleted of thymidine phosphorylase (TP), a protein that maintains m
61 eterozygous mutations in the gene specifying thymidine phosphorylase (TP), located on chromosome 22q1
62 with nuclease P1, alkaline phosphatase, and thymidine phosphorylase (TP), or from chlorinated nucleo
67 s-of-function mutations in the gene encoding thymidine phosphorylase (TP; endothelial cell growth fac
72 ct of thymidine catalyzed by the function of thymidine phosphorylase, upregulates CIITA expression in