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1 e role of E2F3 in vivo, we generated an E2f3 mutant mouse strain.
2 ele of Dscam to use alongside existing Dscam mutant mouse strains.
3 ating glucose metabolism and fat mass in two mutant mouse strains.
4 e scientific community for the generation of mutant mouse strains.
5 ossed Myo15(sh2/sh2) mice to the three other mutant mouse strains.
6 nous imprinted genes in inbred wild-type and mutant mouse strains.
7 n of (59)Fe absorption in both wild-type and mutant mouse strains.
8 ked compositional differences between WT and mutant mouse strains.
10 complementation system (LCS) makes use of a mutant mouse strain, aphakia (ak), homozygotes of which
14 ed a forward genetics approach to identify a mutant mouse strain characterized by the absence of CNS
17 which are defective in the pallid and muted mutant mouse strains, encode small, coiled-coil-forming
19 y important yet simple approach to establish mutant mouse strains for functional study at defined sta
28 we allografted carotid artery loops from six mutant mouse strains into immunocompetent CBA/CaJ recipi
35 er (EOC) in vivo We used the Pten/Kras(G12D)-mutant mouse strain that develops serous EOC with 100% p
37 ological conditions was investigated using a mutant mouse strain that expresses a truncated Cabin1 la
39 strains, ACAID cannot be induced in several mutant mouse strains that are coincidentally deficient i
40 small intestinal phenotype found in most Apc-mutant mouse strains, this strain has been designated th
41 tic defects of GATA-2-/- cells, we interbred mutant mouse strains to assess the effects of p53 loss o
44 he lungs of infected mice revealed that both mutant mouse strains were only transiently impaired in t
47 e-driven breast tumorigenesis in a series of mutant mouse strains with specific DDR deficiencies to r
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