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1 nt mice displayed enhanced susceptibility to Yersinia infection.
2 e cells, and were attenuated in disseminated Yersinia infection.
3 to gain insight into the initial stages of a Yersinia infection.
4 ue and other pathogenic conditions caused by Yersinia infection.
5 nt to support a detectable increased risk of Yersinia infection.
6  important for virulence in murine models of Yersinia infection.
7 novel, antivirulence strategy for preventing Yersinia infection.
8 c colonization in mouse models of intestinal Yersinia infection.
9 ) and TLR2(-/-) mice during enteropathogenic Yersinia infection.
10 ene expression in macrophages in response to Yersinia infection and that YopJ deactivates both pathwa
11 he processing of MyD88 was not restricted to Yersinia infection and to proapoptotic Toll-IL-1R domain
12        Mice lacking T cells are sensitive to Yersinia infection, and a humoral response to Yersinia c
13                   Unless the pathogenesis of Yersinia infection differs markedly between mice and hum
14  YopR are essential for the establishment of Yersinia infections in a mouse model system, suggesting
15                                Nevertheless, Yersinia infection induces inflammatory responses in viv
16 th digitonin to measure Yop targeting during Yersinia infections of HeLa cells.
17                  Successful establishment of Yersinia infections requires the type III machinery, a p
18 y in the HeLa cell nucleus after delivery by Yersinia infection, showing that these LRRs are not esse
19 e expression profile of gammadelta IELs in a Yersinia infection system to better define their roles.
20  TGF-beta+ T-regulatory cells (T-regs) after Yersinia infection that is reduced in ovalbumin T-cell r
21 ction, we postulate that a silent persistent Yersinia infection was reactivated, leading to dissemina
22 ression and targeting of Yop proteins during Yersinia infection, whereas secreted LcrV is required to

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