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1 antigen expression and morphology following pathogen-host interactions.
2 facilitate a comprehensive understanding of pathogen-host interactions.
3 affeensis provide an important interface for pathogen-host interactions.
4 e bacterial cell and the nature of bacterial pathogen-host interactions.
5 at was prominent in proteins associated with pathogen-host interactions.
6 the host cell may provide new insights into pathogen-host interactions.
7 ion dynamics, expanding our understanding of pathogen-host interactions.
8 o be linked to key cellular processes and/or pathogen-host interactions.
9 tly been demonstrated to play vital roles in pathogen-host interactions.
10 generally applied to investigate additional pathogen-host interactions and to provide mechanistic in
12 to reveal insights into new virulence genes, pathogen-host interactions, and the molecular basis of h
14 ocesses, such as transmembrane signaling and pathogen-host interactions, are initiated by a protein r
15 far been used exclusively for investigating pathogen-host interactions, but they should be easily ad
17 ed proteins and secondary metabolism and the pathogen-host interaction database genes are highly enri
22 treatments and may form a basis for modeling pathogen-host interactions in other emerging infectious
23 e structures provide a remarkable example of pathogen-host interactions in which a unique microbial m
26 echanisms that have been identified by which pathogen-host interactions might influence rejection, in
27 in the mga promoter significantly alters the pathogen-host interaction of these asymptomatic carrier
30 e maintaining orthologs of most known fungal pathogen-host interaction proteins, stress response circ
31 ession patterns characterizing each phase of pathogen-host interaction provides avenues for targeted
32 ion on genes proven to affect the outcome of pathogen-host interactions reported in peer reviewed res
34 mucins at epithelial surfaces to facilitate pathogen-host interactions that culminate in toxin deliv
35 of these results for modelling evolution in pathogen-host interactions that lack gene-for-gene deter
36 We have highlighted an emerging principle in pathogen-host interactions: that the cytokine repertoire
37 enient model to study type IV pilus-mediated pathogen-host interactions under physiological condition
38 rkedly expanded our understanding of the key pathogen-host interactions underlying GAS necrotizing fa
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