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1 refore may be useful tools in evaluating the pathogen-host interaction.
2 ree hosts, indicating the uniqueness of each pathogen-host interaction.
3 highlight the functionality of paraCell for pathogen-host interaction.
4 changes in cellular architecture that favor pathogen-host interactions.
5 of cellular targets that enhances subsequent pathogen-host interactions.
6 facilitate a comprehensive understanding of 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 hat serve as tractable models for studies of pathogen-host interactions.
11 antigen expression and morphology following pathogen-host interactions.
12 affeensis provide an important interface for pathogen-host interactions.
13 e bacterial cell and the nature of bacterial pathogen-host interactions.
14 at was prominent in proteins associated with pathogen-host interactions.
15 the host cell may provide new insights into pathogen-host interactions.
16 regulation of gene expression, virulence and pathogen-host interactions.
17 to understanding colonization, movement, and pathogen/host interactions.
18 een successfully applied for (i) identifying pathogen-host interactions and (ii) predicting near-resi
20 ental tissue and are therefore used to study pathogen-host interactions and other complex biological
21 generally applied to investigate additional pathogen-host interactions and to provide mechanistic in
23 to reveal insights into new virulence genes, pathogen-host interactions, and the molecular basis of h
25 ies, and enemy-victim (e.g. predator-prey or pathogen-host) interactions are particularly common.
26 ocesses, such as transmembrane signaling and pathogen-host interactions, are initiated by a protein r
27 far been used exclusively for investigating pathogen-host interactions, but they should be easily ad
28 ology, and controlled vocabularies to curate pathogen-host interaction data, at the level of the host
31 ed proteins and secondary metabolism and the pathogen-host interaction database genes are highly enri
32 ies interactions, using data curated for the Pathogen-Host Interactions database (PHI-base) as a case
38 ed effectors (T3SEs) play important roles in pathogen-host interactions, identifying them is crucial
39 outcomes, but the interpretive complexity of pathogen-host interactions impedes identification of cri
41 al proteases, expanding the understanding of pathogen-host interactions in immune responses, specific
42 esents an innovative approach to investigate pathogen-host interactions in multiple airway conditions
43 treatments and may form a basis for modeling pathogen-host interactions in other emerging infectious
44 e structures provide a remarkable example of pathogen-host interactions in which a unique microbial m
48 To facilitate broader exploration of how pathogen-host interactions might impact transmission and
49 echanisms that have been identified by which pathogen-host interactions might influence rejection, in
50 in the mga promoter significantly alters the pathogen-host interaction of these asymptomatic carrier
51 dicate that we need to better understand the pathogen-host interactions of persister MRSAs in vivo.
52 in vitro platform for investigating enteric pathogen-host interactions, particularly for pathogens l
55 e maintaining orthologs of most known fungal pathogen-host interaction proteins, stress response circ
56 ession patterns characterizing each phase of pathogen-host interaction provides avenues for targeted
57 ion on genes proven to affect the outcome of pathogen-host interactions reported in peer reviewed res
58 abundance during human infections, mitigate pathogen-host interactions, scavenge free ETEC toxins, a
61 mucins at epithelial surfaces to facilitate pathogen-host interactions that culminate in toxin deliv
62 of these results for modelling evolution in pathogen-host interactions that lack gene-for-gene deter
63 resent within the same bat and the different pathogen-host interactions that may regulate the presenc
64 We have highlighted an emerging principle in pathogen-host interactions: that the cytokine repertoire
65 in (Kgp) virulence factor is involved in the pathogen-host interaction through the production of cyto
66 hat CEACAMs play a multifaceted role in ETEC pathogen-host interactions, transiently favoring the pat
67 enient model to study type IV pilus-mediated pathogen-host interactions under physiological condition
68 rkedly expanded our understanding of the key pathogen-host interactions underlying GAS necrotizing fa