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1 st a lethal challenge dose of wild-type (WT) A. hydrophila.
2 cal activities of a diarrheal isolate SSU of A. hydrophila.
3 which could alter the virulence potential of A. hydrophila.
4 e wild-type (WT) and complemented strains of A. hydrophila.
5 )-positive or -negative background strain of A. hydrophila.
6 he detailed mechanisms of action of Act from A. hydrophila.
7 y play an important role in the virulence of A. hydrophila.
8 actone at 10 microM in overnight cultures of A. hydrophila abolishes exoprotease production in azocas
13 of the environmental isolate ATCC 7966(T) of A. hydrophila and the vacB gene of Shigella flexneri.
14 nd the T3SS from a diarrheal isolate, SSU of A. hydrophila, and defined the role of some regulatory g
15 of the TTSS translocon, from wild-type (WT) A. hydrophila as well as from a previously characterized
16 e was then introduced into the chromosome of A. hydrophila by using the suicide vector pJQ200SK, allo
17 d that only the full-length ACD of RtxA from A. hydrophila catalyzed the covalent cross-linking of th
18 her hand, the WT and complemented strains of A. hydrophila caused 80 to 90% of the mice to succumb to
24 rease in gidA and act gene expression in the A. hydrophila Dam-overproducing strain, and these data m
25 tion, we showed that animals challenged with A. hydrophila die because of kidney and liver damage, hy
28 ementation experiments demonstrated that the A. hydrophila fur gene could restore iron regulation in
32 Members of the Aeromonas hydrophila complex (A. hydrophila, HG2, and A. salmonicida), a group that ha
33 table aspects of the metabolic repertoire of A. hydrophila include dissimilatory sulfate reduction an
34 established a role for three enterotoxins in A. hydrophila-induced gastroenteritis in a mouse model w
38 er predominant immune cells inflicted during A. hydrophila infections, such as murine macrophages, wh
39 sition of the S-layer on the cell surface in A. hydrophila is more similar to the X. campestris than
41 y of the effector domains of V. cholerae and A. hydrophila MARTX toxins to elucidate the mechanism of
43 ulture supernatants from deletion mutants of A. hydrophila, namely, a Delta act mutant (a T2SS-associ
45 emonstrated for the first time that VgrG1 of A. hydrophila possessed actin ADPRT activity associated
49 rther, we showed that the full-length ACD of A. hydrophila RtxA disrupted the actin cytoskeleton of H
50 ed the DNA adenine methyltransferase gene of A. hydrophila SSU (dam(AhSSU)) in a T7 promoter-based ve
51 otentially be important for the viability of A. hydrophila SSU as we could delete the chromosomal cop
52 o acid residues ((252)FYDAEKKEY(260)) in the A. hydrophila SSU enolase involved in plasminogen bindin
53 ace-expressed enolase in the pathogenesis of A. hydrophila SSU infections and of any gram-negative ba
54 inished by 55% compared to that of a control A. hydrophila SSU strain harboring the pBAD vector alone
56 am gene to be essential for the viability of A. hydrophila SSU, and, therefore, to better understand
57 the bacterium, and overproduction of Dam in A. hydrophila SSU, using an arabinose-inducible, P(BAD)
61 ns 343, 394, 420, 427, and 430 of enolase in A. hydrophila SSU; the mutated forms of enolase were hyp
62 ateral flagellum, that are reported in other A. hydrophila strains are not identified in the sequence
63 del was used, whereby either single or mixed A. hydrophila strains were injected intramuscularly.
65 Act was noted in the gidA isogenic mutant of A. hydrophila that was generated by marker exchange muta
66 luid secretion compared to that of wild-type A. hydrophila; the triple-knockout mutant failed to indu
67 toxic enterotoxin gene (act)-minus strain of A. hydrophila, thus generating aopB and act/aopB isogeni
73 as well as from the clinical isolate SSU of A. hydrophila, was exclusively expressed and produced du
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