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1 VacA also inhibited the proliferation of purified primar
2 VacA blocks IL-2 secretion in transformed T cell lines b
3 VacA can assemble into multiple types of water-soluble f
4 VacA contains two distinct domains, designated p33 and p
5 VacA cytotoxic activity requires assembly of VacA monome
6 VacA inhibited activation-induced proliferation of prima
7 VacA inhibited both T cell-induced and PMA/anti-IgM-indu
8 VacA inhibited interleukin-2 (IL-2) production by a muri
9 VacA inhibited the proliferation of primary human T cell
10 VacA inserts into membranes and forms a hexameric, anion
11 VacA is a secreted toxin that plays a role in Helicobact
12 VacA is a secreted toxin that plays a role in Helicobact
13 VacA monomers self-assemble into water-soluble oligomeri
14 VacA mutant toxins defective in the capacity to form ani
15 VacA permeabilization induces an influx of extracellular
16 VacA purified from strain 60190 induced apoptosis in a d
17 VacA reduced the mitochondrial membrane potential of CD4
18 VacA suppressed HIV infection of T cells at a stage afte
19 VacA treatment inhibits acid secretion by preventing the
20 VacA-G13A, VacA-G22A, and VacA-G26A induced vacuolation
21 VacA-induced clustering and redistribution of late endoc
22 VacA-induced clusters of late endocytic compartments und
23 VacA-induced death of these cells is a caspase-independe
24 VacA-treated Jurkat T cells secreted markedly diminished
26 panel of C-terminally truncated Delta6-27p88 VacA proteins indicated that a fragment containing amino
27 in lacking amino acids 6 to 27 (Delta6-27p88 VacA) is able to inhibit many activities of wild-type Va
29 e p55 structure into a 19-A cryo-EM map of a VacA dodecamer allows us to propose a model for how VacA
30 nce from the nontoxigenic strain Tx30a) or a VacA mutant protein (VacA Delta 6-27) that lacks a uniqu
31 gineered an H. pylori strain that produced a VacA toxin containing an enterokinase cleavage site loca
35 ave been recognized for vacuolating toxin A (VacA) and urease, H. pylori membrane and secreted factor
40 ed on the roles of H. pylori toxins CagA and VacA on the disease process and have suggested that both
41 r Helicobacter pylori infection and CagA and VacA status by using serum samples from 222 patients.
43 f two known virulence determinants (CagA and VacA) are highly divergent, with 77% and 87% mean amino
44 VacA to form mixed oligomeric complexes, and VacA Delta346-347 inhibited wild-type vacuolating activi
49 accurately detected H. pylori infection and VacA status, but improvements in the interpretation crit
50 gastric epithelial cells with wild-type and VacA-deficient H. pylori strains, treatment of cells wit
51 rs known to inhibit cellular vacuolation and VacA membrane channel activity also inhibit cytochrome c
52 etween VacA-induced cellular vacuolation and VacA-induced cytochrome c release from mitochondria.
53 he efficient induction of Tregs in vivo, and VacA is required to prevent allergen-induced asthma.
56 bilayer and membrane depolarization assays, VacA proteins containing V21L and S25L mutations were de
58 study, we explored the relationship between VacA-induced cellular vacuolation and VacA-induced cytoc
60 The sharing of such peculiar properties by VacA and host ClC channels, together with their similar
62 h isogenic mutants deficient in either CagA, VacA, lipopolysaccharide, or gamma-glutamyl transpeptida
63 unctions of macrophages and dendritic cells, VacA inhibition of T-cell function, and suppressive effe
64 The goal of this study was to characterize VacA-VacA interactions that may mediate assembly of VacA
65 nce of weak bases (e.g., ammonium chloride), VacA induces the formation of large cytoplasmic vacuoles
66 ive epithelial cell signaling; the cytotoxin VacA, which causes epithelial damage; and an adhesin, Ba
67 speptidase GGT and the vacuolating cytotoxin VacA, are required and sufficient for asthma protection
68 speptidase GGT and the vacuolating cytotoxin VacA, contribute critically and nonredundantly to H. pyl
70 cobacter pylori toxin vacuolating cytotoxin (VacA) promotes gastric colonization, and its presence (V
72 ri secretes an 88-kDa vacuolating cytotoxin (VacA) that may contribute to the pathogenesis of peptic
77 two separate domains, as described here for VacA, has rarely been described for pore-forming bacteri
78 mice more efficiently than mutants null for VacA or producing more active forms of it, providing the
79 , including a 60190 isogenic mutant null for VacA, strongly induced interleukin-10 (IL-10) and IL-6 p
80 that amino acids 351 to 360 are required for VacA protein-protein interactions and for dominant-negat
83 Helicobacter pylori secretes a pore-forming VacA toxin that has structural features and activities s
88 decamer allows us to propose a model for how VacA monomers assemble into oligomeric structures capabl
90 cause the non-vacuolating phenotype, but if VacA is unblocked, it confers cell line specificity of v
91 nts (bacterial lysate or the immunomodulator VacA) and subsequently subjected them to four different
96 addition of p55 followed by p33 resulted in VacA internalization and cell vacuolation, whereas seque
104 des cytochrome c release and occurs at lower VacA concentrations, indicating that cellular vacuolatio
105 i strain 60190, which expresses a type s1/m1 VacA toxin, induced significantly higher levels of apopt
108 the more toxigenic 60190 strain contain more VacA (s1i1 type) than vesicles from the SS1 strain (s2i2
109 lower-shaped oligomeric structures, and most VacA activities are dependent on its capacity to oligome
110 of recombinant VacA and identified 10 mutant VacA proteins that lacked vacuolating cytotoxic activity
111 ri vacA gene resulted in secretion of mutant VacA proteins that failed to assemble into large oligome
112 tion, these are the first examples of mutant VacA proteins that have defects in vacuolating activity
113 Through the analysis of a panel of mutant VacA proteins, we demonstrate that VacA-mediated inhibit
115 dependent on interactions between the mutant VacA proteins and wild-type VacA, and they allow mapping
116 bly, we demonstrate that one of these mutant VacA proteins [VacA-Delta(6-27)] abrogates the immunosup
117 causes death of these cells, whereas mutant VacA proteins defective in membrane channel formation do
119 e inhibitory properties of dominant-negative VacA mutant proteins are dependent on interactions betwe
121 n A1 blocks VacA-induced vacuolation but not VacA-induced cytochrome c release, which indicates that
122 propose that the immunomodulatory actions of VacA on T and B lymphocytes, the major effectors of the
124 essential for the intracellular activity of VacA, which suggests that this region may constitute a s
127 ter acinonychis reveals that the ancestry of VacA is different from the African origin that typifies
129 VacA cytotoxic activity requires assembly of VacA monomers into oligomeric structures, formation of a
131 report a previously unrecognized capacity of VacA to induce clustering and perinuclear redistribution
136 otential interactions between two domains of VacA (termed p-33 and p-55) by using a yeast two-hybrid
142 In this study, we investigated effects of VacA on the proliferation of various other types of prim
143 on of purified VacA is required for entry of VacA into cells, and correspondingly, acid activation of
147 eria producing the less active s2/i2 form of VacA colonized mice more efficiently than mutants null f
148 nalysis of a nonoligomerizing mutant form of VacA secreted by H. pylori The nonoligomerizing 88-kDa m
150 comparison to i1 forms of VacA, i2 forms of VacA had a diminished capacity to inhibit the activation
151 rains producing more active (s1/i1) forms of VacA is strongly associated with gastric adenocarcinoma.
152 ne effects of different polymorphic forms of VacA on inflammation and metaplasia in the mouse stomach
153 e compared the ability of i1 and i2 forms of VacA to cause functional alterations in Jurkat cells.
155 pylori strains, including m1 and m2 forms of VacA, allows us to identify structural features of the V
159 ribute to the binding and internalization of VacA and that both domains are required for vacuolating
162 tometry studies indicated that the levels of VacA binding to primary murine CD4+ T cells were signifi
164 me c release are two independent outcomes of VacA intoxication and that both effects are dependent on
167 reatment resulted in complete proteolysis of VacA into p-33 and p-55 domains, which remained physical
168 hin the amino-terminal hydrophobic region of VacA are essential for membrane channel formation, and t
169 unique amino-terminal hydrophobic region of VacA, there are three tandem GXXXG motifs (defined by gl
170 ion has shaped the phylogenetic structure of VacA and CagA, and each of these virulence determinants
172 reconstructions indicate the subdivision of VacA sequences into three main groups with distinct geog
174 ich the s1 sequence at the NH(2) terminus of VacA from strain 60190 was replaced with the s2 sequence
176 e that the assembly of functional oligomeric VacA complexes is dependent on specific sequences, inclu
178 enic H. pylori mutants lacking either GGT or VacA are incapable of preventing LPS-induced DC maturati
180 rminal portion (p55 domain) of wild-type p88 VacA could complement either Delta6-27p33 or Delta(6-27/
186 enic strain Tx30a) or a VacA mutant protein (VacA Delta 6-27) that lacks a unique strongly hydrophobi
187 rate that one of these mutant VacA proteins [VacA-Delta(6-27)] abrogates the immunosuppressive action
188 eover, when an equimolar mixture of purified VacA Delta 6-27 and purified wild-type VacA were added s
190 ri strains, treatment of cells with purified VacA proteins and infection of a mouse model, we show th
199 essing randomly mutated forms of recombinant VacA and identified 10 mutant VacA proteins that lacked
200 zed the functional properties of recombinant VacA fragments corresponding to two putative VacA domain
203 t engineering the SS1 strain to produce s1i1 VacA did not increase the toxin content of its vesicles.
204 hydrophilic N-terminal extension found on s2 VacA blocks vacuolating activity as its removal (to make
205 ype) than vesicles from the SS1 strain (s2i2 VacA), but engineering the SS1 strain to produce s1i1 Va
207 n strains producing m2 forms of the secreted VacA toxin and propose that these functionally interacti
212 ch proteins were present in the supernatant: VacA; a conserved secreted protein (HP1286); putative pe
213 of mutant VacA proteins, we demonstrate that VacA-mediated inhibition of T cell proliferation require
218 f CD4(+) T cells or B cells, indicating that VacA does not alter early signaling events required for
220 ectron microscopic examination revealed that VacA treatment disrupts the radial arrangement of actin
223 programmed necrosis pathway and suggest that VacA can be included among the growing number of bacteri
226 orming bacterial toxins, which suggests that VacA is a pore-forming toxin with unique structural prop
227 nd cytochrome c release, which suggests that VacA must enter cells to produce these two effects.
234 n relatively little study of the role of the VacA intermediate region (i-region) in toxin activity.
235 y, these data help explain the impact of the VacA intermediate region on disease and lead to the hypo
236 we present a 2.4-A crystal structure of the VacA p55 domain, which has an important role in mediatin
237 uggest that, similar to the secretion of the VacA passenger domain, the N-terminal domains of proteas
238 Here we present a structural model of the VacA pore that strongly resembles the structure of an un
239 By providing the most detailed view of the VacA structure to date, these data offer new insights in
240 ws us to identify structural features of the VacA surface that may be important for interactions with
247 novel mechanism of toxin action in which the VacA pore largely mimics the electrophysiological behavi
249 epithelial cells and mouse gastric cells to VacA disrupted induction of autophagy in response to the
250 resistance of primary murine CD4+ T cells to VacA is attributable, at least in part, to impaired VacA
252 a host cell constituent that contributes to VacA-induced cell death and that variation among cell ty
253 We previously found that limited exposure to VacA induces autophagy of gastric cells, which eliminate
255 educed induction of autophagy in response to VacA(+) compared to cells from individuals that did not
256 acA (predicted to be structurally similar to VacA membrane channels) reveals that p55 and the beta-he
257 iation among cell types in susceptibility to VacA-induced cell death is attributable at least in part
264 s against infection with H pylori; the toxin VacA disrupts autophagy to promote infection, which coul
272 hanism by producing the pro-apoptotic toxin, VacA, which was recently demonstrated to (i) localize to
273 the Helicobacter pylori pore-forming toxin, VacA, does not appear to function by either of these mec
275 f the mutations altered the capacity of ToxR-VacA-maltose-binding protein fusion proteins to insert i
276 croscopy map of hexamers formed by wild-type VacA (predicted to be structurally similar to VacA membr
280 Incubation of AZ-521 cells with wild-type VacA results in cell swelling, poly(ADP-ribose) polymera
281 s able to physically interact with wild-type VacA to form mixed oligomeric complexes, and VacA Delta3
282 ified VacA Delta 6-27 and purified wild-type VacA were added simultaneously to AGS cells, the mutant
283 tween the mutant VacA proteins and wild-type VacA, and they allow mapping of a domain involved in the
287 n contrast to VacA-induced cell vacuolation, VacA-induced clustering and redistribution of late endoc
289 terminal portion of p33 is unstructured when VacA is in a monomeric form and that it undergoes a conf
292 IL-2 compared with untreated cells, whereas VacA-treated primary human T cells continued to secrete
293 d anion-selective membrane channels, whereas VacA proteins containing P9A, G14A, and G18A mutations d
295 hese experiments mimics the process by which VacA oligomerizes when in contact with membranes of host
296 c biopsy samples from patients infected with VacA(+), but not nontoxigenic strains of H pylori, had i
299 of Drp1-induced mitochondrial fission within VacA-intoxicated cells inhibited the activation of the p
300 ants/mutants that differ from wild-type (WT) VacA in toxin activity and/or oligomeric structural feat
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