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1 ExoS (453 amino acids) is a bi-functional type III cytot
2 ExoS (453 amino acids) is a bi-functional type-III cytot
3 ExoS (453 amino acids) is a bifunctional type III cytoto
4 ExoS ADP-ribosylated recombinant moesin at a linear velo
5 ExoS ADP-ribosylates Ras and prevents it from interactin
6 ExoS ADP-ribosylation of Rac1 is cell line dependent.
7 ExoS and ExoT are closely related bifunctional proteins
8 ExoS did not ADP-ribosylate Crk-I.
9 ExoS includes both GTPase-activating (GAP) and ADP-ribos
10 ExoS is a bifunctional protein having both GTPase-activa
11 ExoS is a bifunctional Type III cytotoxin of Pseudomonas
12 ExoS is a bifunctional type III cytotoxin produced by Ps
13 ExoS is a bifunctional type III cytotoxin secreted by Ps
14 ExoS is a bifunctional type III cytotoxin that is secret
15 ExoS structural gene sequence comparisons found the gene
16 ExoS(E381D), a mutant deficient in ADP-ribosyltransferas
17 ExoS, ExoT, ExoY, and ExoU all possess enzymatic activit
18 ExoS/ChvI also has important roles in regulating succino
19 1 or with a specific JNK inhibitor abolishes ExoS-triggered apoptosis, demonstrating the requirement
20 , a 14-3-3 family protein, factor-activating ExoS (FAS) had no influence on the activity of the GAP d
27 c cells, and 11 of 33 had antibodies against ExoS, while most CF sera contained antibodies against Po
30 ) visualize the ability of P. aeruginosa and ExoS to align with actin filaments, and (v) demonstrate
32 gest that periplasmically localized ExoR and ExoS-ChvI function together in a unique and critical reg
42 membrane inhibited the actions of RhoGDI and ExoS RhoGAP on the translocation of Cdc42 from membrane
45 rescent energy transfer was detected between ExoS and 14-3-3 proteins but not between ExoS and Rabs p
47 , and RhoA in vivo, the relationship between ExoS RhoGAP and the eukaryotic regulators of Rho GTPases
48 gulator ExoR interacts genetically with both ExoS and ChvI, and localizes to the periplasm of S. meli
55 observed for the ADP-ribosylation of Ras by ExoS, where ADP-ribosylated Ras loses the ability to bin
57 ase subfamily that can be ADP ribosylated by ExoS and indicates that ExoS can inhibit both Ras and Ra
58 anslocated ExoS and that ADP-ribosylation by ExoS affects RalA interaction with its downstream effect
59 nd in vitro, whereas the ADP-ribosylation by ExoS is poly-substrate-specific and includes Ras as an e
60 udied the effect of Rab5 ADP-ribosylation by ExoS on its cellular function, i.e., regulation of early
63 is indicates that within the mammalian cells ExoS undergoes a negatively charged modification, in add
64 nsferase activity, and in J744-Eclone cells, ExoS ADP-ribosyltransferase activity caused a more sever
66 since the expression of the ADPRT-competent ExoS also induced rapid cell death in the Drosophila mel
74 of substrates modified by type III-delivered ExoS identified a 70-kDa protein as an early and predomi
76 ese results indicate that type III-delivered ExoS localizes on the host endosomes and utilizes multip
82 ons in the type III secretion (T3S) effector ExoS to manipulate P. aeruginosa infection, and (iii) hi
83 we determined which of the three effectors (ExoS, ExoT, or ExoY) were required for bleb niche format
84 ne of the major type III secreted effectors, ExoS, prevented triggering of type III secretion by bact
87 y leading to apoptosis, but also establishes ExoS as a valuable tool, in principle, for the elucidati
88 (c20) does not function directly in the ExoR-ExoS/ChvI regulatory pathway and that ExoR(m) is the fun
90 h isogenic mutants secreting wild-type ExoS, ExoS defective in GTPase-activating protein (GAP) activi
91 e type III secretion system effectors (ExoU, ExoS, and PcrV) and for strain relatedness using randoml
92 biochemical and enzymatic functions of ExoU, ExoS, and ExoT, three effector proteins secreted by this
93 cterial strain that naturally secretes ExoU, ExoS, and ExoT were generated to carefully evaluate the
96 oculture of P. aeruginosa strains expressing ExoS with HL-60 myeloid cells revealed the cell line to
97 GST-CpA co-immunoprecipitation studies found ExoS ADP-ribosylation of CpA to efficiently inhibit CpA
98 dy provides insight into a mechanism for how ExoS ADP-ribosylation of Rab5 inhibits Rab5 function.
99 ts provide insight into the mechanism of how ExoS/ChvI regulates its downstream targets and lay a fou
102 e pathogenesis of P. aeruginosa keratitis in ExoS- and ExoT-producing strains is almost entirely due
103 ant negative Rab5(Ser34Asn) does not inhibit ExoS trafficking to the perinuclear region of intoxicate
104 S in the periplasm of S. meliloti to inhibit ExoS/ChvI activity, and that ExoR represents a novel per
105 eLa cells with the presence of intracellular ExoS and further proved the dependence of this process o
106 eb niches and intracellular survival involve ExoS ADP-r activity and implicate a connection between b
107 NAD and FAS, the GAP activity of full-length ExoS was reduced about 10-fold, whereas NAD and FAS did
109 calization domain (residues 51-72) localizes ExoS to a perinuclear region within eukaryotic cells.
113 P-ribosylation by wild-type and E381A mutant ExoS by two-dimensional electrophoresis found the former
116 led that auto-ADP-ribosylation of Arg-146 of ExoS was crucial for inhibition of GAP activity in vitro
119 ted study not only highlights the ability of ExoS ADPRT to modulate host cell signaling, eventually l
122 to cytoskeleton dynamics, and the ability of ExoS to ADP-ribosylate the ERM proteins links ADP-ribosy
124 n of Rab5(TL) does not affect the ability of ExoS to modify intracellular trafficking, while expressi
125 he coordinate function of both activities of ExoS in J774A.1 macrophages was assessed by using P. aer
127 l ADP-ribosyltransferase (ADPRT) activity of ExoS have been found to target but exert opposite effect
129 hough the ADP-ribosyltransferase activity of ExoS is dependent upon FAS, a 14-3-3 family protein, fac
131 e ADP-ribosyltransferase (ADP-r) activity of ExoS, but not the Rho-GAP activity nor the membrane loca
133 not required to observe the pI conformers of ExoS; it enhanced the resolution and formation of pI con
134 r studies also highlight the contribution of ExoS to the opportunistic nature of P. aeruginosa infect
141 sociated with the ADP-ribosylating domain of ExoS, as bacteria expressing plasmids lacking expression
145 as required for the antiphagocytic effect of ExoS and was linked to interference of lamellopodium and
147 ate the mechanisms underlying the effects of ExoS GAP and ADPRT activities on P. aeruginosa internali
148 erential targeting and coordinate effects of ExoS GAP and ADPRT activity on Rac1 within the host cell
150 e ADP-ribosylation and functional effects of ExoS on RalA, ExoS was found to ADP-ribosylate endogenou
151 domains on Rac1 function, limited effects of ExoS-GAP on Rac1 inactivation were evident in HT-29 cell
153 dies provide insight into the enhancement of ExoS ADPRT activity within the eukaryotic cell microenvi
154 study, we demonstrate that the expression of ExoS in HeLa cells by eukaryotic expression vector effec
155 ved, which is required for the expression of ExoS/ChvI-regulated symbiosis genes, we characterized wi
156 GTPase-activating protein-deficient form of ExoS rounded cells, indicating the ADP-ribosyltransferas
165 ors across the host cell plasma membrane) of ExoS is indeed self-regulated and that this inhibition o
166 ganization of the leucines within the MLD of ExoS is different from that of previously described leuc
169 e studies confirm the bifunctional nature of ExoS activity within macrophages when translocated by TT
171 he ADP-ribosyltransferase (ADPRT) portion of ExoS include low molecular weight G-proteins (LMWG-prote
172 s reflected both the increased production of ExoS and the production of ExoS having a higher specific
175 the ADP ribosyltransferase (ADPR) regions of ExoS or ExoT also impaired proapoptotic activity in infe
176 actions is underscored by the requirement of ExoS/ChvI orthologues for virulence of the related alpha
178 se studies draw attention to the key role of ExoS ADPRT activity in causing the effects of bacteriall
179 leb niche formation and the known role(s) of ExoS-mediated apoptosis and/or Rab GTPase inactivation.
180 he MLD did not inhibit type III secretion of ExoS from P. aeruginosa or type III delivery of ExoS int
181 atest impact on virulence while secretion of ExoS had an intermediate effect and ExoT had a minor eff
188 tand the cellular basis for the targeting of ExoS ADPRT activity to Rac1, an inverse relationship was
191 activity demonstrated that the virulence of ExoS was largely dependent on its ADP-ribosyltransferase
193 GTPase-activating protein (GAP) activity, or ExoS defective in ADP-ribosyltransferase activity demons
195 commonly found combinations of ExoU/ExoT or ExoS/ExoT provides redundant and failsafe mechanisms to
196 o detected were antibodies to ExoS, ExoU, or ExoS and ExoU, the latter indicating sequential P. aerug
198 the first detection of antibodies to pooled ExoS/PopB occurred at a time similar to those of detecti
204 tion and functional effects of ExoS on RalA, ExoS was found to ADP-ribosylate endogenous RalA and rec
208 of the host innate immune response requires ExoS-mediated ADP-ribosylation of Ras in neutrophils.
209 s for the type III secretion system restored ExoS secretion but did not always reestablish cytotoxici
211 in was determined to be auto-ADP-ribosylated ExoS, whereas the 25-kDa protein appeared to represent a
213 ophages, where Rac1 was not ADP-ribosylated, ExoS caused a decrease in the levels of active Rac1, and
215 e III-mediated translocation of exoenzyme S (ExoS) into HT-29 epithelial cells by Pseudomonas aerugin
225 P. aeruginosa to be internalized and secrete ExoS within T24 cells, but as with wild-type ExoS, trans
226 d to a more acidic pI than type III secreted ExoS but more basic than auto-ADP-ribosylated ExoS.
228 it was proposed that P. aeruginosa secreting ExoS, upon infection, shuts down host cell survival sign
231 ExoS to intracellular membranes and targeted ExoS to ADP-ribosylate small molecular weight membrane p
232 studies showed that the N-terminus targeted ExoS to intracellular membranes within eukaryotic cells.
233 membrane localization domain [MLD]) targets ExoS to the Golgi-endoplasmic reticulum (Golgi-ER) of ma
235 ane localization domain (MLD), which targets ExoS to perinuclear vesicles within mammalian cells.
238 on and T3S translocation, (iii) confirm that ExoS ADPRT activity targeted a cellular substrate that i
239 noninvasive PA103 strains demonstrated that ExoS or ExoT that is injected into host cells by a type
241 ts with an exoS96::Tn5 mutant indicated that ExoS/ChvI influences the expression of a few hundred gen
242 e ADP ribosylated by ExoS and indicates that ExoS can inhibit both Ras and Rap signaling pathways in
244 T activity-dependent manner, indicating that ExoS alone is sufficient to trigger apoptotic death of h
251 GDI on actin reorganization, suggesting that ExoS RhoGAP functions as a molecular mimic of eukaryotic
255 s suggest that both the ExoR protein and the ExoS/ChvI two-component regulatory system are involved i
256 at the YopE MLD functionally complements the ExoS MLD for intracellular targeting in mammalian cells.
257 train PA14 lacks the coding sequence for the ExoS effector protein and does not seem to express ExoY.
258 The cellular pathway responsible for the ExoS-induced cytotoxicity appears to be well conserved,
260 xpressing plasmids lacking expression of the ExoS GAP activity nonetheless increased the permeation o
267 n addition, also detected were antibodies to ExoS, ExoU, or ExoS and ExoU, the latter indicating sequ
268 epeat region of ExoR that disrupt binding to ExoS and cause a dramatic increase in ExoS/ChvI-dependen
269 her, our results indicate that ExoR binds to ExoS in the periplasm of S. meliloti to inhibit ExoS/Chv
271 an epithelial cells that had been exposed to ExoS-producing Pa, but not an isogenic non-ExoS producin
276 One of the most commonly expressed toxins, ExoS, has two domains that are predicted to affect cytos
277 ed by P. aeruginosa strains that translocate ExoS having GAP or ADPRT mutations allowed the independe
278 llular substrate of bacterially translocated ExoS and that ADP-ribosylation by ExoS affects RalA inte
280 1, was inhibited by bacterially translocated ExoS, indicating an effect of ExoS on cellular RalA func
281 nown cellular substrates of TTS-translocated ExoS (TTS-ExoS) ADPRT activity include proteins in the R
282 cells, where Rac1 is ADP-ribosylated by TTS-ExoS, Rac1 was activated and relocalized to the membrane
283 lar substrates of TTS-translocated ExoS (TTS-ExoS) ADPRT activity include proteins in the Ras superfa
284 sylation of a non-G-protein substrate of TTS-ExoS, cyclophilin A (CpA), a peptidyl-prolyl isomerase (
285 rains expressing and translocating wild-type ExoS or ExoS defective in GAP and/or ADPRT activity.
286 and P. aeruginosa cells expressing wild-type ExoS preferentially bound to the leading edge of T24 cel
287 on with isogenic mutants secreting wild-type ExoS, ExoS defective in GTPase-activating protein (GAP)
288 ExoS within T24 cells, but as with wild-type ExoS, translocation was limited in association with disr
290 S and YopE share structural homology, unlike ExoS, the intracellular localization of YopE within mamm
294 ound to the leading edge of T24 cells, where ExoS altered leading-edge architecture and actin anchori
297 we show that ExoR physically associates with ExoS and that this association is important for regulati
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