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1 the remaining 25-kDa portion of Pseudomonas exotoxin.
2 of IL-13 and a truncated form of Pseudomonas exotoxin.
3 wo unrelated toxins, anthrax and Pseudomonas exotoxin.
4 coccal superantigen, streptococcal pyrogenic exotoxin.
5 -4 is fused to a mutated form of Pseudomonas exotoxin.
6 a colonization factor, and cholera toxin, an exotoxin.
7 ells reflects the action of a potent protein exotoxin.
8 /CaM-dependent kinase kinase and the anthrax exotoxin.
9 d that it decreases the release of pyocyanin exotoxin.
10 -causing GAS mediated by prophage PhiHKU.vir exotoxins.
11 in response to bacterial pathogens and their exotoxins.
12 IgG) and IgG antibody levels to 11 S. aureus exotoxins.
13 mammals are not the primary targets of these exotoxins.
14 e IL-17 after stimulation with gram-positive exotoxins.
15 prevent synthesis of Gram-positive bacterial exotoxins.
16 a family of exotoxins called staphylococcal exotoxins.
17 entral cell-binding component of the anthrax exotoxins.
18 ggregates on the HVEC surfaces, and produced exotoxins.
19 homology with known Streptococcus pyrogenic exotoxins.
20 cidogenesis but not by production of protein exotoxins.
21 cular characterization of PhiHKU.vir-encoded exotoxins.
22 required for the secretion of antiphagocyte exotoxins.
23 ivate several classes of unrelated bacterial exotoxins.
24 rains are attributed to higher prevalence of exotoxins.
25 lation of IL-31 receptor with staphylococcal exotoxins.
26 lation of IL-31 receptor with staphylococcal exotoxins.
27 or with a truncated fragment of Pseudomonas exotoxin 38 are able to specifically kill tumors in vitr
29 by a number of virulence factors, including exotoxin A (ETA) and the type III cytotoxins (ExoS, ExoT
31 termed diphtheria toxin (DT) and Pseudomonas exotoxin A (ETA) sensitivity required gene 1 (DESR1), en
33 3, and NF4 strains were clonal and possessed exotoxin A (ExoA), the NF1 strain was determined to be p
34 d a truncated form of Pseudomonas aeruginosa exotoxin A (IL13-PE38QQR) was developed for the targeted
35 s, a nontoxic form of Pseudomonas aeruginosa exotoxin A (ntPE), Bacillus globigii, Mycoplasma hyopneu
36 composed of a nontoxic form of P. aeruginosa exotoxin A (ntPE), where the C-terminal loop amino acid
47 ced M1 SF370 strain: streptococcal pyrogenic exotoxin A (SpeA) and a streptodornase D (SdaD) homologu
48 erotoxin B (SEB) and streptococcal pyrogenic exotoxin A (SPEA) delivered through the intranasal route
50 Vbeta8-targeting SAg streptococcal pyrogenic exotoxin A (SpeA), or active immunization with either wi
51 rotein expression of streptococcal pyrogenic exotoxin A (SpeA; also known as scarlet fever or erythro
52 joined to a truncated portion of Pseudomonas exotoxin A (termed PE38) have been evaluated in clinical
53 at the P. aeruginosa translational inhibitor Exotoxin A (ToxA), which ribosylates elongation factor 2
54 itor cycloheximide, saponin, and Pseudomonas exotoxin A additionally confirmed that the resistance wa
56 f prophages encoding streptococcal pyrogenic exotoxin A and extracellular DNases and (2) the reciproc
58 (LF) and the catalytic domain of Pseudomonas exotoxin A by (i) mutating the N-terminal amino acids an
60 that elevated furin-dependent activation of exotoxin A caused increased cell death in CF respiratory
64 of the superantigen streptococcal pyrogenic exotoxin A from 90.9 +/- 12.7 ng/mL with the control fib
68 fic polysaccharide conjugated to recombinant exotoxin A of Pseudomonas aeruginosa (O157-rEPA) was saf
69 idate consisting of a genetically detoxified exotoxin A of Pseudomonas aeruginosa covalently linked t
70 Clostridium difficile, diphtheria toxin, and exotoxin A of Pseudomonas aeruginosa; however, this is t
71 th oprI primers, 11 of 13 were positive with exotoxin A primers, and 10 of 13 were positive with algD
72 gyrB or oprI primers, 96% were positive with exotoxin A primers, and 92% were positive with algD prim
73 ribed human diphtheria toxin and Pseudomonas exotoxin A sensitivity required gene 1 and that DPH4 enc
75 y antibodies (VHH) conjugated to Pseudomonas exotoxin A to deplete myeloid cells in vitro and in vivo
77 electin targeting domain, (ii) a Pseudomonas exotoxin A translocation domain, and (iii) a NF-kappaB E
78 portion of the bacterial protein Pseudomonas exotoxin A which consists of the toxin moiety of the RIT
79 or control cells with saporin or Pseudomonas exotoxin A whose intracellular mechanism of activation i
81 ocation and enzymatic domains of Pseudomonas exotoxin A), showed limited promise in initial clinical
83 receptor-binding domain (Ia) of Pseudomonas exotoxin A, AdPEDI-(Abeta1-6)(11), is effective in induc
84 proteins: recombinant Pseudomonas aeruginosa exotoxin A, and ovalbumin, using amide, hydrazone, or th
85 era toxin, ricin, and Pseudomonas aeruginosa exotoxin A, are transported to the lumen of the endoplas
86 ice from lethal challenge with streptococcal exotoxin A, as well as from lethal GAS bacterial infecti
87 rived from the bacterial protein Pseudomonas exotoxin A, as well as to the model Ag keyhole limpet he
88 toxin, cholera toxin, Pseudomonas aeruginosa exotoxin A, Botulinum neurotoxin, ricin, and Zika virus.
89 sed to PE38, a 38-kDa portion of Pseudomonas exotoxin A, has produced many complete remissions in dru
90 helin Fab fused to domain III of Pseudomonas exotoxin A, in which immunogenic B-cell epitopes are sil
91 including Sic, SpeB, streptococcal pyrogenic exotoxin A, Mac protein, and streptococcal phospholipase
92 ticulin, domain II of Pseudomonas aeruginosa exotoxin A, or the sorting signal of the lysosome-associ
94 albumin, recombinant Pseudomonas aeruginosa exotoxin A, recombinant B. anthracis protective antigen
95 syndrome toxin-1 and streptococcal pyrogenic exotoxin A, respectively, across porcine vaginal mucosa
99 ne via the endocytosed translation inhibitor Exotoxin A, which leads to an increase in ZIP-2 protein
111 stent with this hypothesis, we found that C3 exotoxin (a Rho-specific inhibitor) and HA1077 (an inhib
112 d by treatment with Clostridium botulinum C3 exotoxin, a specific inactivator of RhoA family members.
113 Unlike the acute effects of superantigen exotoxins absorbed through the gut or vaginal mucosa, li
116 asured humoral responses to 2 staphylococcal exotoxins, alpha-hemolysin (Hla) and Panton-Valentine le
120 d the cytotoxic action of native Pseudomonas exotoxin and enhanced SS1P toxicity on several human cel
121 antigen and a fusion protein of Pseudomonas exotoxin and lethal factor was tested for anti-lung canc
123 tes examined produce one or more heat-labile exotoxins and may suggest that M. ovis plays a role in t
124 oxin-1 (TSST-1), and streptococcal pyrogenic exotoxins] and anthrax toxin are bioterrorism agents tha
125 sease, is lethal owing to the actions of two exotoxins: anthrax lethal toxin (LT) and oedema toxin (E
126 lls from the lytic effects of three of these exotoxins: anthrolysin O (ALO), listeriolysin O, and pne
130 Prior studies suggest Staphylococcus aureus exotoxins are not produced when the organism is cultured
133 Catalytic rate enhancements by the bacterial exotoxins are small, and thus transition-state analogues
137 ne protease known as streptococcal pyrogenic exotoxin B (SpeB) is a key virulence factor that is prod
141 racellular protease, streptococcal pyrogenic exotoxin B (SpeB), capsular hyaluronic acid, and protein
142 ar toxins, including streptococcal pyrogenic exotoxin B (SpeB), have been implicated in pathogenesis.
145 plasmin receptor and streptococcal pyrogenic exotoxin B are currently considered major putative nephr
148 or the inhibitors 1-butanol, Y-27632, or C3 exotoxin before stimulation with the cholinergic agonist
150 crystal structure of streptococcal pyrogenic exotoxin C (SPE C) with HLA-DR2a (DRA*0101,DRB5*0101) re
154 anthrax protective antigen (PA), an anthrax exotoxin component, to modulate exotoxin cytotoxic activ
155 stridium difficile toxin A (TcdA) is a major exotoxin contributing to disruption of the colonic epith
156 , an anthrax exotoxin component, to modulate exotoxin cytotoxic activity on target macrophage cell li
157 on of CaM between two domains of the anthrax exotoxin (d) binding of Ca2+ ions to only one EF-hand pa
159 duces a potent bacteriophage-encoded protein exotoxin, diphtheria toxin (DT), which causes the sympto
160 that, in addition to Stx, the phage-encoded exotoxin, diphtheria toxin (Dtx) expressed by Corynebact
162 ion of hyaluronic acid capsule synthesis and exotoxins, e.g., streptolysin S (SLS) and pyrogenic exot
163 cytotoxic strains use this system to secrete exotoxin (Exo)U and ExoT causing cytotoxicity and inhibi
166 t the site of the intramuscular injection of exotoxins from an invasive M-type 1 GAS, which caused a
167 tissue destruction, we investigated whether exotoxins from MRSA could stimulate formation of PNAs in
168 ric anthrax toxin lethal factor, Pseudomonas exotoxin fusion protein, was extremely toxic to mice, ca
169 iated isolates typically possessed different exotoxin gene profiles (eg, Panton Valentine leukocidin
171 ized by its ability to internalize bacterial exotoxins, GPI-linked proteins, and extracellular fluid.
174 s blooms coupled with the presence of potent exotoxins; however, no chemical standards are currently
176 uman IL-13 and a mutated form of Pseudomonas exotoxin (IL-13-PE) might affect pathological features o
177 IL-13 and a truncated version of Pseudomonas exotoxin (IL13-PE), the proliferation of primary usual i
178 IL-13 and a truncated version of Pseudomonas exotoxin (IL13-PE), which targets and kills IL-13 recept
179 be useful in the management of Gram-positive exotoxin illnesses; its action appears to be membrane st
180 n composed of IL-4 and truncated Pseudomonas exotoxin in animal models of pancreatic ductal adenocarc
181 evels of the anthrax protective antigen (PA) exotoxin in biological fluids, we have developed a metal
182 first gene in this operon (rtxA) encodes an exotoxin in vibrios, while other genes code for proteins
184 The expression of type 3 secretion system exotoxins in bacteremic isolates of P. aeruginosa confer
187 ibosylation of RhoA by Clostridium botulinum exotoxin inactivated RhoA signaling and resulted in the
188 ins, leading to inhibition of staphylococcal exotoxins, included the two-component system SrrA-SrrB.
189 in vivo production of potent staphylococcal exotoxins, including Panton-Valentine leukocidin (PVL) a
190 in composed of IL-13 and mutated Pseudomonas exotoxin induced specific killing of IL-13Ralpha2(+) tum
191 markable features describing how a bacterial exotoxin induces virulence exclusively in specific cells
193 gy of an intracellular pathogen, in which an exotoxin is delivered from an intracellular location to
196 he prophage encoding streptococcal pyrogenic exotoxin K (SpeK) and extracellular phospholipase A(2) (
199 anthrax toxin is the toxic component of the exotoxin (lethal toxin) secreted by toxic strains of Bac
201 ands in S. aureus which encode enterotoxins, exotoxins, leukocidins, and leukotoxins not found in S.
204 g a mutated human IL-13 fused to Pseudomonas exotoxin (mhIL-13-PE) that specifically binds to IL13Ral
207 hat thermostable direct haemolysin (TDH), an exotoxin of the food-borne pathogen Vibrio parahaemolyti
210 he bicomponent pore-forming leukocidin (Luk) exotoxins of the major pathogen Staphylococcus aureus as
211 the ability of GML to inhibit the effects of exotoxins on mammalian cells and prevent rabbit lethalit
213 ment with Clostridium botulinum exoenzyme C3 exotoxin or expression of dominant negative RhoA blocks
220 tality risk, are due to diphtheria toxin, an exotoxin produced by the pathogen that inhibits protein
222 we examined the early role played by another exotoxin produced by this pathogen, adenylate cyclase to
223 tending toxins (CDTs) are tripartite protein exotoxins produced by a diverse group of pathogenic Gram
224 This is primarily due to the pathogenic exotoxins produced by Bacillus anthracis as well as othe
228 GAS SAgs, namely the streptococcal pyrogenic exotoxins produced by the globally disseminated M1T1 GAS
230 bin (as low as 1 mug/mL) inhibited S. aureus exotoxin production while increasing production of prote
233 hion and that a chimeric 5-Helix/Pseudomonas exotoxin protein recognizes cells expressing Env from a
234 us pyogenes (GAS) express superantigen (SAg) exotoxin proteins capable of inducing lethal shock.
237 six genes (rtxACHBDE), where rtxA encodes an exotoxin, rtxC encodes an RtxA activator, rtxH encodes a
238 hages were prestimulated with staphylococcal exotoxins (SEB, alpha-toxin) to up-regulate the IL-31 re
239 ed a transcytosis pathway used by cholix, an exotoxin secreted by nonpandemic forms of the intestinal
242 his paper describes a biosensing concept for exotoxins secreted by Staphylococcus aureus and Pseudomo
244 lates into 22 distinct subgroups, designated exotoxin sequence types (ETST), while the standard seven
245 ed in pathogenesis (e.g., staphylocoagulase, exotoxin, Ser-Asp fibrinogen-binding bone sialoprotein-b
247 rulence factors, the streptococcal pyrogenic exotoxin (Spe) A and the cysteine protease SpeB, was rec
249 superantigen (ssa), streptococcal pyrogenic exotoxins (speC, speH, and speI), and DNases (spd1 and s
253 zolid resulted in significant suppression of exotoxin synthesis and improved survival outcomes in a r
254 coccal enterotoxin B (SEB), a shock-inducing exotoxin synthesized by Staphylococcus aureus, is an imp
255 nteracts with the type III-secreted effector exotoxin T (ExoT) and plays a key role in vivo in limiti
257 t, an albumin-binding domain and Pseudomonas exotoxin targeting PD-1-expressing cells, selectively re
260 idium difficile infections are caused by two exotoxins, TcdA and TcdB, which target host colonocytes
261 major nosocomial pathogen that produces two exotoxins, TcdA and TcdB, with TcdB thought to be the pr
264 rcularly permuted human IL-4 and Pseudomonas exotoxin termed IL4(38-37)-PE38KDEL, or IL-4 cytotoxin.
265 (Hp) secrete VacA, a diffusible pore-forming exotoxin that is epidemiologically linked to gastric dis
266 Here we identify cytolysin-a two-subunit exotoxin that is secreted by Enterococcus faecalis(5,6)-
267 ny pathogenic gram-positive bacteria release exotoxins that belong to the family of cholesterol-depen
268 s (SEs) belong to a large group of bacterial exotoxins that cause severe immunopathologies, especiall
269 lentine leukocidin (PVL) and alpha-toxin are exotoxins that create lytic pores in the host cell membr
270 ubstrate tryptophan to synthesize diffusible exotoxins that kill the nematode Caenorhabditis elegans.
271 us has numerous virulence factors, including exotoxins that may increase the severity of infection.
272 esumably through the release of allelopathic exotoxins that offer advantages for Prymnesium in its in
273 ed and seems to be not valid for the anthrax exotoxin, the CaM-regulated K+-channel and possibly also
274 s from environmental exposure to Pseudomonas exotoxin, the component of the RIT that elicits the neut
276 ents using constitutively active Cdc42 or C3 exotoxin to inhibit Rho GTPase supported a role of Rho G
278 particular toxin, allowing bacteria-bearing exotoxins to kill a broader spectrum of predators, incre
280 ile infection (CDI) is mediated by two major exotoxins, toxin A (TcdA) and toxin B (TcdB), that damag
281 C. difficile releases 2 structurally similar exotoxins, toxin A and toxin B, animal experiments sugge
283 s primarily from the 2 C. difficile-secreted exotoxins-toxin A (TcdA) and toxin B (TcdB)-that disrupt
286 or a type three secretion system, a putative exotoxin, two different RTX toxins, and four pilus syste
290 ously we found that pertussis toxin (PT), an exotoxin virulence factor produced by Bordetella pertuss
291 o determine whether pertussis toxin (PT), an exotoxin virulence factor produced exclusively by Bordet
292 ples of chemical entities designed to target exotoxin virulence factors from important human bacteria
293 c knockout mutants of the PhiHKU.vir-encoded exotoxins, we find that SpeC and Spd1 act synergisticall
294 hich point both IgG titers against S. aureus exotoxins were determined, and the functionality of the
296 tibacter actinomycetemcomitans is a powerful exotoxin, which can cause imbalance in host response.
298 ins is the NAD(+)-dependent ADP-ribosylating exotoxins, which include pertussis, cholera, and diphthe
299 ective antigen component of the B. anthracis exotoxin with high affinity and conjugated to polyethyle