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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 d that it decreases the release of pyocyanin exotoxin.
5 coccal superantigen, streptococcal pyrogenic exotoxin.
6 -4 is fused to a mutated form of Pseudomonas exotoxin.
7 a colonization factor, and cholera toxin, an exotoxin.
8 ells reflects the action of a potent protein exotoxin.
9 /CaM-dependent kinase kinase and the anthrax exotoxin.
10 ety (IL-4) and a mutated form of Pseudomonas exotoxin.
11 IgG) and IgG antibody levels to 11 S. aureus exotoxins.
12 mammals are not the primary targets of these exotoxins.
13 prevent synthesis of Gram-positive bacterial exotoxins.
14 a family of exotoxins called staphylococcal exotoxins.
15 entral cell-binding component of the anthrax exotoxins.
16 ggregates on the HVEC surfaces, and produced exotoxins.
17 homology with known Streptococcus pyrogenic exotoxins.
18 cidogenesis but not by production of protein exotoxins.
19 required for the secretion of antiphagocyte exotoxins.
20 ivate several classes of unrelated bacterial exotoxins.
21 rains are attributed to higher prevalence of exotoxins.
22 lation of IL-31 receptor with staphylococcal exotoxins.
23 lation of IL-31 receptor with staphylococcal exotoxins.
24 in response to bacterial pathogens and their exotoxins.
25 or with a truncated fragment of Pseudomonas exotoxin 38 are able to specifically kill tumors in vitr
27 by a number of virulence factors, including exotoxin A (ETA) and the type III cytotoxins (ExoS, ExoT
29 termed diphtheria toxin (DT) and Pseudomonas exotoxin A (ETA) sensitivity required gene 1 (DESR1), en
30 ysaccharide (LPS), phosholipase C (PLC), and exotoxin A (ETA) were evaluated for their ability to ind
31 e cholera toxin (CT), Pseudomonas aeruginosa exotoxin A (ETA), and ricin, move from the plasma membra
33 d a truncated form of Pseudomonas aeruginosa exotoxin A (IL13-PE38QQR) was developed for the targeted
34 s, a nontoxic form of Pseudomonas aeruginosa exotoxin A (ntPE), Bacillus globigii, Mycoplasma hyopneu
35 composed of a nontoxic form of P. aeruginosa exotoxin A (ntPE), where the C-terminal loop amino acid
47 eractions, including streptococcal pyrogenic exotoxin A (scarlet fever toxin) and two uncharacterized
48 ced M1 SF370 strain: streptococcal pyrogenic exotoxin A (SpeA) and a streptodornase D (SdaD) homologu
49 erotoxin B (SEB) and streptococcal pyrogenic exotoxin A (SPEA) delivered through the intranasal route
51 Vbeta8-targeting SAg streptococcal pyrogenic exotoxin A (SpeA), or active immunization with either wi
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
61 h intratumoral injections of IL4-Pseudomonas exotoxin A experienced complete disappearance of establi
63 of the superantigen streptococcal pyrogenic exotoxin A from 90.9 +/- 12.7 ng/mL with the control fib
66 xin in which a truncated form of Pseudomonas exotoxin A is joined to the variable region of a broadly
69 fic polysaccharide conjugated to recombinant exotoxin A of Pseudomonas aeruginosa (O157-rEPA) was saf
70 idate consisting of a genetically detoxified exotoxin A of Pseudomonas aeruginosa covalently linked t
71 Clostridium difficile, diphtheria toxin, and exotoxin A of Pseudomonas aeruginosa; however, this is t
72 th oprI primers, 11 of 13 were positive with exotoxin A primers, and 10 of 13 were positive with algD
73 ers for gyrB or oprI, 98% were positive with exotoxin A primers, and 90% were positive with algD prim
74 gyrB or oprI primers, 96% were positive with exotoxin A primers, and 92% were positive with algD prim
75 ribed human diphtheria toxin and Pseudomonas exotoxin A sensitivity required gene 1 and that DPH4 enc
77 etween the rise of anti-cell lysate and anti-exotoxin A titer and a WCXR score of 5 or more (P =.24 a
78 y antibodies (VHH) conjugated to Pseudomonas exotoxin A to deplete myeloid cells in vitro and in vivo
80 electin targeting domain, (ii) a Pseudomonas exotoxin A translocation domain, and (iii) a NF-kappaB E
81 portion of the bacterial protein Pseudomonas exotoxin A which consists of the toxin moiety of the RIT
82 or control cells with saporin or Pseudomonas exotoxin A whose intracellular mechanism of activation i
84 ocation and enzymatic domains of Pseudomonas exotoxin A), showed limited promise in initial clinical
86 receptor-binding domain (Ia) of Pseudomonas exotoxin A, AdPEDI-(Abeta1-6)(11), is effective in induc
88 proteins: recombinant Pseudomonas aeruginosa exotoxin A, and ovalbumin, using amide, hydrazone, or th
89 era toxin, ricin, and Pseudomonas aeruginosa exotoxin A, are transported to the lumen of the endoplas
90 ice from lethal challenge with streptococcal exotoxin A, as well as from lethal GAS bacterial infecti
91 oding TonB, alkaline protease,PrpL protease, exotoxin A, as well as fumarase C, Mn-dependent superoxi
92 rived from the bacterial protein Pseudomonas exotoxin A, as well as to the model Ag keyhole limpet he
93 toxin, cholera toxin, Pseudomonas aeruginosa exotoxin A, Botulinum neurotoxin, ricin, and Zika virus.
94 sed to PE38, a 38-kDa portion of Pseudomonas exotoxin A, has produced many complete remissions in dru
95 helin Fab fused to domain III of Pseudomonas exotoxin A, in which immunogenic B-cell epitopes are sil
96 including Sic, SpeB, streptococcal pyrogenic exotoxin A, Mac protein, and streptococcal phospholipase
97 ticulin, domain II of Pseudomonas aeruginosa exotoxin A, or the sorting signal of the lysosome-associ
99 albumin, recombinant Pseudomonas aeruginosa exotoxin A, recombinant B. anthracis protective antigen
100 syndrome toxin-1 and streptococcal pyrogenic exotoxin A, respectively, across porcine vaginal mucosa
103 y of a recombinant cytotoxin IL4-Pseudomonas exotoxin A, which is composed of a targeting moiety (IL-
105 ne via the endocytosed translation inhibitor Exotoxin A, which leads to an increase in ZIP-2 protein
116 stent with this hypothesis, we found that C3 exotoxin (a Rho-specific inhibitor) and HA1077 (an inhib
117 d by treatment with Clostridium botulinum C3 exotoxin, a specific inactivator of RhoA family members.
118 Unlike the acute effects of superantigen exotoxins absorbed through the gut or vaginal mucosa, li
121 asured humoral responses to 2 staphylococcal exotoxins, alpha-hemolysin (Hla) and Panton-Valentine le
125 d the cytotoxic action of native Pseudomonas exotoxin and enhanced SS1P toxicity on several human cel
126 antigen and a fusion protein of Pseudomonas exotoxin and lethal factor was tested for anti-lung canc
127 tes examined produce one or more heat-labile exotoxins and may suggest that M. ovis plays a role in t
129 oxin-1 (TSST-1), and streptococcal pyrogenic exotoxins] and anthrax toxin are bioterrorism agents tha
130 sease, is lethal owing to the actions of two exotoxins: anthrax lethal toxin (LT) and oedema toxin (E
131 lls from the lytic effects of three of these exotoxins: anthrolysin O (ALO), listeriolysin O, and pne
135 Prior studies suggest Staphylococcus aureus exotoxins are not produced when the organism is cultured
138 Catalytic rate enhancements by the bacterial exotoxins are small, and thus transition-state analogues
141 ne protease known as streptococcal pyrogenic exotoxin B (SpeB) is a key virulence factor that is prod
145 racellular protease, streptococcal pyrogenic exotoxin B (SpeB), capsular hyaluronic acid, and protein
146 ar toxins, including streptococcal pyrogenic exotoxin B (SpeB), have been implicated in pathogenesis.
149 plasmin receptor and streptococcal pyrogenic exotoxin B are currently considered major putative nephr
152 or the inhibitors 1-butanol, Y-27632, or C3 exotoxin before stimulation with the cholinergic agonist
154 crystal structure of streptococcal pyrogenic exotoxin C (SPE C) with HLA-DR2a (DRA*0101,DRB5*0101) re
159 anthrax protective antigen (PA), an anthrax exotoxin component, to modulate exotoxin cytotoxic activ
160 d/or Shiga toxin 2 (Stx2), both of which are exotoxins comprised of active (A) and binding (B) subuni
161 eurotoxin SP-PE35, a substance P-Pseudomonas exotoxin conjugate, selectively targets striatal choline
162 , an anthrax exotoxin component, to modulate exotoxin cytotoxic activity on target macrophage cell li
163 on of CaM between two domains of the anthrax exotoxin (d) binding of Ca2+ ions to only one EF-hand pa
165 duces a potent bacteriophage-encoded protein exotoxin, diphtheria toxin (DT), which causes the sympto
166 that, in addition to Stx, the phage-encoded exotoxin, diphtheria toxin (Dtx) expressed by Corynebact
168 ion of hyaluronic acid capsule synthesis and exotoxins, e.g., streptolysin S (SLS) and pyrogenic exot
169 cytotoxic strains use this system to secrete exotoxin (Exo)U and ExoT causing cytotoxicity and inhibi
172 t the site of the intramuscular injection of exotoxins from an invasive M-type 1 GAS, which caused a
173 tissue destruction, we investigated whether exotoxins from MRSA could stimulate formation of PNAs in
174 human IL-13 and a derivative of Pseudomonas exotoxin, from days 38 to 44 after the conidia challenge
175 ric anthrax toxin lethal factor, Pseudomonas exotoxin fusion protein, was extremely toxic to mice, ca
176 iated isolates typically possessed different exotoxin gene profiles (eg, Panton Valentine leukocidin
178 ized by its ability to internalize bacterial exotoxins, GPI-linked proteins, and extracellular fluid.
179 represent a non-functional heavy atom in an exotoxin group that has diverged from related bacterial
183 s blooms coupled with the presence of potent exotoxins; however, no chemical standards are currently
185 uman IL-13 and a mutated form of Pseudomonas exotoxin (IL-13-PE) might affect pathological features o
186 n protein comprised of IL-13 and Pseudomonas exotoxin (IL13-PE) on the development of pulmonary granu
187 IL-13 and a truncated version of Pseudomonas exotoxin (IL13-PE), the proliferation of primary usual i
188 IL-13 and a truncated version of Pseudomonas exotoxin (IL13-PE), which targets and kills IL-13 recept
189 be useful in the management of Gram-positive exotoxin illnesses; its action appears to be membrane st
190 n composed of IL-4 and truncated Pseudomonas exotoxin in animal models of pancreatic ductal adenocarc
191 evels of the anthrax protective antigen (PA) exotoxin in biological fluids, we have developed a metal
192 first gene in this operon (rtxA) encodes an exotoxin in vibrios, while other genes code for proteins
194 The expression of type 3 secretion system exotoxins in bacteremic isolates of P. aeruginosa confer
197 ibosylation of RhoA by Clostridium botulinum exotoxin inactivated RhoA signaling and resulted in the
198 ins, leading to inhibition of staphylococcal exotoxins, included the two-component system SrrA-SrrB.
199 in vivo production of potent staphylococcal exotoxins, including Panton-Valentine leukocidin (PVL) a
200 in composed of IL-13 and mutated Pseudomonas exotoxin induced specific killing of IL-13Ralpha2(+) tum
201 markable features describing how a bacterial exotoxin induces virulence exclusively in specific cells
203 gy of an intracellular pathogen, in which an exotoxin is delivered from an intracellular location to
206 he prophage encoding streptococcal pyrogenic exotoxin K (SpeK) and extracellular phospholipase A(2) (
209 anthrax toxin is the toxic component of the exotoxin (lethal toxin) secreted by toxic strains of Bac
211 ands in S. aureus which encode enterotoxins, exotoxins, leukocidins, and leukotoxins not found in S.
214 g a mutated human IL-13 fused to Pseudomonas exotoxin (mhIL-13-PE) that specifically binds to IL13Ral
218 the ability of GML to inhibit the effects of exotoxins on mammalian cells and prevent rabbit lethalit
220 ment with Clostridium botulinum exoenzyme C3 exotoxin or expression of dominant negative RhoA blocks
227 we examined the early role played by another exotoxin produced by this pathogen, adenylate cyclase to
228 tending toxins (CDTs) are tripartite protein exotoxins produced by a diverse group of pathogenic Gram
229 This is primarily due to the pathogenic exotoxins produced by Bacillus anthracis as well as othe
233 GAS SAgs, namely the streptococcal pyrogenic exotoxins produced by the globally disseminated M1T1 GAS
235 bin (as low as 1 mug/mL) inhibited S. aureus exotoxin production while increasing production of prote
239 hion and that a chimeric 5-Helix/Pseudomonas exotoxin protein recognizes cells expressing Env from a
240 us pyogenes (GAS) express superantigen (SAg) exotoxin proteins capable of inducing lethal shock.
242 h-killing P. shumwayae do not secrete potent exotoxins; rather, fish mortality results from micropred
244 six genes (rtxACHBDE), where rtxA encodes an exotoxin, rtxC encodes an RtxA activator, rtxH encodes a
245 hages were prestimulated with staphylococcal exotoxins (SEB, alpha-toxin) to up-regulate the IL-31 re
249 his paper describes a biosensing concept for exotoxins secreted by Staphylococcus aureus and Pseudomo
251 lates into 22 distinct subgroups, designated exotoxin sequence types (ETST), while the standard seven
252 ed in pathogenesis (e.g., staphylocoagulase, exotoxin, Ser-Asp fibrinogen-binding bone sialoprotein-b
254 rulence factors, the streptococcal pyrogenic exotoxin (Spe) A and the cysteine protease SpeB, was rec
256 superantigen (ssa), streptococcal pyrogenic exotoxins (speC, speH, and speI), and DNases (spd1 and s
259 zolid resulted in significant suppression of exotoxin synthesis and improved survival outcomes in a r
260 coccal enterotoxin B (SEB), a shock-inducing exotoxin synthesized by Staphylococcus aureus, is an imp
261 nteracts with the type III-secreted effector exotoxin T (ExoT) and plays a key role in vivo in limiti
265 idium difficile infections are caused by two exotoxins, TcdA and TcdB, which target host colonocytes
266 major nosocomial pathogen that produces two exotoxins, TcdA and TcdB, with TcdB thought to be the pr
268 rcularly permuted human IL-4 and Pseudomonas exotoxin termed IL4(38-37)-PE38KDEL, or IL-4 cytotoxin.
269 ny pathogenic gram-positive bacteria release exotoxins that belong to the family of cholesterol-depen
270 s (SEs) belong to a large group of bacterial exotoxins that cause severe immunopathologies, especiall
271 ubstrate tryptophan to synthesize diffusible exotoxins that kill the nematode Caenorhabditis elegans.
272 us has numerous virulence factors, including exotoxins that may increase the severity of infection.
273 Staphylococcal enterotoxins are superantigen exotoxins that mediate food poisoning and toxic shock sy
274 esumably through the release of allelopathic exotoxins that offer advantages for Prymnesium in its in
275 ed and seems to be not valid for the anthrax exotoxin, the CaM-regulated K+-channel and possibly also
276 s from environmental exposure to Pseudomonas exotoxin, the component of the RIT that elicits the neut
278 a and P. shumwayae reportedly secrete potent exotoxins thought to cause fish lesion events, acute fis
279 ents using constitutively active Cdc42 or C3 exotoxin to inhibit Rho GTPase supported a role of Rho G
281 particular toxin, allowing bacteria-bearing exotoxins to kill a broader spectrum of predators, incre
283 C. difficile releases 2 structurally similar exotoxins, toxin A and toxin B, animal experiments sugge
287 or a type three secretion system, a putative exotoxin, two different RTX toxins, and four pilus syste
291 ously we found that pertussis toxin (PT), an exotoxin virulence factor produced by Bordetella pertuss
292 o determine whether pertussis toxin (PT), an exotoxin virulence factor produced exclusively by Bordet
293 ples of chemical entities designed to target exotoxin virulence factors from important human bacteria
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.
297 tor of the geranylgeranylation of Rho; by C3 exotoxin, which inactivates Rho; and by the adenoviral e
299 ins is the NAD(+)-dependent ADP-ribosylating exotoxins, which include pertussis, cholera, and diphthe
300 ective antigen component of the B. anthracis exotoxin with high affinity and conjugated to polyethyle
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