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1 acillus anthracis collectively known as the "anthrax toxin".
2 ry capacity does not affect the synthesis of anthrax toxin.
3 odies that mitigate the biological action of anthrax toxin.
4 approach to generating potent inhibitors of anthrax toxin.
5 ity, they are likely relevant targets of the anthrax toxin.
6 the two previously identified receptors for anthrax toxin.
7 s, completing the assembly of the tripartite anthrax toxin.
8 binding sites on the heptameric component of anthrax toxin.
9 hrax is thought to include neutralization of anthrax toxin.
10 (CMG2), the two known cellular receptors for anthrax toxin.
11 tective antigen (PA), a central component of anthrax toxin.
12 hanism of acidic pH-induced translocation of anthrax toxin.
13 was recently identified as the receptor for anthrax toxin.
14 ole for ARAP3 in cellular internalization of anthrax toxin.
15 pproved drug that can block the action of an anthrax toxin.
16 immunized mice against lethal challenge with anthrax toxin.
17 g the mechanism of membrane translocation by anthrax toxin.
18 understand the mechanism of translocation by anthrax toxin.
19 uses, like influenza virus, and toxins, like anthrax toxin.
20 ainst protective antigen, a component of the anthrax toxin.
21 from anthrax spore challenge and neutralizes anthrax toxins.
22 s with high activity and specificity for the anthrax toxins.
23 inst the protective antigen component of the anthrax toxins.
24 encapsulated, toxigenic B. anthracis or with anthrax toxins.
25 pore-like form retained the capacity to bind anthrax toxin A moieties and cell surface receptors, but
31 cytosolic domain plays no essential role in anthrax toxin action was obtained by showing that TEM8 a
33 of the protective antigen (PA) component of anthrax toxin allows it to self-associate into a ring-sh
37 ate talin-1 are exploited for association of anthrax toxin and its principal receptor, CMG2, with hig
39 he mechanisms by which antibodies neutralize anthrax toxin and may have future application in the eva
40 ly to the heptameric cell-binding subunit of anthrax toxin and prevents the interaction between cell-
41 terium's major virulence factors are (a) the anthrax toxins and (b) an antiphagocytic polyglutamic ca
44 This review focuses on the activities of anthrax toxins and their roles in initial and late stage
45 both at the cell surface (protecting against anthrax toxin) and in the secretory pathway (blocking pr
46 nd edema factor, which are the components of anthrax toxin, and other proteins with known or potentia
47 idate the process by which the components of anthrax toxin, and perhaps other binary bacterial toxins
48 , and streptococcal pyrogenic exotoxins] and anthrax toxin are bioterrorism agents that cause disease
53 Taken together, these studies indicate that anthrax toxins are required for dissemination of bacteri
57 encodes a host membrane protein exploited by anthrax toxin as a principal receptor, dramatically alte
58 en (PA) and lethal factor (LF) components of anthrax toxin as a system for in vivo delivery of cytoto
59 doing so we targeted a protease component of anthrax toxin as well as host proteases exploited by thi
60 disease, harbors virulence plasmids encoding anthrax toxins as well as hyaluronic acid (HA) and B. ce
63 acis that produce two key virulence factors, anthrax toxin (Atx) and a poly-gamma-D-glutamic acid cap
64 The protective antigen (PA) component of the anthrax toxin (ATx) plays an essential role in the patho
67 asive assay that uses nontoxic, reengineered anthrax toxin-beta-lactamase fusion proteins with altere
68 lethal factor (LF) and edema factor (EF) of anthrax toxin bind by means of their amino-terminal doma
69 ages and human lymphoblastoid cells affected anthrax toxin binding, internalization, and sensitivity.
74 ve antigen (PA), the B subunit of the binary anthrax toxin, binds to the cellular receptors capillary
75 ted by the protective antigen (PA) moiety of anthrax toxin by more than four orders of magnitude, wit
77 MEK1 cleaved with the lethal factor of the anthrax toxin can still be activated by its upstream mit
78 ET and LT demonstrates how the components of anthrax toxin can work together to increase lethality.
79 We used our method to prepare two different anthrax toxin cargo proteins: one containing an (alpha)t
80 tency in cell assays and protected mice from anthrax toxin challenge with much better efficacy than t
83 trate that the acid-induced translocation by anthrax toxin closely resembles that of diphtheria toxin
89 on-antimicrobial drugs with activity against anthrax toxin components; and agents that inhibit bindin
98 nted here demonstrate the versatility of the anthrax toxin delivery system and indicate that this sys
99 for PA supports its potency in neutralizing anthrax toxin, demonstrating its potential utility as a
101 igen (PA), the cell-binding component of the anthrax toxin determinant for toxin entrance into cells.
107 to the protective antigen (PA) component of anthrax toxin elicited by approved anthrax vaccines is a
113 seful as a therapeutic agent to compete with anthrax toxins for cellular receptors during active infe
114 of the protective antigen (PA) component of anthrax toxin forms a heptameric channel, (PA63)7, in ac
116 rm, the protective antigen (PA) component of anthrax toxin forms a heptameric prepore, which converts
122 The protective antigen (PA) component of the anthrax toxin forms pores within the low pH environment
123 of protease activation specificity converts anthrax toxin from a highly lethal to a potent tumoricid
124 zed full-length protective antigen (PA83) of anthrax toxin from Bacillus anthracis as a foreign antig
130 regulator AtxA controls transcription of the anthrax toxin genes and capsule biosynthetic operon.
131 non-B. anthracis isolate that possesses the anthrax toxin genes and is capable of causing a severe i
132 but carrying pXO1 (182 kb) that harbors the anthrax toxin genes, are attenuated in animal models.
133 ing the protective antigen (PA) component of anthrax toxin genetically fused to a dendritic cell (DC)
135 by protective antigen (PA), the B moiety of anthrax toxin, has focused attention on understanding ho
137 igen (PA), the receptor-binding component of anthrax toxin, heptamerizes and inserts into the endosom
138 ized that host cells would be protected from anthrax toxins if anthrax toxin receptor expression was
140 rstanding of the molecular events induced by anthrax toxin in different target cells at each stage of
141 peutic value for alleviating the symptoms of anthrax toxin in infected individuals and for medium-ter
142 A comprehensive study of the effects of anthrax toxin in mice demonstrates that toxin-induced de
143 ttern-matched polyvalent liposomes inhibited anthrax toxin in vitro at concentrations four orders of
147 e polypeptide-based polyvalent inhibitors of anthrax toxin in which multiple copies of an inhibitory
150 furin inhibitor hexa-D-arginine amide delays anthrax toxin-induced toxemia both in cells and in live
151 This work demonstrates a receptor-directed anthrax-toxin inhibitor and represents a promising strat
158 usative agent of anthrax, and the tripartite anthrax toxin is an essential element of its pathogenesi
167 tective antigen (PA), the binding subunit of anthrax toxin, is the major component in the current ant
168 he level of PA is crucial to pathogenesis by anthrax toxins, it is important to understand how the ho
169 genes for the 255 amino-terminal residues of anthrax toxin lethal factor (LFn) and the TcdB(1-556) co
170 des the protective antigen binding region of anthrax toxin lethal factor and mediates the cell entry
171 er as a fusion to the N-terminal fragment of anthrax toxin lethal factor or when naturally delivered
172 a recombinant cytotoxin, FP59, consisting of anthrax toxin lethal factor residues 1-254 fused to the
173 a recombinant cytotoxin, FP59, consisting of anthrax toxin lethal factor residues 1-254 fused to the
174 e antigen, when administered with a chimeric anthrax toxin lethal factor, Pseudomonas exotoxin fusion
178 dependent on the cytotoxic components of the anthrax toxin, lethal factor (LF) and edema factor (EF).
179 resistance of mice to the other component of anthrax toxin, lethal toxin (LT; LF plus PA), has been s
180 is dependent on the expression of both major anthrax toxins, lethal toxin (LT) and edema toxin (ET).
182 partners reduced PA/integrin endocytosis and anthrax toxin lethality, and hyaluronic acid--which inte
186 ted disruption of the Rab11/Sec15 exocyst by anthrax toxins may contribute to toxin-dependent barrier
187 The protective antigen (PA) component of anthrax toxin mediates entry of the toxin's lethal facto
188 Protective antigen (PA), a key component of anthrax toxin, mediates the entry of lethal factor (LF)
189 ining the protective antigen (PA) carrier of anthrax toxin moieties and protected targeted cells from
192 f IQNPA that neutralized 50% of the toxin in anthrax toxin neutralization assays was 0.3 nM, while 0.
195 and have been identified; however, the major anthrax toxin-neutralizing humoral responses to these an
196 engagement, with minimal protection against anthrax toxin observed in FcgammaR-deficient mice follow
197 l blockers of three binary bacterial toxins: anthrax toxin of Bacillus anthracis, C2 toxin of Clostri
199 lays a role in the proteolytic activation of anthrax toxin PA, and that PACE4 can activate substrates
200 id-based expression of protective antigen of anthrax toxin (PA83) fused with the export protein ClyA
201 f the gene for the protective antigen of the anthrax toxin, pagA, or that of the toxin regulator, atx
202 e virulence plasmids proposed to provide for anthrax toxin (pBCXO1) and/or capsule expression (pBC218
203 molysin pore from Staphylococcus aureus, the anthrax toxin pore and the 1.2-MDa mouse mechanosensitiv
205 has previously been demonstrated to inhibit anthrax toxin, postexposure use of DNI-based vaccines, i
207 nhibited HVEC and macrophage cytotoxicity by anthrax toxin, prevented erythrocyte lysis by purified h
209 sCMG2, respectively) receptor decoys bind to anthrax toxin protective antigen (PA) and compete with c
212 ctive cytotoxins, we constructed two mutated anthrax toxin protective antigen (PA) proteins in which
214 h alanine substitutions in the small loop of anthrax toxin protective antigen domain 4 was created to
217 Replacing the furin activation sequence in anthrax toxin protective antigen with an artificial pept
220 Using a defined in vitro assembly system, anthrax toxins, protective antigen, lethal factor and th
221 selective cytotoxins, we constructed mutated anthrax toxin-protective antigen (PrAg) proteins in whic
223 Bacillus anthracis structural genes for the anthrax toxin proteins and biosynthetic operon for capsu
224 ure supernatant directly cleaved each of the anthrax toxin proteins as well as an additional secreted
225 Expression of the structural genes for the anthrax toxin proteins is coordinately controlled by hos
231 Morphogenesis Gene 2 (CMG2) gene encodes an Anthrax toxin receptor (ANTXR2), but the normal physiolo
236 this corresponded with the higher levels of anthrax toxin receptor 1 (ANTXR1) in these cells than in
237 r endothelial marker 8 (TEM8), also known as anthrax toxin receptor 1 (ANTXR1), is a highly conserved
239 ficant amounts of the protective Ag receptor anthrax toxin receptor 1 (TEM8/ANTXR1) and anthrax toxin
240 which consisted of the first 14 exons of the anthrax toxin receptor 1 gene (2p13.1) and varying combi
242 tasis of other membrane proteins as CFTR and anthrax toxin receptor 2, two poor folders involved in s
243 These studies distinguish CMG2 as a second anthrax toxin receptor and identify a potent antitoxin t
245 evention depended on both the Bcl-XL and the anthrax toxin receptor binding/translocation moieties.
247 egion of domain 4 known to interact with the anthrax toxin receptor CMG-2 and within a conformation-d
248 ls would be protected from anthrax toxins if anthrax toxin receptor expression was effectively silenc
254 capillary morphogenesis protein 2 (CMG2) and anthrax toxin receptor/tumor endothelial marker 8 (ATR/T
256 een shown to bind to two cellular receptors: anthrax toxin receptor/tumor endothelial marker 8 and ca
258 ion and was recently shown to function as an anthrax-toxin receptor, its physiologic role is unclear.
259 ET increases cell surface expression of the anthrax toxin receptors (ANTXR) in monocyte-derived cell
261 subunits bind a single group of cell-surface anthrax toxin receptors (ATRs), encoded by the tumor end
263 xin (EdTx) is an AB-type toxin that binds to anthrax toxin receptors on target cells via the binding
264 Thus, even tumors genetically deficient in anthrax toxin receptors were still susceptible to the to
266 nthrax toxins enter cells via two identified anthrax toxin receptors: tumor endothelial marker 8 (TEM
267 isplay to identify a peptide that binds both anthrax-toxin receptors and attached this peptide to a s
269 including influenza virus, Pseudomonas, and anthrax toxins, require processing by host proprotein co
270 acis protective antigen (PA), a component of anthrax toxin, results in significantly augmented protec
274 vated, the protective antigen (PA) moiety of anthrax toxin self-associates to form symmetric, ring-sh
275 membrane by the protective antigen moiety of anthrax toxin serve as portals for entry of the enzymati
279 cell surface recognition unit of the binary anthrax toxin system and the primary immunogenic compone
282 y of protective antigen (PA), the protein of anthrax toxin that mediates entry of edema factor (EF) o
283 aracterized a new set of 15 VHHs against the anthrax toxins that act by binding to the edema factor (
284 acid substitutions within PA domain 4 create anthrax toxins that selectively kill human tumor cells.
285 inds the membrane-translocating component of anthrax toxin, the protective antigen (PA); domains II,
286 elucidating the process of translocation in anthrax toxin, these findings may aid in developing syst
288 trate a highly sensitive nano aptasensor for anthrax toxin through the detection of its polypeptide e
289 membrane by the Protective Antigen moiety of anthrax toxin translocate the enzymatic moieties of the
292 We reported earlier that a nontoxic form of anthrax toxin was capable of delivering a cytotoxic T-ly
293 r (LF), the principal virulence component of anthrax toxin, was a zinc-metalloprotease that cleaved a
294 lethal factor (LF) and edema factor (EF) in anthrax toxin, we asked whether LF entry into the cell m
295 ior work on targeting of tumor with modified anthrax toxins, we used phage display to select PA varia
296 zee Fabs reactive with lethal factor (LF) of anthrax toxin were isolated and converted into complete
297 n the membrane and the protective antigen of anthrax toxin, where a heptameric complex is essential f
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