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1 g mouse bioassay for BoNT and/or culture for Clostridium botulinum.
2 bacterial toxin C3 transferase derived from Clostridium botulinum.
3 from the anaerobic, spore-forming bacterium Clostridium botulinum.
4 ifically inactivated by exoenzyme C3 (C3) of Clostridium botulinum.
5 e neurotoxins produced in a single strain of Clostridium botulinum.
6 tulism, are produced by different strains of Clostridium botulinum.
7 toxins (BoNTs) are a product of the bacteria Clostridium botulinum.
8 ns of the anaerobic, spore-forming bacterium Clostridium botulinum.
9 The case was caused by a type B strain of Clostridium botulinum.
10 ally related neurotoxin proteins produced by Clostridium botulinum.
11 ted by a RhoA inhibitor, C3 transferase from Clostridium botulinum.
12 by bird ingestion of neurotoxins produced by Clostridium botulinum, a spore-forming, gram-positive, a
13 s (A-G), each produced by various strains of Clostridium botulinum, act on the neuromuscular junction
14 linum neurotoxins, produced by the bacterium Clostridium botulinum, act on their hosts by a high-affi
16 ulture were inhibited by microinjection of a Clostridium botulinum ADP-ribosyltransferase (C3) and tr
17 d, are each produced by different strains of Clostridium botulinum along with a group of neurotoxin-a
18 ost nephritogenic peptide, pCB, derived from Clostridium botulinum, also induced modest (25%) to seve
19 Botulinum neurotoxin (BoNT) is produced by Clostridium botulinum and associates with nontoxic neuro
20 tection of protease-based toxins produced by Clostridium botulinum and Bacillus anthracis represents
22 otulinum neurotoxins (BoNTs) are produced by Clostridium botulinum and cause the neuroparalytic syndr
25 uding the pathogens Clostridium perfringens, Clostridium botulinum and Clostridium tetani, has shown
26 linum neurotoxins (BoNTs) are synthesized by Clostridium botulinum and exist as seven immunologically
27 A priority pathogens; Bacillus anthracis and Clostridium botulinum, and Category B priority pathogens
28 phylococcus aureus, Clostridium perfringens, Clostridium botulinum, and Clostridium difficile were id
29 rax toxin of Bacillus anthracis, C2 toxin of Clostridium botulinum, and iota toxin of Clostridium per
30 Botulinum neurotoxins (BoNTs) produced by Clostridium botulinum are the most poisonous substances
33 kholderia mallei, Burkholderia pseudomallei, Clostridium botulinum, Brucella melitensis, Brucella abo
36 uption, direct cytoskeletal disassembly with Clostridium botulinum C2 toxin was insufficient to induc
39 nucleotide dissociation inhibitor (GDI), or Clostridium botulinum C3 ADP-ribosyl transferase (C3) to
41 c antisense oligonucleotides or treated with Clostridium botulinum C3 exoenzyme and then stimulated w
45 m difficile toxin B, but was not affected by Clostridium botulinum C3 exoenzyme, pertussis toxin, or
46 to be insensitive to the Rho GTPase-specific Clostridium botulinum C3 exoenzyme, raising the possibil
48 was shown to be inhibited by treatment with Clostridium botulinum C3 exotoxin, a specific inactivato
49 , an inhibitor of ARF activation, but not by Clostridium botulinum C3 exotoxin, an inhibitor of the a
52 process that is blocked by RhoA(19N) and the Clostridium botulinum C3 toxin, which inhibit Rho signal
56 hibition of RhoA by expression of either the Clostridium botulinum C3 transferase or a dominant negat
59 ho has no effect, the inhibition of rho with Clostridium botulinum C3 transferase stimulates the outg
60 like insulin, this activation was blocked by Clostridium botulinum C3 transferase, suggesting a requi
61 Rho function, dominant negative N19RhoA and Clostridium botulinum C3 transferase, to examine the pos
65 Ts), produced by the spore-forming bacterium Clostridium botulinum, cause botulism, a rare but fatal
67 prioritize the antibacterial drug targets in Clostridium botulinum (Clb), the causative agent of flac
69 e with a RhoA inhibitor, C3 transferase from Clostridium botulinum, effectively blocked fMLP-induced
73 xin-producing Clostridium species other than Clostridium botulinum from food and stool requires devia
74 ant negative N19RhoA and the C3 exoenzyme of Clostridium botulinum, further supporting a role for Rho
75 accid, paralysis that results when spores of Clostridium botulinum germinate in a wound and elaborate
77 SmpB has been included, and genomic data for Clostridium botulinum has revealed a group I (subgroup I
80 al metabolite brefeldin A, and C3 exoenzyme (Clostridium botulinum), implicating the activation of Rh
82 imens from week 1 and type A toxin-producing Clostridium botulinum in stool specimens from weeks 3 to
83 hewanella oneidensis, Shewanella woodyi, and Clostridium botulinum, indicating that the binding site
86 ighly toxic botulinum neurotoxin (BoNT) from Clostridium botulinum is of critical importance because
93 study binding and transcytosis of iodinated Clostridium botulinum neurotoxin serotypes A, B, and C,
94 osensor for the ultra-sensitive detection of Clostridium botulinum Neurotoxin Type A (BoNT/A) in comp
96 ation of zinc from our structural studies on Clostridium botulinum neurotoxin type B in complex with
97 biochemical analysis on several mutations on Clostridium botulinum neurotoxin type E light chain with
98 ructure of the catalytic light chain (LC) of Clostridium botulinum neurotoxin type G (BoNT/G-LC) at 2
104 asurement of chicken and human antibodies to Clostridium botulinum neurotoxins A, B, and E was accomp
108 he seven antigenically distinct serotypes of Clostridium botulinum neurotoxins cleave specific solubl
109 uminescence (ECL) assays were used to detect Clostridium botulinum neurotoxins serotypes A, B, E, and
110 os were microinjected with C3 exoenzyme from Clostridium botulinum or with wild-type, constitutively
111 homolog from a bacteriophage and unravel the Clostridium botulinum phage c-st type III partition syst
114 Through elaboration of its botulinum toxins, Clostridium botulinum produces clinical syndromes of inf
116 cid sequence of Spo0A is highly conserved in Clostridium botulinum relative to Bacillus subtilis but
117 The bacterial enzyme C3 transferase from Clostridium botulinum selectively ADP-ribosylates Rho in
119 s of botulinum neurotoxins (A-G) produced by Clostridium botulinum share significant sequence homolog
120 adequate refrigeration likely contributed to Clostridium botulinum spore survival, germination, and t
122 entified in California in 1976, results from Clostridium botulinum spores that germinate, multiply, a
131 st potent toxins known in nature produced by Clostridium botulinum strains, which can cause life-thre
132 A derivative of the type A neurotoxin from Clostridium botulinum (termed LH(N)/A) that retains cata
133 cific features for a candidate "IStron" from Clostridium botulinum that allow the element to carefull
134 A recombinant BoNT/A toxoid was produced in Clostridium botulinum that contained a double amino acid
135 a very small group of strains of proteolytic Clostridium botulinum that form type A5 neurotoxin.
136 ctivated by treatment with C3 exoenzyme from Clostridium botulinum, the ability of Galpha13Q226L to a
139 ergic receptor antagonist rauwolscine and by Clostridium botulinum toxin as well as by antibodies dir
141 The inhibition of RhoA by the C3 toxin (Clostridium botulinum toxin) restored endothelial barrie
142 firmed) infant botulism (75 caused by type A Clostridium botulinum toxin, and 47 by type B toxin); tr
143 cin heavy chain, ricin holotoxin, serotype A Clostridium botulinum toxin, Staphylococcus enterotoxin
144 toxic substance known to man, is produced by Clostridium botulinum type A as a complex with a group o
145 ative 900-kDa type A neurotoxin complex from Clostridium botulinum type A-Hall (Allergan) strain.
146 Disrupting Nt-Syr1 function by cleavage with Clostridium botulinum type C toxin or competition with a
148 Francisella tularensis, Brucella melitensis, Clostridium botulinum, Vaccinia virus, and one biologica
149 ne of seven highly potent toxins produced by Clostridium botulinum which inhibit neurotransmission at
150 of a transgene encoding C3 transferase from Clostridium botulinum which selectively ADP-ribosylates
152 mechanisms, we characterized the enzyme from Clostridium botulinum, which belongs to a subclass of cl
153 unding is fully blocked by the C3 toxin from Clostridium botulinum, which specifically ADP-ribosylate