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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
15                              Exoenzyme C3 of Clostridium botulinum ADP-ribosylates Rho at Asn41, a mo
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
21         Laboratory testing was performed for Clostridium botulinum and botulinum neurotoxin.
22 otulinum neurotoxins (BoNTs) are produced by Clostridium botulinum and cause the neuroparalytic syndr
23 by C. perfringens, as well as sporulation by Clostridium botulinum and Clostridium sporogenes.
24        An upsurge in wound infections due to Clostridium botulinum and Clostridium tetani among users
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
31         Botulinum toxins (BoNTs) produced by Clostridium botulinum are the most potent known bacteria
32 e A is initially released from the bacterium Clostridium botulinum as a stable 900-kDa complex.
33 kholderia mallei, Burkholderia pseudomallei, Clostridium botulinum, Brucella melitensis, Brucella abo
34      Nitric oxide (NO) is extremely toxic to Clostridium botulinum, but its molecular targets are unk
35                                     Here the Clostridium botulinum C2 binding/translocation domain wa
36 uption, direct cytoskeletal disassembly with Clostridium botulinum C2 toxin was insufficient to induc
37                                  The natural Clostridium botulinum C2 toxin was then delivered to hum
38 a-galactosidase and the enzymatic subunit of Clostridium botulinum C2 toxin.
39  nucleotide dissociation inhibitor (GDI), or Clostridium botulinum C3 ADP-ribosyl transferase (C3) to
40                       To express recombinant Clostridium botulinum C3 exoenzyme (using double subgeno
41 c antisense oligonucleotides or treated with Clostridium botulinum C3 exoenzyme and then stimulated w
42                                              Clostridium botulinum C3 exoenzyme inactivates the small
43                               Scrape loading Clostridium botulinum C3 exoenzyme into primary peripher
44                            Pretreatment with Clostridium botulinum C3 exoenzyme which inactivates the
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
47 cytoskeleton, is specifically antagonized by Clostridium botulinum C3 exoenzyme.
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
50                           Co-transfection of Clostridium botulinum C3 toxin blocked activation of PKD
51                             Co-expression of Clostridium botulinum C3 toxin specifically blocked indu
52 process that is blocked by RhoA(19N) and the Clostridium botulinum C3 toxin, which inhibit Rho signal
53          Mice treated with the Rho inhibitor Clostridium botulinum C3 transferase (10 microgram/d) or
54            Furthermore, inhibition of Rho by Clostridium botulinum C3 transferase (50 microg/ml) or b
55                Rho inhibition by coexpressed Clostridium botulinum C3 transferase did not alter estro
56 hibition of RhoA by expression of either the Clostridium botulinum C3 transferase or a dominant negat
57                 Indeed, inhibition of Rho by Clostridium botulinum C3 transferase or overexpression o
58            Furthermore, inhibition of Rho by Clostridium botulinum C3 transferase or Rho-kinase by ov
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
62            The treatment of HEp-2 cells with Clostridium botulinum C3, an enzyme that ADP-ribosylates
63                       Inhibition of Rho with Clostridium botulinum C3-transferase disturbed intercell
64 ases (ADPRTs) Staphylococcus aureus EDIN and Clostridium botulinum C3.
65 Ts), produced by the spore-forming bacterium Clostridium botulinum, cause botulism, a rare but fatal
66 ial protein, transcription terminator Rho of Clostridium botulinum (Cb-Rho), could form a prion.
67 prioritize the antibacterial drug targets in Clostridium botulinum (Clb), the causative agent of flac
68  poisoning often occurs through ingestion of Clostridium botulinum-contaminated food.
69 e with a RhoA inhibitor, C3 transferase from Clostridium botulinum, effectively blocked fMLP-induced
70                                              Clostridium botulinum encompasses bacteria that produce
71       Inactivation of RhoA by treatment with Clostridium botulinum exoenzyme C3 exotoxin or expressio
72                  ADP-ribosylation of RhoA by Clostridium botulinum exotoxin inactivated RhoA signalin
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
76                                              Clostridium botulinum HA is a component of the large bot
77 SmpB has been included, and genomic data for Clostridium botulinum has revealed a group I (subgroup I
78 ns (Proteus mirabilis, Escherichia coli, and Clostridium botulinum) have been detected herein.
79                           A unique strain of Clostridium botulinum (IBCA10-7060) was recently discove
80 al metabolite brefeldin A, and C3 exoenzyme (Clostridium botulinum), implicating the activation of Rh
81 ulinum neurotoxins are produced by anaerobic Clostridium botulinum in an inactive form.
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
84                                              Clostridium botulinum is a taxonomic designation for man
85       The hemagglutinating protein HA33 from Clostridium botulinum is associated with the large botul
86 ighly toxic botulinum neurotoxin (BoNT) from Clostridium botulinum is of critical importance because
87                                              Clostridium botulinum isolates from 4 patients were clos
88               The ribosyltransferase C3 from Clostridium botulinum modifies Rho proteins and inhibits
89                                              Clostridium botulinum neurotoxin (BoNT) is the causative
90                         BAcTrace is based on Clostridium botulinum neurotoxin A, Botox, which we engi
91                                              Clostridium botulinum neurotoxin serotype A (BoNT/A) is
92                                          The Clostridium botulinum neurotoxin serotype A light chain
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
95                                              Clostridium botulinum neurotoxin type A (BoNT/A) is one
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
99             The seven serologically distinct Clostridium botulinum neurotoxins (BoNTs A-G) are zinc e
100                                              Clostridium botulinum neurotoxins (BoNTs) are effective
101                                              Clostridium botulinum neurotoxins (BoNTs) are the most t
102                              The dynamics of Clostridium botulinum neurotoxins (BoNTs) protein-transl
103                                              Clostridium botulinum neurotoxins (BoNTs), the most pote
104 asurement of chicken and human antibodies to Clostridium botulinum neurotoxins A, B, and E was accomp
105                                              Clostridium botulinum neurotoxins are the most potent to
106                                              Clostridium botulinum neurotoxins are the most potent to
107                                              Clostridium botulinum neurotoxins are zinc endopeptidase
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
112 actin-like ParM is encoded on the large pCBH Clostridium botulinum plasmid.
113                                              Clostridium botulinum produces botulinum neurotoxins (Bo
114 Through elaboration of its botulinum toxins, Clostridium botulinum produces clinical syndromes of inf
115                                              Clostridium botulinum produces seven antigenically disti
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
118                                              Clostridium botulinum serotype A produces a neurotoxin c
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
121 gulations that could have led to survival of Clostridium botulinum spores during sterilization.
122 entified in California in 1976, results from Clostridium botulinum spores that germinate, multiply, a
123               Recently, it was reported that Clostridium botulinum strain Af84 has three neurotoxin g
124                  Sequencing of the genome of Clostridium botulinum strain Hall A revealed a gene (CBO
125                                         Only Clostridium botulinum strain IBCA10-7060 produces the re
126 enced the 2 botulinum toxin gene clusters of Clostridium botulinum strain IBCA10-7060 type Bh.
127                                              Clostridium botulinum strain IBCA10-7060 was recently re
128                                              Clostridium botulinum strain IBCA10-7060, isolated from
129                     A retrospective study of Clostridium botulinum strains isolated from patients fro
130                                      Rarely, Clostridium botulinum strains that produce two serotypes
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
137                                           In Clostridium botulinum, the nrn gene is replaced by a gen
138            The addition of C3 exoenzyme from clostridium botulinum to specifically ribosylate and inh
139 ergic receptor antagonist rauwolscine and by Clostridium botulinum toxin as well as by antibodies dir
140                        In prior studies, the Clostridium botulinum toxin C3 exoenzyme has been used t
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
147                                              Clostridium botulinum type E has been associated with bo
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
151                    We used C3 transferase of Clostridium botulinum, which ADP-ribosylates and inactiv
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

 
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