ライフサイエンスコーパス: Clostridium botulinum

1 bacterial toxin C3 transferase derived from Clostridium botulinum.

2 from the anaerobic, spore-forming bacterium Clostridium botulinum.

3 ifically inactivated by exoenzyme C3 (C3) of Clostridium botulinum.

4 e neurotoxins produced in a single strain of Clostridium botulinum.

5 tulism, are produced by different strains of Clostridium botulinum.

6 ns of the anaerobic, spore-forming bacterium Clostridium botulinum.

7 The case was caused by a type B strain of Clostridium botulinum.

8 ally related neurotoxin proteins produced by Clostridium botulinum.

9 ted by a RhoA inhibitor, C3 transferase from Clostridium botulinum.

10 by bird ingestion of neurotoxins produced by Clostridium botulinum, a spore-forming, gram-positive, a

11 s (A-G), each produced by various strains of Clostridium botulinum, act on the neuromuscular junction

12 linum neurotoxins, produced by the bacterium Clostridium botulinum, act on their hosts by a high-affi

13 Exoenzyme C3 of Clostridium botulinum ADP-ribosylates Rho at Asn41, a mo

14 ulture were inhibited by microinjection of a Clostridium botulinum ADP-ribosyltransferase (C3) and tr

15 d, are each produced by different strains of Clostridium botulinum along with a group of neurotoxin-a

16 ost nephritogenic peptide, pCB, derived from Clostridium botulinum, also induced modest (25%) to seve

17 Botulinum neurotoxin (BoNT) is produced by Clostridium botulinum and associates with nontoxic neuro

18 tection of protease-based toxins produced by Clostridium botulinum and Bacillus anthracis represents

19 Laboratory testing was performed for Clostridium botulinum and botulinum neurotoxin.

20 otulinum neurotoxins (BoNTs) are produced by Clostridium botulinum and cause the neuroparalytic syndr

21 by C. perfringens, as well as sporulation by Clostridium botulinum and Clostridium sporogenes.

22 An upsurge in wound infections due to Clostridium botulinum and Clostridium tetani among users

23 uding the pathogens Clostridium perfringens, Clostridium botulinum and Clostridium tetani, has shown

24 linum neurotoxins (BoNTs) are synthesized by Clostridium botulinum and exist as seven immunologically

25 A priority pathogens; Bacillus anthracis and Clostridium botulinum, and Category B priority pathogens

26 phylococcus aureus, Clostridium perfringens, Clostridium botulinum, and Clostridium difficile were id

27 rax toxin of Bacillus anthracis, C2 toxin of Clostridium botulinum, and iota toxin of Clostridium per

28 Botulinum neurotoxins (BoNTs) produced by Clostridium botulinum are the most poisonous substances

29 e A is initially released from the bacterium Clostridium botulinum as a stable 900-kDa complex.

30 kholderia mallei, Burkholderia pseudomallei, Clostridium botulinum, Brucella melitensis, Brucella abo

31 Nitric oxide (NO) is extremely toxic to Clostridium botulinum, but its molecular targets are unk

32 Here the Clostridium botulinum C2 binding/translocation domain wa

33 uption, direct cytoskeletal disassembly with Clostridium botulinum C2 toxin was insufficient to induc

34 The natural Clostridium botulinum C2 toxin was then delivered to hum

35 a-galactosidase and the enzymatic subunit of Clostridium botulinum C2 toxin.

36 nucleotide dissociation inhibitor (GDI), or Clostridium botulinum C3 ADP-ribosyl transferase (C3) to

37 To express recombinant Clostridium botulinum C3 exoenzyme (using double subgeno

38 c antisense oligonucleotides or treated with Clostridium botulinum C3 exoenzyme and then stimulated w

39 Clostridium botulinum C3 exoenzyme inactivates the small

40 Scrape loading Clostridium botulinum C3 exoenzyme into primary peripher

41 Pretreatment with Clostridium botulinum C3 exoenzyme which inactivates the

42 m difficile toxin B, but was not affected by Clostridium botulinum C3 exoenzyme, pertussis toxin, or

43 to be insensitive to the Rho GTPase-specific Clostridium botulinum C3 exoenzyme, raising the possibil

44 cytoskeleton, is specifically antagonized by Clostridium botulinum C3 exoenzyme.

45 was shown to be inhibited by treatment with Clostridium botulinum C3 exotoxin, a specific inactivato

46 , an inhibitor of ARF activation, but not by Clostridium botulinum C3 exotoxin, an inhibitor of the a

47 Co-transfection of Clostridium botulinum C3 toxin blocked activation of PKD

48 Co-expression of Clostridium botulinum C3 toxin specifically blocked indu

49 process that is blocked by RhoA(19N) and the Clostridium botulinum C3 toxin, which inhibit Rho signal

50 Mice treated with the Rho inhibitor Clostridium botulinum C3 transferase (10 microgram/d) or

51 Furthermore, inhibition of Rho by Clostridium botulinum C3 transferase (50 microg/ml) or b

52 Rho inhibition by coexpressed Clostridium botulinum C3 transferase did not alter estro

53 hibition of RhoA by expression of either the Clostridium botulinum C3 transferase or a dominant negat

54 Indeed, inhibition of Rho by Clostridium botulinum C3 transferase or overexpression o

55 Furthermore, inhibition of Rho by Clostridium botulinum C3 transferase or Rho-kinase by ov

56 ho has no effect, the inhibition of rho with Clostridium botulinum C3 transferase stimulates the outg

57 like insulin, this activation was blocked by Clostridium botulinum C3 transferase, suggesting a requi

58 Rho function, dominant negative N19RhoA and Clostridium botulinum C3 transferase, to examine the pos

59 The treatment of HEp-2 cells with Clostridium botulinum C3, an enzyme that ADP-ribosylates

60 Inhibition of Rho with Clostridium botulinum C3-transferase disturbed intercell

61 ases (ADPRTs) Staphylococcus aureus EDIN and Clostridium botulinum C3.

62 ial protein, transcription terminator Rho of Clostridium botulinum (Cb-Rho), could form a prion.

63 prioritize the antibacterial drug targets in Clostridium botulinum (Clb), the causative agent of flac

64 poisoning often occurs through ingestion of Clostridium botulinum-contaminated food.

65 e with a RhoA inhibitor, C3 transferase from Clostridium botulinum, effectively blocked fMLP-induced

66 Clostridium botulinum encompasses bacteria that produce

67 Inactivation of RhoA by treatment with Clostridium botulinum exoenzyme C3 exotoxin or expressio

68 ADP-ribosylation of RhoA by Clostridium botulinum exotoxin inactivated RhoA signalin

69 xin-producing Clostridium species other than Clostridium botulinum from food and stool requires devia

70 ant negative N19RhoA and the C3 exoenzyme of Clostridium botulinum, further supporting a role for Rho

71 accid, paralysis that results when spores of Clostridium botulinum germinate in a wound and elaborate

72 Clostridium botulinum HA is a component of the large bot

73 SmpB has been included, and genomic data for Clostridium botulinum has revealed a group I (subgroup I

74 A unique strain of Clostridium botulinum (IBCA10-7060) was recently discove

75 al metabolite brefeldin A, and C3 exoenzyme (Clostridium botulinum), implicating the activation of Rh

76 ulinum neurotoxins are produced by anaerobic Clostridium botulinum in an inactive form.

77 imens from week 1 and type A toxin-producing Clostridium botulinum in stool specimens from weeks 3 to

78 hewanella oneidensis, Shewanella woodyi, and Clostridium botulinum, indicating that the binding site

79 Clostridium botulinum is a taxonomic designation for man

80 The hemagglutinating protein HA33 from Clostridium botulinum is associated with the large botul

81 ighly toxic botulinum neurotoxin (BoNT) from Clostridium botulinum is of critical importance because

82 The ribosyltransferase C3 from Clostridium botulinum modifies Rho proteins and inhibits

83 Clostridium botulinum neurotoxin (BoNT) is the causative

84 The Clostridium botulinum neurotoxin serotype A light chain

85 study binding and transcytosis of iodinated Clostridium botulinum neurotoxin serotypes A, B, and C,

86 osensor for the ultra-sensitive detection of Clostridium botulinum Neurotoxin Type A (BoNT/A) in comp

87 Clostridium botulinum neurotoxin type A (BoNT/A) is one

88 ation of zinc from our structural studies on Clostridium botulinum neurotoxin type B in complex with

89 biochemical analysis on several mutations on Clostridium botulinum neurotoxin type E light chain with

90 ructure of the catalytic light chain (LC) of Clostridium botulinum neurotoxin type G (BoNT/G-LC) at 2

91 The seven serologically distinct Clostridium botulinum neurotoxins (BoNTs A-G) are zinc e

92 Clostridium botulinum neurotoxins (BoNTs) are effective

93 Clostridium botulinum neurotoxins (BoNTs) are the most t

94 The dynamics of Clostridium botulinum neurotoxins (BoNTs) protein-transl

95 Clostridium botulinum neurotoxins (BoNTs), the most pote

96 asurement of chicken and human antibodies to Clostridium botulinum neurotoxins A, B, and E was accomp

97 Clostridium botulinum neurotoxins are the most potent to

98 Clostridium botulinum neurotoxins are the most potent to

99 Clostridium botulinum neurotoxins are zinc endopeptidase

100 he seven antigenically distinct serotypes of Clostridium botulinum neurotoxins cleave specific solubl

101 uminescence (ECL) assays were used to detect Clostridium botulinum neurotoxins serotypes A, B, E, and

102 os were microinjected with C3 exoenzyme from Clostridium botulinum or with wild-type, constitutively

103 homolog from a bacteriophage and unravel the Clostridium botulinum phage c-st type III partition syst

104 Clostridium botulinum produces botulinum neurotoxins (Bo

105 Through elaboration of its botulinum toxins, Clostridium botulinum produces clinical syndromes of inf

106 Clostridium botulinum produces seven antigenically disti

107 cid sequence of Spo0A is highly conserved in Clostridium botulinum relative to Bacillus subtilis but

108 The bacterial enzyme C3 transferase from Clostridium botulinum selectively ADP-ribosylates Rho in

109 Clostridium botulinum serotype A produces a neurotoxin c

110 s of botulinum neurotoxins (A-G) produced by Clostridium botulinum share significant sequence homolog

111 adequate refrigeration likely contributed to Clostridium botulinum spore survival, germination, and t

112 gulations that could have led to survival of Clostridium botulinum spores during sterilization.

113 entified in California in 1976, results from Clostridium botulinum spores that germinate, multiply, a

114 Recently, it was reported that Clostridium botulinum strain Af84 has three neurotoxin g

115 Sequencing of the genome of Clostridium botulinum strain Hall A revealed a gene (CBO

116 Only Clostridium botulinum strain IBCA10-7060 produces the re

117 enced the 2 botulinum toxin gene clusters of Clostridium botulinum strain IBCA10-7060 type Bh.

118 Clostridium botulinum strain IBCA10-7060 was recently re

119 Clostridium botulinum strain IBCA10-7060, isolated from

120 A retrospective study of Clostridium botulinum strains isolated from patients fro

121 Rarely, Clostridium botulinum strains that produce two serotypes

122 A derivative of the type A neurotoxin from Clostridium botulinum (termed LH(N)/A) that retains cata

123 A recombinant BoNT/A toxoid was produced in Clostridium botulinum that contained a double amino acid

124 a very small group of strains of proteolytic Clostridium botulinum that form type A5 neurotoxin.

125 ctivated by treatment with C3 exoenzyme from Clostridium botulinum, the ability of Galpha13Q226L to a

126 The addition of C3 exoenzyme from clostridium botulinum to specifically ribosylate and inh

127 ergic receptor antagonist rauwolscine and by Clostridium botulinum toxin as well as by antibodies dir

128 In prior studies, the Clostridium botulinum toxin C3 exoenzyme has been used t

129 The inhibition of RhoA by the C3 toxin (Clostridium botulinum toxin) restored endothelial barrie

130 firmed) infant botulism (75 caused by type A Clostridium botulinum toxin, and 47 by type B toxin); tr

131 toxic substance known to man, is produced by Clostridium botulinum type A as a complex with a group o

132 ative 900-kDa type A neurotoxin complex from Clostridium botulinum type A-Hall (Allergan) strain.

133 Disrupting Nt-Syr1 function by cleavage with Clostridium botulinum type C toxin or competition with a

134 Clostridium botulinum type E has been associated with bo

135 Francisella tularensis, Brucella melitensis, Clostridium botulinum, Vaccinia virus, and one biologica

136 ne of seven highly potent toxins produced by Clostridium botulinum which inhibit neurotransmission at

137 of a transgene encoding C3 transferase from Clostridium botulinum which selectively ADP-ribosylates

138 We used C3 transferase of Clostridium botulinum, which ADP-ribosylates and inactiv

139 unding is fully blocked by the C3 toxin from Clostridium botulinum, which specifically ADP-ribosylate