ライフサイエンスコーパス: antitoxin

1 by direct interaction with a structured RNA antitoxin.

2 ely mediated by active site hindrance by its antitoxin.

3 tially toxic protein, and a small RNA (sRNA) antitoxin.

4 i-F botulinum antitoxins but not with anti-E antitoxin.

5 overed antitoxin gene be named ralA for RalR antitoxin.

6 lasmic protein toxin and its cognate protein antitoxin.

7 nhibition that can be rescued by the cognate antitoxin.

8 tates, an unprecedented rearrangement for an antitoxin.

9 ls a second strain lacking the corresponding antitoxin.

10 by the co-expression of its cognate RelB2sca antitoxin.

11 protease, inorganic polyphosphate, and toxin-antitoxins.

12 factor and may have potential application as antitoxins.

13 re organized into operons with their cognate antitoxins.

14 phylaxis related to HBAT and other botulinum antitoxins.

15 d for HBAT and previously employed botulinum antitoxins.

16 in activity and the regulated proteolysis of antitoxins.

17 ios >/=1190:1 for neutralization by existing antitoxins.

18 rved PPVs and NPVs of ST for other botulinum antitoxins (302 patients) were 0-56% and 50%-100%, respe

19 The humanized antitoxin A mAb PA-50 and antitoxin B mAb PA-41 have pic

20 A heptavalent F(ab')2 botulinum antitoxin A-G obtained from the US Army also did not neu

21 hese produce a stable toxin (T) and a labile antitoxin (A) conditioning cell survival to plasmid main

22 by ClpXP, and this degradation requires the antitoxin, a ClpXP adaptor.

23 E operon was negatively autoregulated by the antitoxin, AbiEi, a member of a widespread family of put

24 The RNA chaperone Hfq is required for RalA antitoxin activity and appears to stabilize RalA.

25 and inhibiting multiple toxin partners, when antitoxin activity is generally considered to be limited

26 Prompt antitoxin administration and meticulous intensive care a

27 dren (persons <18 years of age) or botulinum antitoxin administration to children.

28 d a meta-analysis on the effect of timing of antitoxin administration, antitoxin type, and toxin expo

29 value of skin testing (ST) before botulinum antitoxin administration.

30 viously, we identified a potent neutralizing antitoxin against BoNT/A1 termed ciA-C2, derived from a

31 Hence, more potent and safer antitoxins against BoNT/H are needed.

32 strong platform for the development of novel antitoxin agents and for the rational design of BoNT/A v

33 In addition, antitoxin agents are not only promising for therapeutic

34 Development of successful antitoxin agents would likely decrease the use of antibi

35 eview of (1) allergic reactions to botulinum antitoxin and (2) the predictive value of skin testing (

36 AbrB transition state regulator and the MazE antitoxin and MraW is known to methylate the 16S rRNA, m

37 ically evaluated the literature on botulinum antitoxin and other treatments.

38 vior of some of these systems, such as toxin-antitoxin and restriction modification modules.

39 sses of defense systems, in particular toxin-antitoxin and restriction-modification systems, show non

40 properties of defense systems such as toxins-antitoxins and an important role of horizontal mobility

41 njection blocking, abortive infection, toxin-antitoxin, and CRISPR-Cas systems.

42 been selected to bind structurally disparate antitoxins, and exhibit distinct toxin activities includ

43 The antitoxin antibodies actoxumab and bezlotoxumab bind to

44 (9)(2)-STa(1)(3) fusions induce neutralizing antitoxin antibodies and provided important information

45 Circulating neutralizing antitoxin antibodies are protective in C. difficile infe

46 In this study, we show that the antitoxin antibodies are protective in multiple murine m

47 alizing activity and suggest that engineered antitoxin antibodies will have improved therapeutic effi

48 -old woman that arose despite the protective antitoxin antibody in her serum.

49 Patients who develop strong antitoxin antibody responses can clear C. difficile infe

50 ssociate acute stage toxemia with subsequent antitoxin antibody responses.

51 toxic peptide (PepA1) and the SprA1(AS) RNA antitoxin are within a pathogenicity island on opposite

52 Antitoxins are becoming recognized as proteins that regu

53 Antitoxins are more labile than toxins and are readily d

54 Furthermore, it is unclear how antitoxins are selected for proteolysis by cellular prot

55 ression of HigB toxin in the absence of HigA antitoxin arrests growth and causes cell death in M. tub

56 The humanized antitoxin A mAb PA-50 and antitoxin B mAb PA-41 have picomolar potencies in vitro

57 r the zorO-orzO type I system where the OrzO antitoxin base pairs to the 174-nucleotide zorO 5 UTR.

58 ation for the Type III TA class, and the RNA antitoxin bears a novel structural feature of an extende

59 This is distinct from antitoxins belonging to other superfamilies that typical

60 Additionally, protein antitoxins bind their own promoters and repress transcri

61 at typically acts as a gate to direct RNA or antitoxin binding.

62 indicating that Dmd can act as a promiscuous antitoxin, binding and inhibiting multiple toxin partner

63 at consists of the toxin gene, brnT, and its antitoxin, brnA.

64 te with anti-A, anti-B, and anti-F botulinum antitoxins but not with anti-E antitoxin.

65 y and mortality, but concerns that botulinum antitoxin can induce anaphylaxis exist.

66 olded state of the partially disordered CcdA antitoxin can therefore provide insight into general mec

67 d structural study of the binding of an IDP (antitoxin CcdA) to its molecular target (gyrase poison C

68 arget, DNA gyrase, but retain binding to the antitoxin, CcdA.

69 to a Type II TA system, while the cjrA (RNA antitoxin)/cjpT (proteic toxin) pair in 81-176 belongs t

70 ve risk of death among patients treated with antitoxin compared with patients not treated with antito

71 stal structure of the Escherichia coli toxin-antitoxin complex YafQ-(DinJ)2-YafQ, a key component of

72 death in Myxococcus via the MrpC-MazF toxin-antitoxin complex.

73 ensity information to an intracellular toxin-antitoxin complex.

74 The features of toxin-antitoxin complexes that are important to inhibit toxin

75 d in the systems characterized the toxin and antitoxin components together form a trimeric assembly.

76 provides a reproducible platform for testing antitoxin compounds and immunotherapeutics with outcome

77 formational states play a role in regulating antitoxin concentrations and the activity of CcdA's cogn

78 ing other functions, for example, toxins and antitoxins, confirming the recently discovered potential

79 main of unknown function (DUF) 4433, and the antitoxin (DarG) a macrodomain protein.

80 Diphtheria antitoxin (DAT) has been the cornerstone of the treatmen

81 he ClpXP protease is responsible for Epsilon antitoxin degradation.

82 The antitoxin DinJ dimer adopts a ribbon-helix-helix motif r

83 e, we investigated the physiological role of antitoxin DinJ of the YafQ/DinJ TA pair and found DinJ a

84 y virtue of its interaction with its cognate antitoxin, DinJ.

85 However, these antitoxins do not functionally complement each other, ev

86 ite, regulation of enzymatic activity by the antitoxin EcMazE diverges from its B. subtilis homolog.

87 systems consist of stable toxins and labile antitoxins encoded within small genetic modules widespre

88 osynthesis through complex formation with an antitoxin, EsaG, which binds to its C-terminal nuclease

89 may be members of the very large VapBC toxin-antitoxin family.

90 Furthermore, we evolved an antitoxin for the new toxin ArT from two unrelated antit

91 monstrate that the peptide competes with the antitoxin for toxin binding and directly activates the l

92 Here we show that an antitoxin from a type V system (GhoS, an endoribonucleas

93 expressed and neutralized with their cognate antitoxins from a TA (toxin-antitoxin) operon in normall

94 Therefore, toxins and antitoxins from disparate systems can be interconverted.

95 We suggest the newly discovered antitoxin gene be named ralA for RalR antitoxin.

96 hia coli contains at least 36 putative toxin-antitoxin gene pairs, and some pathogens such as Mycobac

97 ng a 30-amino acid hydrophobic toxin and the antitoxin gene sr5 overlap at their 3' ends by 112 bp.

98 es bacterial growth and a toxin-neutralizing antitoxin gene, usually encoded in a single operon.

99 Toxin-antitoxin genes play important roles in the regulation o

100 ma factors, transcription factors, and toxin-antitoxin genes.

101 rium tuberculosis contains at least 88 toxin-antitoxin genes.

102 d by cleavage of its messenger RNA (mRNA) by antitoxin GhoS, and TA system MqsR/MqsA controls GhoT/Gh

103 Children who received antitoxin had better survival; serious adverse events we

104 iated, equine-derived, heptavalent botulinum antitoxin (HBAT) is licensed in the United States.

105 Equine-derived heptavalent botulinum antitoxin (HBAT), the only currently available treatment

106 ound that, unlike most other TA systems, the antitoxin HigA makes minimal interactions with toxin Hig

107 crobial therapy and prompt administration of antitoxin, if necessary.

108 emonstrate that durable levels of protective antitoxin immunity exist in the majority of vaccinated i

109 terial toxins--are routinely used to promote antitoxin immunity for the treatment and prevention of b

110 is toxoid, they may induce antibacterial and antitoxin immunity.

111 eine variant [C117S]YmoB can replace TomB as antitoxins in E. coli.

112 the adaptor that works with ClpCP to degrade antitoxins in S. aureus.

113 completely eliminated by existing serotype A antitoxins, including those contained in multivalent the

114 ncoding the intracellular toxin MazF and its antitoxin inhibitor MazE.

115 We further demonstrate that ParD antitoxin is dimeric, stably folded, and largely helical

116 ed until 6-8 h post-induction, suggesting an antitoxin is unnecessary earlier.

117 Nine of these toxin-antitoxin loci belong to the mazEF family, encoding the

118 Type I toxin-antitoxin loci consist of two genes: a small, hydrophobi

119 Gpp triggers slow growth by activating toxin-antitoxin loci through a regulatory cascade depending on

120 tatives from all three families act as toxin-antitoxin loci within Escherichia coli and at least two

121 Toxin-antitoxin loci, which encode a toxic protein alongside w

122 at the zorO-orzO pair is a true type I toxin-antitoxin locus.

123 eing inhibited by a toxin encoded by a toxin-antitoxin locus.

124 Novel antitoxin mAbs were generated in mice and were humanized

125 ibe the isolation of diverse and efficacious antitoxin mAbs.

126 s of MazF in complex with mRNA substrate and antitoxin MazE in Bacillus subtilis.

127 s inactivated through binding to its cognate antitoxin, MazE.

128 f protein-protein interactions using a toxin-antitoxin model.

129 The toxin Doc from the phd/doc toxin-antitoxin module targets the cellular translation machin

130 Bacterial type II toxin-antitoxin modules are protein-protein complexes whose fu

131 The majority of 14 toxin-antitoxin modules contributed to intracellular persister

132 In several different organisms, toxin-antitoxin modules function as effectors of ppGpp-induced

133 In Escherichia coli, toxin-antitoxin modules have been linked to persister formatio

134 Toxin and antitoxin modules in bacteria are believed to be one pos

135 one of many chromosomally encoded toxin and antitoxin modules in Escherichia coli and the HipA7 alle

136 Deleting toxin-antitoxin modules in S. aureus did not affect the level

137 Bacteria encode multiple type II toxin-antitoxin modules that cleave ribosome-bound mRNAs in re

138 ylococcus aureus genome contains three toxin-antitoxin modules, including one mazEF module, SamazEF.

139 the transcriptional repression of two toxin/antitoxin modules, mqsR/mqsA and dinJ/yafQ.

140 e contains an unusually high number of toxin-antitoxin modules, some of which have been suggested to

141 by small RNAs (sRNAs), denoted type I toxin-antitoxin modules, were first discovered on plasmids whe

142 Gpp and requires chromosomally encoded toxin-antitoxin modules.

143 owing persisters through the action of toxin-antitoxin modules.

144 lated antitoxin templates, the protein-based antitoxin MqsA and RNA-based antitoxin ToxI, and showed

145 hesis; for example, we found previously that antitoxin MqsA of the Escherichia coli toxin/antitoxin (

146 rsister cells is mqsR, a gene that, with the antitoxin mqsA, constitutes a TA module.

147 in the presence and absence of the proposed antitoxin MrpC.

148 Among patients who received antitoxin (n = 193), 23 (12%) reported an adverse event,

149 The association of toxins with their cognate antitoxins neutralizes toxin activity, allowing for norm

150 e activated Lon to degrade all known type II antitoxins of E. coli.

151 Therapeutic agents other than antitoxin offered no clear benefit.

152 or, but instead functions to destabilize the antitoxin-operator complex under all conditions, and thu

153 th their cognate antitoxins from a TA (toxin-antitoxin) operon in normally growing cells.

154 ycobacterium tuberculosis have over 90 toxin-antitoxin operons.

155 into the critical interactions between toxin-antitoxin pairs necessary to inhibit toxin activity and

156 Unlike many other antitoxins, ParD2 could prevent but not reverse ParE2 to

157 ranslation machinery and is inhibited by its antitoxin partner Phd.

158 g those contained in multivalent therapeutic antitoxin products that are the mainstay of human botuli

159 The antitoxin protein CcdA is a homodimer composed of two mo

160 n in the 3' end of the shpB gene encoding an antitoxin protein.

161 sponse to stress is selective proteolysis of antitoxin proteins which releases their cognate toxin pa

162 the biochemical properties of both toxin and antitoxin proteins.

163 e II TA systems relies on the proteolysis of antitoxin proteins.

164 An antitoxin raised against IBCA10-7060 toxoid protected mi

165 ion-provided monovalent polyclonal botulinum antitoxins raised against BoNT types A-G.

166 reactions may occur among 1%-2% of botulinum antitoxin recipients and will require epinephrine and an

167 Timely administration of antitoxin reduces mortality; despite appropriate treatme

168 16% (8/687 patients) for all other botulinum antitoxins (relative risk, 1.41 [95% confidence interval

169 Moreover, the RelBE2sca complex, or the antitoxin RelB2sca alone, specifically interacted with t

170 Interestingly, the E. coli antitoxin RelBeco was able to alleviate the toxicity of

171 Notably, cjrA (antitoxin) represents the first noncoding small RNA demo

172 956 which encode the HigB toxin and the HigA antitoxin respectively.

173 phage rac form a type I TA pair in which the antitoxin RNA is a trans-encoded small RNA with 16 nucle

174 es, suggesting that the regulation of RNA or antitoxin selection may be distinct from other canonical

175 Finally, we explain the origins of ToxI antitoxin selectivity through our crystal structure of t

176 rotease ClpXP; this degradation requires the antitoxin, SocA, as a proteolytic adaptor.

177 ortality; despite appropriate treatment with antitoxin, some patients suffer respiratory failure.

178 rves as the target site of the corresponding antitoxin sRNA.

179 These data suggest that antitoxin strategies against this organism will require

180 ee homologues of the plasmid RK2 ParDE toxin-antitoxin system are present in the Vibrio cholerae geno

181 The bacterial toxin-antitoxin system CcdB-CcdA provides a mechanism for the

182 omponent of the Escherichia coli RelBE toxin-antitoxin system has been extensively studied in vitro a

183 olecular Cell, Aarke et al. identify a toxin-antitoxin system in Caulobacter crescentus that acts by

184 BsrE/SR5 is a new type I toxin/antitoxin system located on the prophage-like region P6

185 MazEF is a type II toxin-antitoxin system present on the chromosome of Escherichi

186 from bacteriophage P1 (of the phd-doc toxin-antitoxin system) has served as a model for the family o

187 Loss of GmvAT and a second toxin-antitoxin system, CcdAB, from pINV reduces S. sonnei pla

188 GmvAT, a toxin-antitoxin system, is responsible for the difference in s

189 ron that also has characteristics of a toxin-antitoxin system, thus joining several enigmatic feature

190 to human infections, e.g. Fic and VbhA toxin-antitoxin system.

191 o-residing plasmid encoding a putative toxin-antitoxin system; iii) a mutation in the host's global t

192 Lastly, we describe the role of toxin-antitoxin systems (TAS) in the induction of the VBNC sta

193 s the expansion and diversification of toxin-antitoxin systems and other paralogous protein families

194 pulation dynamics for a large class of toxin-antitoxin systems and suggests answers to several of the

195 This study shows that active Type III toxin-antitoxin systems are far more diverse than previously k

196 Toxin-antitoxin systems are ubiquitous and have been implicate

197 Toxin-antitoxin systems are ubiquitous in nature and present o

198 Toxin-antitoxin systems are ubiquitous in prokaryotic and arch

199 Toxin-antitoxin systems are widespread in bacteria and archaea

200 Multiple toxin-antitoxin systems can be cooperatively marshaled for gre

201 The recently discovered Type III toxin-antitoxin systems encode protein toxins that are inhibit

202 Toxin-antitoxin systems have been divided into three types, de

203 e and regulation of this operon, since toxin-antitoxin systems have been suggested to play a part in

204 The generic architecture of toxin-antitoxin systems provides the potential for bistability

205 Additionally, the toxin/antitoxin systems that we investigated (MqsR, MazF, GhoT

206 In type I toxin-antitoxin systems, a small RNA acts as an antitoxin, whi

207 s, such as restriction-modification or toxin-antitoxin systems, and qualitative, including the discov

208 al, but thousands were associated with toxin-antitoxin systems, DNA repair, cell membrane function, d

209 In type III toxin-antitoxin systems, small processed RNAs directly antagon

210 Using bacterial toxin-antitoxin systems, we demonstrate the plausibility of th

211 To discover novel type I toxin-antitoxin systems, we developed a set of search paramete

212 epression complex in contrast to other toxin-antitoxin systems.

213 etic phase variation and activation of toxin/antitoxin systems.

214 persister frequency and the number of toxin-antitoxin systems.

215 ding acting as antitoxic components in toxin-antitoxin systems.

216 regulatory sequences-encode functional toxin-antitoxin systems.

217 istinct from the majority derived from toxin-antitoxin systems: it does not cleave RNA; in fact P1 Do

218 Toxin-antitoxin (TA) gene cassettes are widely distributed acr

219 Toxin-antitoxin (TA) loci are widespread in bacteria and can c

220 t of several protein toxins encoded in toxin-antitoxin (TA) loci as well as of man-made antibiotics s

221 Toxin-antitoxin (TA) loci encode inhibitors of translation, re

222 l organism Escherichia coli depends on toxin-antitoxin (TA) loci.

223 tion) to the activation of a metabolic toxin-antitoxin (TA) module (the ppGpp biochemical network) re

224 We report a functional type I toxin-antitoxin (TA) module expressed by a human pathogen, Sta

225 ealed that shpAB is a newly discovered toxin-antitoxin (TA) module.

226 Toxin/antitoxin (TA) modules are involved in persister formati

227 A large cohort of Toxin-Antitoxin (TA) modules contribute to this persistence.

228 Toxin-antitoxin (TA) modules have an important role in the for

229 The role of chromosomal toxin-antitoxin (TA) modules in bacterial physiology remains e

230 hia coli codes for at least 11 type II toxin-antitoxin (TA) modules, all implicated in bacterial pers

231 by an up-regulation of genes known as toxin-antitoxin (TA) modules.

232 e harbors an unusually large number of toxin-antitoxin (TA) modules.

233 antitoxin MqsA of the Escherichia coli toxin/antitoxin (TA) pair MqsR/MqsA directly represses the gen

234 The mazEFSa toxin-antitoxin (TA) system is ubiquitous in clinical isolates

235 n that, along with mqsA, forms a novel toxin.antitoxin (TA) system.

236 herichia coli form an oxygen-dependent toxin-antitoxin (TA) system.

237 Type II toxin-antitoxin (TA) systems are expressed from two-gene opero

238 Toxin-antitoxin (TA) systems are found on both bacterial plasm

239 Toxin-antitoxin (TA) systems are gene modules that are ubiquit

240 Bacterial toxin-antitoxin (TA) systems are genetic elements, which are e

241 Toxin-antitoxin (TA) systems are implicated in the downregulat

242 Genes encoding toxin-antitoxin (TA) systems are near ubiquitous in bacterial

243 Toxin-antitoxin (TA) systems are ubiquitous on bacterial chrom

244 Toxin/antitoxin (TA) systems are ubiquitous within bacterial g

245 Toxin-antitoxin (TA) systems are unique modules that effect pl

246 Toxin-antitoxin (TA) systems are widely distributed in bacteri

247 Toxin-antitoxin (TA) systems are widespread in prokaryotes.

248 All free-living bacteria carry the toxin-antitoxin (TA) systems controlling cell growth and death

249 Toxin-antitoxin (TA) systems form a ubiquitous class of prokar

250 Toxin-antitoxin (TA) systems have been implicated in facilitat

251 Since toxins of toxin/antitoxin (TA) systems have been postulated to be respon

252 The relBE family of Type II toxin-antitoxin (TA) systems have been widely reported in bact

253 The discovery and study of toxin-antitoxin (TA) systems helps us advance our understandin

254 The prevalence of toxin/antitoxin (TA) systems in almost all genomes suggests th

255 come specialized toward the control of toxin-antitoxin (TA) systems known to promote bacterial adapta

256 lmost all free-living bacteria contain toxin-antitoxin (TA) systems on their genomes and the targets

257 Toxin/antitoxin (TA) systems perhaps enable cells to reduce th

258 Toxin-antitoxin (TA) systems play key roles in bacterial persi

259 Bacterial toxin-antitoxin (TA) systems regulate key cellular processes t

260 For toxin/antitoxin (TA) systems, no toxin has been identified tha

261 ial genomes contain different types of toxin-antitoxin (TA) systems.

262 as a tool to identify and characterize toxin-antitoxin (TA)-acting Abi systems.

263 xin for the new toxin ArT from two unrelated antitoxin templates, the protein-based antitoxin MqsA an

264 ized BoNT/H and represents a potential human antitoxin that could be developed for the prevention and

265 VapB is an antitoxin that interacts with and neutralizes VapC via i

266 has been increased effort toward developing antitoxin therapies, rather than antibacterial treatment

267 were identified as associated with botulinum antitoxin therapy among 11 patients who received it.

268 ells can be rescued by the expression of the antitoxin, thereby raising the possibility that vapC20 c

269 ng and to prevent degradation of its cognate antitoxin, thus facilitating inhibition of the toxin.

270 We employ rational design and a toxin/antitoxin titering approach to produce and screen a smal

271 ed as the Dmd protein acts as an alternative antitoxin to LsoA, thus preventing its anti-bacteriophag

272 al requirements of the Escherichia coli DinJ antitoxin to suppress its toxin partner, YafQ.

273 ne-third most homologous to BoNT/A) requires antitoxin to toxin ratios >/=1190:1 for neutralization b

274 creased by giving millions of doses of horse antitoxin to wounded soldiers.

275 The combining of antitoxins to neutralize the toxicity of known bivalent

276 e protein-based antitoxin MqsA and RNA-based antitoxin ToxI, and showed that the evolved MqsA and Tox

277 esent study, we sought to define how the RNA antitoxin, ToxI, inhibits its potentially lethal protein

278 might exist in B. subtilis that can promote antitoxin/toxin RNA interaction.

279 Reduced mortality was associated with any antitoxin treatment (odds ratio [OR], 0.16; 95% confiden

280 ht to quantify the allergy risk of botulinum antitoxin treatment and the usefulness of skin testing t

281 ; 95% confidence interval [CI], .09-.30) and antitoxin treatment within 48 hours of illness onset (OR

282 ffect of timing of antitoxin administration, antitoxin type, and toxin exposure type.

283 that the antitoxin, YeeU, is a novel type of antitoxin (type IV TA system), which does not form a com

284 During steady-state cell growth, antitoxins typically interact with their cognate toxins

285 r studies published on botulism or botulinum antitoxin use during pregnancy and the postpartum period

286 comes associated with botulism and botulinum antitoxin use during pregnancy and the postpartum period

287 inations of cognate and noncognate Mtb toxin-antitoxins using in vivo toxicity and rescue experiments

288 open new possibilities in the preparation of antitoxin vaccines against the many virulence factors th

289 The virA (proteic antitoxin)/virT (proteic toxin) pair in IA3902 belongs t

290 oxin compared with patients not treated with antitoxin was 0.24 (95% confidence interval, .14-.40; P

291 Antitoxin was administered, resulting in patient improve

292 subsequent in vivo analysis showed that the antitoxin was degraded by ClpP.

293 Diphtheria antitoxin was issued in two (9.5%) cases; both survived.

294 We did not identify an interval beyond which antitoxin was not beneficial.

295 nic strains and the only available treatment antitoxin which can target the neurotoxin at the extrace

296 in-antitoxin systems, a small RNA acts as an antitoxin, which prevents the synthesis of the toxin.

297 Current treatments rely on antitoxins, which, while effective, cannot reverse sympt

298 f interface mutants, we show that toxins and antitoxins with high specificity are frequently connecte

299 We have developed an antitoxin, XOMA 3AB, consisting of three recombinant mAb

300 Here, we demonstrate that the antitoxin, YeeU, is a novel type of antitoxin (type IV T