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1 ls a second strain lacking the corresponding antitoxin.
2 by the co-expression of its cognate RelB2sca antitoxin.
3  is counteracted by its HD domain-containing antitoxin.
4  by direct interaction with a structured RNA antitoxin.
5 ely mediated by active site hindrance by its antitoxin.
6 tially toxic protein, and a small RNA (sRNA) antitoxin.
7 i-F botulinum antitoxins but not with anti-E antitoxin.
8 overed antitoxin gene be named ralA for RalR antitoxin.
9 -ribosylating toxin and ParS for the cognate antitoxin.
10 pINV, consist of a toxic protein and protein antitoxin.
11 phylaxis related to HBAT and other botulinum antitoxins.
12 d for HBAT and previously employed botulinum antitoxins.
13 in activity and the regulated proteolysis of antitoxins.
14 ios >/=1190:1 for neutralization by existing antitoxins.
15 pment of a mechanistic class of C. difficile antitoxins.
16 e association and co-evolution of toxins and antitoxins.
17 ution patterns and in their range of cognate antitoxins.
18 rved PPVs and NPVs of ST for other botulinum antitoxins (302 patients) were 0-56% and 50%-100%, respe
19              A heptavalent F(ab')2 botulinum antitoxin A-G obtained from the US Army also did not neu
20 hese produce a stable toxin (T) and a labile antitoxin (A) conditioning cell survival to plasmid main
21  by ClpXP, and this degradation requires the antitoxin, a ClpXP adaptor.
22 E operon was negatively autoregulated by the antitoxin, AbiEi, a member of a widespread family of put
23   The RNA chaperone Hfq is required for RalA antitoxin activity and appears to stabilize RalA.
24 orylates Ser78 of the toxin), and HepT/MntA (antitoxin adds three AMPs to Tyr104 of the toxin).
25                                       Prompt antitoxin administration and meticulous intensive care a
26 travenous magnesium sulphate and intrathecal antitoxin administration as methods of spasm control tha
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 with the timely administration of diphtheria antitoxin and antimicrobial therapy.
37 xpansive diversity of inovirus-encoded toxin-antitoxin and gene expression modulation systems, alongs
38 AbrB transition state regulator and the MazE antitoxin and MraW is known to methylate the 16S rRNA, m
39 ically evaluated the literature on botulinum antitoxin and other treatments.
40 vior of some of these systems, such as toxin-antitoxin and restriction modification modules.
41 es for TA systems based on the nature of the antitoxin and the way that the antitoxin inactivates the
42 veral conditionally essential genes encoding antitoxins and/or immunity proteins.
43 njection blocking, abortive infection, toxin-antitoxin, and CRISPR-Cas systems.
44                Although this module's toxin, antitoxin, and toxin-antitoxin complex have been more th
45 tability, and consists of wound debridement, antitoxin, antibiotics, and supportive care.
46                                          The antitoxin antibodies actoxumab and bezlotoxumab bind to
47                     Circulating neutralizing antitoxin antibodies are protective in C. difficile infe
48              In this study, we show that the antitoxin antibodies are protective in multiple murine m
49 alizing activity and suggest that engineered antitoxin antibodies will have improved therapeutic effi
50 -old woman that arose despite the protective antitoxin antibody in her serum.
51                  Patients who develop strong antitoxin antibody responses can clear C. difficile infe
52                         Further, a wild-type antitoxin appears optimized for specificity as no substi
53 tor interaction, enabling the development of antitoxin approaches and improved animal models to explo
54               Furthermore, it is unclear how antitoxins are selected for proteolysis by cellular prot
55 r the zorO-orzO type I system where the OrzO antitoxin base pairs to the 174-nucleotide zorO 5 UTR.
56 ation for the Type III TA class, and the RNA antitoxin bears a novel structural feature of an extende
57                        This is distinct from antitoxins belonging to other superfamilies that typical
58   A typical regulatory strategy involves the antitoxin binding and repressing its own promoter while
59 at typically acts as a gate to direct RNA or antitoxin binding.
60  free antitoxin is readily degraded in vivo, antitoxin bound to toxin is protected from proteolysis,
61  other TA proteins in the sense that not the antitoxin but the toxin possesses a flexible region.
62 te with anti-A, anti-B, and anti-F botulinum antitoxins but not with anti-E antitoxin.
63                 Selective degradation of the antitoxin by proteases leads to the unopposed action of
64 y and mortality, but concerns that botulinum antitoxin can induce anaphylaxis exist.
65 olded state of the partially disordered CcdA antitoxin can therefore provide insight into general mec
66 signate those TA systems in which the enzyme antitoxin chemically modifies the toxin post-translation
67  to a Type II TA system, while the cjrA (RNA antitoxin)/cjpT (proteic toxin) pair in 81-176 belongs t
68 ve risk of death among patients treated with antitoxin compared with patients not treated with antito
69 gh this module's toxin, antitoxin, and toxin-antitoxin complex have been more thoroughly investigated
70 stal structure of the Escherichia coli toxin-antitoxin complex YafQ-(DinJ)2-YafQ, a key component of
71                  Chromosomally-encoded toxin-antitoxin complexes are ubiquitous in bacteria and regul
72                        The features of toxin-antitoxin complexes that are important to inhibit toxin
73 formational states play a role in regulating antitoxin concentrations and the activity of CcdA's cogn
74 ing other functions, for example, toxins and antitoxins, confirming the recently discovered potential
75 xible region in the toxin rather than in the antitoxin controls operon expression and toxin activity.
76 main of unknown function (DUF) 4433, and the antitoxin (DarG) a macrodomain protein.
77                                          The antitoxin, DarG(Mtb) , forms a cytosolic complex with DN
78 t is rescued by expression of an orthologous antitoxin, DarG(Taq) , from Thermus aquaticus.
79                                   Diphtheria antitoxin (DAT) has been the cornerstone of the treatmen
80 ecies and toxin confirmation, and diphtheria antitoxin (DAT) is obtained from CDC for treatment.
81  the administration and safety of diphtheria antitoxin (DAT), the standard treatment for diphtheria.
82 l horse sera directed against DT (diphtheria antitoxin; DAT).
83     Stress-induced transcription arises from antitoxin degradation and relief of transcriptional auto
84 he ClpXP protease is responsible for Epsilon antitoxin degradation.
85                                          The antitoxin DinJ dimer adopts a ribbon-helix-helix motif r
86 y virtue of its interaction with its cognate antitoxin, DinJ.
87 ite, regulation of enzymatic activity by the antitoxin EcMazE diverges from its B. subtilis homolog.
88  they comprise two proteins, a toxin, and an antitoxin, encoded by adjacent genes and forming a compl
89 us isolates, and was influenced by the toxin/antitoxin encoding locus mazEF.
90 osynthesis through complex formation with an antitoxin, EsaG, which binds to its C-terminal nuclease
91 obacterium tuberculosis (Mtb), three contain antitoxins essential for bacterial viability.
92 ntiToxSAS system with its multiple different antitoxins exemplifies how ancient nucleotide-based sign
93                   Furthermore, we evolved an antitoxin for the new toxin ArT from two unrelated antit
94                         Here we show that an antitoxin from a type V system (GhoS, an endoribonucleas
95                        Therefore, toxins and antitoxins from disparate systems can be interconverted.
96              We suggest the newly discovered antitoxin gene be named ralA for RalR antitoxin.
97 hia coli contains at least 36 putative toxin-antitoxin gene pairs, and some pathogens such as Mycobac
98 ng a 30-amino acid hydrophobic toxin and the antitoxin gene sr5 overlap at their 3' ends by 112 bp.
99 es bacterial growth and a toxin-neutralizing antitoxin gene, usually encoded in a single operon.
100                                        Toxin-antitoxin genes play important roles in the regulation o
101 ma factors, transcription factors, and toxin-antitoxin genes.
102 n by the protein products of six neighboring antitoxin genes.
103 d by cleavage of its messenger RNA (mRNA) by antitoxin GhoS, and TA system MqsR/MqsA controls GhoT/Gh
104 e show that Pseudomonas putida graTA-encoded antitoxin GraA and toxin GraT differ from other TA prote
105                        Children who received antitoxin had better survival; serious adverse events we
106 iated, equine-derived, heptavalent botulinum antitoxin (HBAT) is licensed in the United States.
107         Equine-derived heptavalent botulinum antitoxin (HBAT), the only currently available treatment
108                                     Botulism Antitoxin Heptavalent (A,B,C,D,E,F,G)-(Equine) (BAT) man
109 he cognate toxin is the direct target of the antitoxin: Hha/TomB (antitoxin oxidizes Cys18 of the tox
110 ound that, unlike most other TA systems, the antitoxin HigA makes minimal interactions with toxin Hig
111 crobial therapy and prompt administration of antitoxin, if necessary.
112  month prior had significantly greater serum antitoxin IgA and IgG against toxins A (P = .02 for both
113                              For comparison, antitoxin IgG and NAb were measured in cord blood from 5
114 emonstrate that durable levels of protective antitoxin immunity exist in the majority of vaccinated i
115 eine variant [C117S]YmoB can replace TomB as antitoxins in E. coli.
116 the adaptor that works with ClpCP to degrade antitoxins in S. aureus.
117 nature of the antitoxin and the way that the antitoxin inactivates the toxin.
118 completely eliminated by existing serotype A antitoxins, including those contained in multivalent the
119 itional and distinct TA systems in which the antitoxin is an enzyme and the cognate toxin is the dire
120                 Under stress conditions, the antitoxin is degraded liberating the active toxin.
121                   Importantly, although free antitoxin is readily degraded in vivo, antitoxin bound t
122      We find that the C-terminus of the HigA antitoxin is required for dimerization and transcription
123 egulated at the transcriptional level by the antitoxin itself.
124                         The widespread toxin-antitoxin loci and 'open' state of the pangenome provide
125                                 Type I toxin-antitoxin loci consist of two genes: a small, hydrophobi
126                                        Toxin-antitoxin loci, which encode a toxic protein alongside w
127 at the zorO-orzO pair is a true type I toxin-antitoxin locus.
128 ibe the isolation of diverse and efficacious antitoxin mAbs.
129 s inactivated through binding to its cognate antitoxin, MazE.
130 T, is bactericidal unless neutralized by its antitoxin MbcA.
131            Here, we discovered that the MntA antitoxin (MNT-domain protein) acts as an adenylyltransf
132 f protein-protein interactions using a toxin-antitoxin model.
133 ncoded by a three-component parDE-like toxin-antitoxin module from Escherichia coli O157:H7.
134         The toxin Doc from the phd/doc toxin-antitoxin module targets the cellular translation machin
135                      Bacterial type II toxin-antitoxin modules are protein-protein complexes whose fu
136                     The majority of 14 toxin-antitoxin modules contributed to intracellular persister
137        In several different organisms, toxin-antitoxin modules function as effectors of ppGpp-induced
138                   In Escherichia coli, toxin-antitoxin modules have been linked to persister formatio
139                                    Toxin and antitoxin modules in bacteria are believed to be one pos
140  one of many chromosomally encoded toxin and antitoxin modules in Escherichia coli and the HipA7 alle
141                               Deleting toxin-antitoxin modules in S. aureus did not affect the level
142       Bacteria encode multiple type II toxin-antitoxin modules that cleave ribosome-bound mRNAs in re
143 es, and signaling molecules, including toxin-antitoxin modules, adenosine triphosphate, and guanosine
144 ylococcus aureus genome contains three toxin-antitoxin modules, including one mazEF module, SamazEF.
145  the transcriptional repression of two toxin/antitoxin modules, mqsR/mqsA and dinJ/yafQ.
146 Gpp and requires chromosomally encoded toxin-antitoxin modules.
147 owing persisters through the action of toxin-antitoxin modules.
148 that assessed the efficacy and safety of the antitoxin monoclonal antibodies bezlotoxumab and actoxum
149 lated antitoxin templates, the protein-based antitoxin MqsA and RNA-based antitoxin ToxI, and showed
150                                 Notably, the antitoxin MqsA possesses a C-terminal DNA-binding domain
151                  Among patients who received antitoxin (n = 193), 23 (12%) reported an adverse event,
152 se that inhibits cell growth, while the HipB antitoxin neutralizes the toxin.
153 The association of toxins with their cognate antitoxins neutralizes toxin activity, allowing for norm
154 e activated Lon to degrade all known type II antitoxins of E. coli.
155                Therapeutic agents other than antitoxin offered no clear benefit.
156 or, but instead functions to destabilize the antitoxin-operator complex under all conditions, and thu
157 pression of the Proteus vulgaris higBA toxin-antitoxin operon from the Rts1 plasmid.
158 ycobacterium tuberculosis have over 90 toxin-antitoxin operons.
159                                        Toxin-antitoxin or toxin-antidote (TA) elements are genetic dy
160 he direct target of the antitoxin: Hha/TomB (antitoxin oxidizes Cys18 of the toxin), TglT/TakA (antit
161             The mqsRA operon encodes a toxin-antitoxin pair that was characterized to participate in
162                                Type II toxin-antitoxin pairs are regulated at the transcriptional lev
163 into the critical interactions between toxin-antitoxin pairs necessary to inhibit toxin activity and
164            Though thousands of various toxin-antitoxins pairs have been predicted bioinformatically,
165 ranslation machinery and is inhibited by its antitoxin partner Phd.
166 xin oxidizes Cys18 of the toxin), TglT/TakA (antitoxin phosphorylates Ser78 of the toxin), and HepT/M
167 c is an equine-derived heptavalent botulinum antitoxin product indicated for the treatment of symptom
168 g those contained in multivalent therapeutic antitoxin products that are the mainstay of human botuli
169 ion and is associated with repression of the antitoxin promoter and enhanced processing of its transc
170                                          The antitoxin protein CcdA is a homodimer composed of two mo
171 sponse to stress is selective proteolysis of antitoxin proteins which releases their cognate toxin pa
172 the biochemical properties of both toxin and antitoxin proteins.
173 e II TA systems relies on the proteolysis of antitoxin proteins.
174                                           An antitoxin raised against IBCA10-7060 toxoid protected mi
175 ion-provided monovalent polyclonal botulinum antitoxins raised against BoNT types A-G.
176 reactions may occur among 1%-2% of botulinum antitoxin recipients and will require epinephrine and an
177                     Timely administration of antitoxin reduces mortality; despite appropriate treatme
178               Here, we examined how the HigA antitoxin regulates the expression of the Proteus vulgar
179 16% (8/687 patients) for all other botulinum antitoxins (relative risk, 1.41 [95% confidence interval
180      Moreover, the RelBE2sca complex, or the antitoxin RelB2sca alone, specifically interacted with t
181                   Interestingly, the E. coli antitoxin RelBeco was able to alleviate the toxicity of
182                               Notably, cjrA (antitoxin) represents the first noncoding small RNA demo
183 phage rac form a type I TA pair in which the antitoxin RNA is a trans-encoded small RNA with 16 nucle
184 stasis and that co-expression of the cognate antitoxin Rv2515c restores bacterial growth.
185 es, suggesting that the regulation of RNA or antitoxin selection may be distinct from other canonical
186 oxin sequences are more closely related than antitoxin sequences in M. tuberculosis Furthermore, the
187 ortality; despite appropriate treatment with antitoxin, some patients suffer respiratory failure.
188  This mRNA is translationally silenced by an antitoxin sRNA, IstR-1, that base pairs to the standby s
189 rves as the target site of the corresponding antitoxin sRNA.
190 estions were investigated for a type I toxin-antitoxin system (AapA1-IsoA1) expressed from the chromo
191                          The bacterial toxin-antitoxin system CcdB-CcdA provides a mechanism for the
192 re, we describe the AtaT2 toxin from a toxin-antitoxin system from Escherichia coli O157:H7.
193 olecular Cell, Aarke et al. identify a toxin-antitoxin system in Caulobacter crescentus that acts by
194               BsrE/SR5 is a new type I toxin/antitoxin system located on the prophage-like region P6
195                     MazEF is a type II toxin-antitoxin system present on the chromosome of Escherichi
196  from bacteriophage P1 (of the phd-doc toxin-antitoxin system) has served as a model for the family o
197             Loss of GmvAT and a second toxin-antitoxin system, CcdAB, from pINV reduces S. sonnei pla
198                               GmvAT, a toxin-antitoxin system, is responsible for the difference in s
199 ron that also has characteristics of a toxin-antitoxin system, thus joining several enigmatic feature
200 to human infections, e.g. Fic and VbhA toxin-antitoxin system.
201 , persistence is promoted by the HipBA toxin-antitoxin system.
202 ing potential novel regulation in this toxin-antitoxin system.
203 o-residing plasmid encoding a putative toxin-antitoxin system; iii) a mutation in the host's global t
204        Lastly, we describe the role of toxin-antitoxin systems (TAS) in the induction of the VBNC sta
205 vival mechanism modulated, in part, by toxin-antitoxin systems (TAS).
206 s the expansion and diversification of toxin-antitoxin systems and other paralogous protein families
207 pulation dynamics for a large class of toxin-antitoxin systems and suggests answers to several of the
208                                        Toxin-antitoxin systems are found in many bacterial chromosome
209                              Bacterial toxin-antitoxin systems are important factors implicated in gr
210                                        Toxin-antitoxin systems are mediators of diverse activities in
211                                        Toxin-antitoxin systems are ubiquitous and have been implicate
212                                        Toxin-antitoxin systems are ubiquitous in nature and present o
213                                        Toxin-antitoxin systems are ubiquitous in prokaryotic and arch
214                        Using bacterial toxin-antitoxin systems as a model, we screened a combinatoria
215 xification; antimicrobial peptides and toxin-antitoxin systems associated with symbiosis, immunity, a
216 e and regulation of this operon, since toxin-antitoxin systems have been suggested to play a part in
217                      Additionally, the toxin/antitoxin systems that we investigated (MqsR, MazF, GhoT
218                              In type I toxin-antitoxin systems, a small RNA acts as an antitoxin, whi
219 s, such as restriction-modification or toxin-antitoxin systems, and qualitative, including the discov
220 al, but thousands were associated with toxin-antitoxin systems, DNA repair, cell membrane function, d
221                        Using bacterial toxin-antitoxin systems, we demonstrate the plausibility of th
222 epression complex in contrast to other toxin-antitoxin systems.
223 ation as compared to classical type II toxin-antitoxin systems.
224 istinct from the majority derived from toxin-antitoxin systems: it does not cleave RNA; in fact P1 Do
225                                Type II toxin-antitoxins systems are widespread in prokaryotic genomes
226      YoeB-YefM, the widespread type II toxin-antitoxin (TA) module, binds to its own promoter to auto
227                              Bacterial toxin-antitoxin (TA) modules are tightly regulated to maintain
228                      A large cohort of Toxin-Antitoxin (TA) modules contribute to this persistence.
229                    Of the ~80 putative toxin-antitoxin (TA) modules encoded by the bacterial pathogen
230                                        Toxin-antitoxin (TA) modules have an important role in the for
231 hia coli codes for at least 11 type II toxin-antitoxin (TA) modules, all implicated in bacterial pers
232 reminiscent of those typically seen in toxin-antitoxin (TA) operons.
233 T is predicted to be the most abundant toxin/antitoxin (TA) system in prokaryotes.
234 herichia coli form an oxygen-dependent toxin-antitoxin (TA) system.
235                                        Toxin-antitoxin (TA) systems are gene modules that are ubiquit
236                                        Toxin-antitoxin (TA) systems are implicated in the downregulat
237                         Genes encoding toxin-antitoxin (TA) systems are near ubiquitous in bacterial
238                                        Toxin/antitoxin (TA) systems are present in nearly all bacteri
239                                        Toxin-antitoxin (TA) systems are ubiquitous genetic elements i
240                                        Toxin/antitoxin (TA) systems are ubiquitous within bacterial g
241                                        Toxin-antitoxin (TA) systems are widely distributed in bacteri
242                                        Toxin-antitoxin (TA) systems are widespread in prokaryotes.
243                        Since toxins of toxin/antitoxin (TA) systems have been postulated to be respon
244            The relBE family of Type II toxin-antitoxin (TA) systems have been widely reported in bact
245             The discovery and study of toxin-antitoxin (TA) systems helps us advance our understandin
246                      The prevalence of toxin/antitoxin (TA) systems in almost all genomes suggests th
247                                        Toxin-antitoxin (TA) systems interfere with essential cellular
248    In particular, regulation of type I toxin-antitoxin (TA) systems is achieved through sophisticated
249 come specialized toward the control of toxin-antitoxin (TA) systems known to promote bacterial adapta
250 lmost all free-living bacteria contain toxin-antitoxin (TA) systems on their genomes and the targets
251                                        Toxin/antitoxin (TA) systems perhaps enable cells to reduce th
252                                        Toxin-antitoxin (TA) systems play key roles in bacterial persi
253                                        Toxin-antitoxin (TA) systems regulate fundamental cellular pro
254                              Bacterial toxin-antitoxin (TA) systems regulate key cellular processes t
255 aeal chromosomes encode a diversity of toxin-antitoxin (TA) systems that contribute to a variety of s
256                                        Toxin-antitoxin (TA) systems were proposed as perfect candidat
257 Shigella flexneri, pINV harbours three toxin-antitoxin (TA) systems, CcdAB, GmvAT and VapBC that prom
258                                    For toxin/antitoxin (TA) systems, no toxin has been identified tha
259 sually large representation of type II toxin-antitoxin (TA) systems, whose functions and targets are
260 istance have previously been linked to toxin-antitoxin (TA) systems.
261 ial genomes contain different types of toxin-antitoxin (TA) systems.
262 me harbors an unusually high number of toxin-antitoxin (TA) systems.
263 as a tool to identify and characterize toxin-antitoxin (TA)-acting Abi systems.
264 xin for the new toxin ArT from two unrelated antitoxin templates, the protein-based antitoxin MqsA an
265 ized BoNT/H and represents a potential human antitoxin that could be developed for the prevention and
266 onsist of a toxin that reduces growth and an antitoxin that masks toxin activity.
267 were identified as associated with botulinum antitoxin therapy among 11 patients who received it.
268 ng and to prevent degradation of its cognate antitoxin, thus facilitating inhibition of the toxin.
269        We employ rational design and a toxin/antitoxin titering approach to produce and screen a smal
270 ture of the toxin bound to a fragment of the antitoxin to 1.50 angstrom.
271 fection, they must be paired with diphtheria antitoxin to limit morbidity.
272 y induced by chromosomal inactivation of the antitoxin to select mutations that suppress toxicity.
273 al requirements of the Escherichia coli DinJ antitoxin to suppress its toxin partner, YafQ.
274 ne-third most homologous to BoNT/A) requires antitoxin to toxin ratios >/=1190:1 for neutralization b
275 creased by giving millions of doses of horse antitoxin to wounded soldiers.
276                             The combining of antitoxins to neutralize the toxicity of known bivalent
277 e protein-based antitoxin MqsA and RNA-based antitoxin ToxI, and showed that the evolved MqsA and Tox
278 esent study, we sought to define how the RNA antitoxin, ToxI, inhibits its potentially lethal protein
279  might exist in B. subtilis that can promote antitoxin/toxin RNA interaction.
280    Reduced mortality was associated with any antitoxin treatment (odds ratio [OR], 0.16; 95% confiden
281 ht to quantify the allergy risk of botulinum antitoxin treatment and the usefulness of skin testing t
282 ; 95% confidence interval [CI], .09-.30) and antitoxin treatment within 48 hours of illness onset (OR
283 ffect of timing of antitoxin administration, antitoxin type, and toxin exposure type.
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 reened a combinatorially complete library of antitoxin variants at three key positions against two to
288                            The virA (proteic antitoxin)/virT (proteic toxin) pair in IA3902 belongs t
289 oxin compared with patients not treated with antitoxin was 0.24 (95% confidence interval, .14-.40; P
290                                              Antitoxin was administered, resulting in patient improve
291  subsequent in vivo analysis showed that the antitoxin was degraded by ClpP.
292                                   Diphtheria antitoxin was issued in two (9.5%) cases; both survived.
293 We did not identify an interval beyond which antitoxin was not beneficial.
294 nic strains and the only available treatment antitoxin which can target the neurotoxin at the extrace
295  essential cellular processes, and a cognate antitoxin which counteracts this activity.
296 in-antitoxin systems, a small RNA acts as an antitoxin, which prevents the synthesis of the toxin.
297 /activity of the toxin is counteracted by an antitoxin, which, in type I systems, is an antisense RNA
298  monomeric and interacts with dimeric PaParD antitoxin with a K(D) in the lower picomolar range, yiel
299 f interface mutants, we show that toxins and antitoxins with high specificity are frequently connecte
300 gyrase, and overexpression in the absence of antitoxin yielded an expected filamentous morphology wit

 
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