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1 uberculosis) and diphtheria (Corynebacterium diphtheriae).
2 gnition of the toxin gene in Corynebacterium diphtheriae.
3 mmalian HO-1 and the HO from Corynebacterium diphtheriae.
4 antigenically distinct from other pili of C. diphtheriae.
5 sights into transcriptional regulation in C. diphtheriae.
6 he SpaABC pili and possibly other pili of C. diphtheriae.
7 n linked to the virulence of Corynebacterium diphtheriae.
8 iosynthesis and transport in Corynebacterium diphtheriae.
9 esent a potential reservoir for toxigenic C. diphtheriae.
10 tatic and virulence genes in Corynebacterium diphtheriae.
11 nes were constructed on the chromosome of C. diphtheriae.
12 of known virulence genes in Corynebacterium diphtheriae.
13 disease caused by toxigenic Corynebacterium diphtheriae.
14 ed the precise amount of DtxR per cell in C. diphtheriae.
15 than another studied HO from Corynebacterium diphtheriae.
16 l of iron-sensitive genes in Corynebacterium diphtheriae.
17 l ion-activated repressor in Corynebacterium diphtheriae.
18 cobacterium tuberculosis and Corynebacterium diphtheriae.
19 ecretion of diphtheria toxin by wild-type C. diphtheriae.
20 n(2+) transport systems may be present in C. diphtheriae.
21 egulated promoters (IRPs) in Corynebacterium diphtheriae.
22 loregulatory proteins to be identified in C. diphtheriae.
23 t time that dtxR is a dispensable gene in C. diphtheriae.
24 tem previously identified in Corynebacterium diphtheriae.
25 nose swab to be positive for Corynebacterium diphtheriae.
26 mmunicable disease caused by Corynebacterium diphtheriae.
27 ane when expressed in Escherichi coli and C. diphtheriae.
28 infectious disease caused by Corynebacterium diphtheriae.
29 nd may function as the haemin receptor in C. diphtheriae.
30 d the need for laboratories to screen for C. diphtheriae.
31 ay a crucial role in the pathogenicity of C. diphtheriae.
32 in from toxigenic strains of Corynebacterium diphtheriae.
33 emoglobin as iron sources by Corynebacterium diphtheriae.
34 negative global regulator in Corynebacterium diphtheriae.
35 ease caused by the bacterium Corynebacterium diphtheriae.
36 cobacterium tuberculosis and Corynebacterium diphtheriae.
37 scheme, which is currently restricted to C. diphtheriae.
38 the general oxidative folding machine in C. diphtheriae.
39 n-mediated disease caused by Corynebacterium diphtheriae.
40 al host iron sources that are utilized by C. diphtheriae.
41 -TOF MS) were conclusive for Corynebacterium diphtheriae.
42 ad no effect on hemin iron utilization in C. diphtheriae.
43 virulence and other genes in Corynebacterium diphtheriae.
44 se reaction intermediates in Corynebacterium diphtheriae.
45 nction as cell surface hemin receptors in C. diphtheriae.
46 currently the method of choice for typing C. diphtheriae.
47 h ferrous ion homeostasis in Corynebacterium diphtheriae.
48 of the regulation of heme homeostasis in C. diphtheriae.
49 onsillectomy and immunity to Corynebacterium diphtheriae (1931), 2 papers from a longitudinal study o
50 r the clinically significant Corynebacterium diphtheriae (4 of 4) and Corynebacterium jeikeium (8 of
52 To further define the DtxR regulon in C. diphtheriae, a DtxR repressor titration assay (DRTA) was
53 release measurements are compatible with C. diphtheriae acquiring heme passively released from hemog
55 ria toxin (Dtx) expressed by Corynebacterium diphtheriae also can function as part of an anti-predato
56 imed to describe the outbreak of toxigenic C diphtheriae among asylum seekers arriving by small boats
57 me oxygenase mutants of both Corynebacterium diphtheriae and C. ulcerans fail to use heme as an iron
59 espiratory illness caused by Corynebacterium diphtheriae and C. ulcerans, and use of diphtheria anti-
60 etions in the hmuO gene from Corynebacterium diphtheriae and Corynebacterium ulcerans and show that t
64 ection caused by a nontoxigenic strain of C. diphtheriae and discuss the epidemiology, possible sourc
65 of the SpaA-type pilus from Corynebacterium diphtheriae and FimA of the type 2 pilus from Actinomyce
67 inc specific transcriptional regulator in C. diphtheriae and give new insights into the intricate reg
68 are and contrast galactan biosynthesis in C. diphtheriae and M. tuberculosis In each species, the gal
69 n of amino acids, as well as Corynebacterium diphtheriae and Mycobacterium tuberculosis, which cause
70 lts of this work provide insight into how C. diphtheriae and other pathogenic and commensal corynebac
73 utilization of heme as an iron source by C. diphtheriae and that the heme oxygenase activity of HmuO
74 , the heterotrimeric pili in Corynebacterium diphtheriae and the heterodimeric pili in Actinomyces or
75 -based mutagenesis technique for use with C. diphtheriae, and we used it to construct the first trans
76 Diagnostic tests for toxinogenicity of C. diphtheriae are based either on immunoassays or on bioas
77 cobacterium tuberculosis and Corynebacterium diphtheriae are characterized by their complex, multi-la
78 We show here that pili of Corynebacterium diphtheriae are composed of three pilin subunits, SpaA,
80 ix sortase genes encoded in the genome of C. diphtheriae are required for precursor processing, pilus
81 toxin repressor (DtxR) from Corynebacterium diphtheriae, are iron-dependent regulatory proteins that
84 ncing to determine the genome sequence of C. diphtheriae BQ11 and mechanism of beta-lactam resistance
85 ncing to determine the genome sequence of C. diphtheriae BQ11 and the mechanism of B-lactam resistanc
86 cobacterium tuberculosis and Corynebacterium diphtheriae, but unlike the linear chromosomes of the mo
88 1 was toxigenic and 3 were non-toxigenic C. diphtheriae by culture and Elek, 6 were culture-negative
89 , 1 was toxigenic and 3 were nontoxigenic C. diphtheriae by culture and Elek, 6 were culture-negative
91 ia cases caused by toxigenic Corynebacterium diphtheriae (C diphtheriae) was reported among asylum se
92 ized with either pentavalent Corynebacterium diphtheriae C7 (beta197) cross-reactive material (CRM197
93 operon contained a large deletion in the C. diphtheriae C7 strain, but the sid genes were unaffected
95 d under high-iron conditions in wild-type C. diphtheriae C7(beta), but they were expressed constituti
97 xR(E175K) mutant allele from Corynebacterium diphtheriae can be expressed in Mycobacterium tuberculos
98 Unlike other Cas9 orthologs, Corynebacterium diphtheriae Cas9 (CdCas9) recognizes the promiscuous NNR
100 ation enzyme in the pathogen Corynebacterium diphtheriae, catalyzes the oxygen-dependent conversion o
104 eted by lysogenic strains of Corynebacterium diphtheriae, causes the disease diphtheria in humans by
106 reductase A of the pathogen Corynebacterium diphtheriae (Cd-MsrA) and shown that this enzyme is coup
107 r-lacZ fusion was dependent on the cloned C. diphtheriae chrA and chrS genes (chrAS), which encode th
108 In this study, two clones isolated from a C. diphtheriae chromosomal library were shown to activate t
109 ephages are capable of inserting into the C. diphtheriae chromosome at two specific sites, attB1 and
110 each of these systems was cloned from the C. diphtheriae chromosome, and constructs each carrying one
111 organism showed that several genotypes of C. diphtheriae circulated on different continents of the wo
112 ed the predominant strain of nontoxigenic C. diphtheriae circulating in the United Kingdom to see if
115 e, we characterized a large collection of C. diphtheriae clinical isolates for their pilin gene pool
117 he findings from this study indicate that C. diphtheriae contains at least 18 DtxR binding sites and
119 ief has been disproven with many notable non-diphtheriae Corynebacterium species being found to be pa
128 omologous to elements of the Corynebacterium diphtheriae DtxR regulon, which controls, in response to
132 ings demonstrated that the irp6 operon in C. diphtheriae encodes a putative ABC transporter, that spe
134 egmatis (EsxA and EsxB), and Corynebacterium diphtheriae (EsxA and EsxB) are heterodimers and fold in
135 The Gram-positive pathogen Corynebacterium diphtheriae exports through the Sec apparatus many extra
136 o immune system-induced oxidative stress, C. diphtheriae expresses antioxidant enzymes, among which a
137 In this study, we describe a Corynebacterium diphtheriae ferric uptake regulator-family protein, Zur,
138 a heme degradation enzyme in Corynebacterium diphtheriae, forms a stoichiometric complex with iron pr
140 T-PCR assay to detect tox and distinguish C. diphtheriae from the closely related species C. ulcerans
142 ts and on the results of experiments with C. diphtheriae genes cloned in Escherichia coli or analyzed
149 on hemin utilization, which suggests that C. diphtheriae has an additional system for transporting he
150 olecular characterization of Corynebacterium diphtheriae has become a priority in order to be able to
153 rom the pathogenic bacterium Corynebacterium diphtheriae has been subcloned and expressed in Escheric
154 iology of diseases caused by Corynebacterium diphtheriae has changed dramatically over the decades, a
155 f tools, genetic analysis of Corynebacterium diphtheriae has primarily relied on analysis of chemical
156 rom the pathogenic bacterium Corynebacterium diphtheriae, have been investigated by (1)H NMR spectros
157 txR mutant of C7, and in a hmuO mutant of C. diphtheriae HC1 provided further evidence that transcrip
158 nation and spin-state of the Corynebacterium diphtheriae heme oxygenase (Hmu O) and the proximal Hmu
163 n and heme whereas transcription from the C. diphtheriae hmuO promoter shows both significant iron re
164 ces from the mammalian HO-1 and bacterial C. diphtheriae HO structures, which suggests a structural b
165 endent activation at the hmuO promoter in C. diphtheriae; however, it was observed that significant l
166 report, we identify and characterize the C. diphtheriae hrtAB genes, which encode a putative ABC typ
169 ents (77%), including all 5 patients with C. diphtheriae IE, required hospital admission for C. dipht
170 h a proposed mechanism of hemin uptake in C. diphtheriae in which hemin is initially obtained from Hb
171 2015, and indicating silent circulation of C diphtheriae in Yemen before the outbreak was declared.
173 significant implications for treatment of C. diphtheriae infection and may lead to clinical failure.
178 ificant implications for the treatment of C. diphtheriae infection, and may lead to clinical failure.
180 orted the improbability of importation of C. diphtheriae into this area and rather strongly suggest t
183 , represses transcription of Corynebacterium diphtheriae iron-regulated promoters in vivo and binds t
185 toxin repressor (DtxR) from Corynebacterium diphtheriae is a divalent metal-activated repressor of c
188 of the pathogenic bacterium Corynebacterium diphtheriae is conferred by diphtheria toxin, whose expr
191 iptional regulator DtxR from Corynebacterium diphtheriae is the prototype for a family of metal-depen
192 toxin repressor (DtxR) from Corynebacterium diphtheriae is the prototypic member of a superfamily of
195 we describe the genomic variation of 502 C. diphtheriae isolates across 16 countries and territories
196 e distribution of each genetic cluster of C. diphtheriae isolates across multiple countries in Europe
197 tion of 53 U.S. and Canadian Corynebacterium diphtheriae isolates by multilocus enzyme electrophoresi
199 tive composite transposon associated with C. diphtheriae isolates that dominated the diphtheria outbr
205 Here, we solved the solution structure of C. diphtheriae MsrB (Cd-MsrB) and unraveled its catalytic a
206 min iron utilization assays using various C. diphtheriae mutants indicate that deletion of the chtA-c
208 f important pathogens (e.g., Corynebacterium diphtheriae, Mycobacterium tuberculosis), and (iii) prov
210 m were infected by toxigenic Corynebacterium diphtheriae of both mitis and gravis biotypes, showing t
212 -regulated promoters in vivo and binds to C. diphtheriae operators in a metal-dependent manner in vit
215 he source of galactan length variation, a C. diphtheriae ortholog of the M. tuberculosis carbohydrate
217 y was caused by one major clonal group of C. diphtheriae (PFGE type A, ribotype R1), which was identi
218 44 patients (median age, 44 years) had a C. diphtheriae-positive clinical culture, with most detecti
220 heme and hemoglobin, which suggests that C. diphtheriae possesses a novel mechanism for utilizing he
221 Therefore, recent clinical isolates of C. diphtheriae produce a single antigenic type of DT, and d
224 Nontoxigenic strains of Corynebacterium diphtheriae represent a potential reservoir for the emer
225 of the Hb-Hp complex as an iron source by C. diphtheriae requires multiple iron-regulated surface com
226 The use of hemin iron by Corynebacterium diphtheriae requires the DtxR- and iron-regulated ABC he
229 espiratory diphtheria caused by toxigenic C. diphtheriae resistant to penicillin and all other B-lact
230 espiratory diphtheria caused by toxigenic C. diphtheriae resistant to penicillin and all other beta-l
231 muO, the heme oxygenase from Corynebacterium diphtheriae, restores iron and heme levels, as well as A
232 dtxR genes in recent clinical isolates of C. diphtheriae revealed several tox alleles that encode ide
233 nematodes from infection by Corynebacterium diphtheriae, revealing the importance of this minor pool
234 rate that the cohort of CR domains within C. diphtheriae's hemin-uptake system have dissociation cons
235 thogenic bacteria, including Corynebacterium diphtheriae, Salmonella enterica, and Vibrio cholerae, a
237 MR, and in situ binding measurements that C. diphtheriae selectively captures iron-loaded hemoglobin
244 significant genetic diversity within the C. diphtheriae species, and ribotyping and MEE data general
245 ently, cell wall extracts of a particular C. diphtheriae strain (DSM43989) lacking mycolic acid ester
246 We report that an htaA deletion mutant of C. diphtheriae strain 1737 is unable to use the Hb-Hp compl
247 ae, FimA, is expressed in corynebacteria, C. diphtheriae strain NCTC13129 polymerized FimA to form sh
248 demic of 1993 to 1998 and 13 non-Georgian C. diphtheriae strains (10 Russian and 3 reference isolates
250 n mostly caused by toxigenic Corynebacterium diphtheriae strains and occasionally by toxigenic C. ulc
253 nd the emergence of epidemic Corynebacterium diphtheriae strains globally have highlighted the need f
254 reservoir for the emergence of toxigenic C. diphtheriae strains if they possessed functional diphthe
255 closely related to each other than to the C. diphtheriae strains isolated in other parts of the Unite
256 atory element (dtxR) from 72 Corynebacterium diphtheriae strains isolated in Russia and Ukraine befor
258 strated that the majority (87.5%; 7/8) of C. diphtheriae strains represented new sequence types (STs)
260 PD typing, ribotyping, and PFGE typing of C. diphtheriae strains were improved to enable rapid and co
262 erium diphtheriae strains, 9 nontoxigenic C. diphtheriae strains, and 44 strains representing the div
263 n hemoglobin-iron utilization, whereas in C. diphtheriae strains, deletion of hmuO caused no or only
265 eight (40.0%) were caused by Corynebacterium diphtheriae strains; six were biovar mitis, which were a
266 endent regulatory protein in Corynebacterium diphtheriae that controls gene expression by binding to
267 d characterized two novel genetic loci in C. diphtheriae that encode factors that bind hemin and Hb.
268 an extracellular protein of Corynebacterium diphtheriae that inhibits protein synthesis and kills su
269 iron-dependent repressor in Corynebacterium diphtheriae that regulates transcription from multiple p
270 d for the fusion toxin using Corynebacterium diphtheriae that secretes fully folded, biologically act
271 eted by lysogenic strains of Corynebacterium diphtheriae, that causes the disease diphtheria in human
272 y human pathogens, including Corynebacterium diphtheriae, the causative agent of diphtheria, use host
278 livered to the cytoplasm of non-lysogenic C. diphtheriae, they integrated into either the attB1 or at
279 toxin produced by the causative organism, C. diphtheriae; this detection is the definitive test for t
280 chtC gene has no affect on the ability of C. diphtheriae to use hemin or Hb as iron sources; however,
281 nd binary toxin (CDTa-CDTb), Corynebacterium diphtheriae toxin (DT), and Pseudomonas aeruginosa exoto
282 of a heterotrimeric pilus in Corynebacterium diphtheriae, uncovering the molecular switch that termin
290 confirm cases biologically, Corynebacterium diphtheriae was isolated and identified from throat swab
291 ical diphtheritic lesions but from whom no C diphtheriae was isolated from clinical swabs was also in
294 by toxigenic Corynebacterium diphtheriae (C diphtheriae) was reported among asylum seekers arriving
295 prototypical SpaA pilus from Corynebacterium diphtheriae We show that sortase-catalyzed introduction
296 d the systems for genetic manipulation of C. diphtheriae, we constructed plasmid vectors capable of i
297 y toxin-producing strains of Corynebacterium diphtheriae, with similar illness produced occasionally