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1 data and analysis tools for the analysis of Yersinia.
2 iaTree for constructing phylogenetic tree of Yersinia.
3 the function of the pathogenic machinery in Yersinia.
4 lling the host colonization and virulence of Yersinia.
5 Gram-negative bacterial pathogens, including Yersinia.
6 sphatase, is essential for full virulence of Yersinia.
7 spiratory electron acceptor tetrathionate by Yersinia.
8 pe III secretion system (T3SS) of pathogenic Yersinia.
9 bacter: 738, Salmonella: 624, Shigella: 376, Yersinia: 17) were identified and followed for a median
11 initially low-affinity antibacterial (e.g., Yersinia) Abs cross-reactive with TSHR, eventually leadi
14 avirulent strains of Gram-negative bacteria, Yersinia and Klebsiella, and less so by their wild-type
15 compartment showed extreme susceptibility to Yersinia and were deficient in monocyte and neutrophil-d
16 luding enteric Escherichia coli, Salmonella, Yersinia, and Shigella, to subvert cell signaling and ho
23 tion system, whereas the delivery of GBP2 to Yersinia-containing vacuoles (YCVs) requires hypersecret
24 nded DNA (dsDNA) to a type I-F CRISPR system yersinia (Csy) surveillance complex leads to large quate
25 of Rac1 but not of RhoA, -B, or -C inhibited Yersinia effector translocation in CNF-Y-treated and con
27 tably Aeromonas sp. (23.8%) by FilmArray and Yersinia enterocolitica (48.1%) by the Luminex assay.
28 ed defective clearance of the ileal pathogen Yersinia enterocolitica and an elevated inflammatory cyt
29 ) spp., Shigella spp., Campylobacter spp. or Yersinia enterocolitica and matched each with up to 4 un
32 ent the first three-dimensional structure of Yersinia enterocolitica and Shigella flexneri injectisom
33 rrelation spectroscopy, we show that in live Yersinia enterocolitica bacteria these soluble proteins
37 e III secretion system of the human pathogen Yersinia enterocolitica enabled efficient identification
38 t an aberrant acute inflammatory response to Yersinia enterocolitica infection leads to long-lasting
41 gainst siderophilic extracellular pathogens (Yersinia enterocolitica O9) by controlling non-transferr
42 conjugation-ready tetrasaccharide of O-PS of Yersinia enterocolitica O:50 strain 3229 and the trisacc
46 er Yersinia species, and differences between Yersinia enterocolitica subsp. enterocolitica and Yersin
48 rophomonas maltophilia, Vibrio cholerae, and Yersinia enterocolitica T2S-expressing plant pathogens i
49 ins, fused to the N-terminal fragment of the Yersinia enterocolitica T3S substrate YopE, are effectiv
50 btype the important human-pathogenic species Yersinia enterocolitica to whole-genome resolution level
52 , Bacillus cereus was the most sensitive and Yersinia enterocolitica was found to be the most resista
54 , is composed of ~22 copies of SctQ (YscQ in Yersinia enterocolitica), which require the presence of
56 41, norovirus, rotavirus A, Vibrio cholerae, Yersinia enterocolitica, Entamoeba histolytica, Cryptosp
57 lmonella spp., Vibrio spp., Vibrio cholerae, Yersinia enterocolitica, enteroaggregative E. coli, ente
58 eserved stool specimens for the detection of Yersinia enterocolitica, enterotoxigenic Escherichia col
59 lence of a Gram-negative bacterial pathogen, Yersinia enterocolitica, when subjected to low temperatu
60 Staphylococcus aureus, Escherichia coli and Yersinia enterocolitica--demonstrated that the zone of i
61 re that CNF-Y increases Yop translocation in Yersinia enterocolitica-infected cells up to 5-fold.
69 acilitate the ongoing and future research of Yersinia, especially those generally considered non-path
70 comparative genomics, and investigations of Yersinia-flea interactions have disclosed the important
71 ved two structures of an ASBT homologue from Yersinia frederiksenii (ASBTYf) in a lipid environment,
72 Pathogenic bacteria such as Listeria and Yersinia gain initial entry by binding to host target ce
74 T) for comparative pathogenomics analysis of Yersinia genomes; (3) YersiniaTree for constructing phyl
75 and analysis platform is needed to hold the Yersinia genomic data and analysis tools for the Yersini
76 ialized platform to hold the rapidly-growing Yersinia genomic data and to provide analysis tools part
81 ociated with urinary E. coli isolates is the Yersinia high pathogenicity island (HPI), which directs
83 zation interface of PcrH mirrors that of the Yersinia homolog SycD and not the dimerization interface
85 and other Enterobacteriaceae expressing the Yersinia HPI also secrete escherichelin, a second metall
86 e escherichelin biosynthetic capacity of the Yersinia HPI while eliminating the Ybt biosynthetic capa
87 fect may relate to the apparent selection of Yersinia HPI-positive E. coli in uncomplicated clinical
92 unity." The Gram-negative bacterial pathogen Yersinia inactivates critical proteins of the NF-kappaB
94 PK1-dependent cell death, we now reveal that Yersinia-induced apoptosis is critical for host survival
97 3 and caspase-8 or FADD completely abrogated Yersinia-induced cell death and caspase-1 activation.
98 ticle, we report a key role for TNF/TNFR1 in Yersinia-induced cell death of murine macrophages, which
101 he processing of MyD88 was not restricted to Yersinia infection and to proapoptotic Toll-IL-1R domain
108 accurate and reproducible identification of Yersinia isolates to the species level, a process often
111 ichia, Salmonella, Klebsiella, Shigella, and Yersinia opportunistic pathogens, the structure of GusR
113 antigens (rAgs) of HEV genotypes 1 and 3 and Yersinia outer protein D (YopD) on a flow-through chemil
116 dent upon type III secretion system effector Yersinia outer protein J (YopJ), is minimally affected b
117 de host immune defences through injection of Yersinia outer proteins (Yops) into phagocytic cells.
119 an injectisome and effector proteins, called Yersinia outer proteins (Yops), that modulate activation
122 a) in a 19th century intestinal specimen and Yersinia pestis ("Black Death" plague) in a medieval too
124 s from cultures of two attenuated strains of Yersinia pestis [KIM D27 (pgm-) and KIM D1 (lcr-)] grown
125 Here we studied the interaction between the Yersinia pestis ABC heme importer (HmuUV) and its partne
127 specially potential bioterrorism agents like Yersinia pestis and Bacillus anthracis which feature on
129 tant of 20 nM between EGFP-labeled LcrV from Yersinia pestis and its cognate membrane-bound protein Y
130 tant to pigmentation locus-negative (pgm(-)) Yersinia pestis and that this phenotype maps to a 30-cen
131 s both the protective F1 capsular antigen of Yersinia pestis and the LcrV protein required for secret
132 e identification of new virulence factors in Yersinia pestis and understanding their molecular mechan
133 owed differences in virulence genes found in Yersinia pestis and Yersinia pseudotuberculosis compared
134 nt of YopJ-dependent cytotoxicity induced by Yersinia pestis and Yersinia pseudotuberculosis paradoxi
135 ion of either Yersinia pseudotuberculosis or Yersinia pestis bacteria express the small RNAs YSR35 or
136 molecule cyclic diguanylate is essential for Yersinia pestis biofilm formation that is important for
142 Braun lipoprotein (Lpp) and MsbB attenuated Yersinia pestis CO92 in mouse and rat models of bubonic
144 ts the most severe form of disease caused by Yersinia pestis due to its ease of transmission, rapid p
147 ere, we report the oldest direct evidence of Yersinia pestis identified by ancient DNA in human teeth
148 tudies (influenza A in lesser snow geese and Yersinia pestis in coyotes), we argue that with careful
149 ery that regulates the entry and survival of Yersinia pestis in host macrophages is poorly understood
150 ated with iron(III)-yersiniabactin import in Yersinia pestis In this study, we compared the impact of
152 n lymph nodes (LNs), or buboes, characterize Yersinia pestis infection, yet how they form and functio
165 rate chain to the 2' position of lipid A, in Yersinia pestis produced bisphosphoryl hexa-acylated lip
167 roinflammatory responses through TLRs by the Yersinia pestis T3S needle protein, YscF, the Salmonella
169 mal system for interrogating such couplings: Yersinia pestis transmission exerts intense selective pr
170 the possible role of Na(+)/H(+) antiport in Yersinia pestis virulence and found that Y. pestis strai
171 .3, raised to the LcrV virulence factor from Yersinia pestis were characterised for their Fab affinit
173 flammatory response induced by other lethal (Yersinia pestis) and non-lethal (Legionella pneumophila,
174 cessfully produce disease, the causal agent (Yersinia pestis) must rapidly sense and respond to rapid
175 a and Salmonella enterica serovar Typhi, and Yersinia pestis), and 3 protozoa (Leishmania spp., Plasm
176 ymerization of a single protein, e.g., YscF (Yersinia pestis), PscF (Pseudomonas aeruginosa), PrgI (S
177 n, the serine/threonine kinase YopO (YpkA in Yersinia pestis), uses monomeric actin as bait to recrui
180 he consequence of a singular introduction of Yersinia pestis, after which the disease established its
183 acids from BT organisms (Bacillus anthracis, Yersinia pestis, Francisella tularensis, Brucella spp.,
184 -six distinct strains of Bacillus anthracis, Yersinia pestis, Francisella tularensis, Burkholderia ma
185 ns cause host cell death upon infection, and Yersinia pestis, infamous for its role in large pandemic
188 lague, caused by the Gram-negative bacterium Yersinia pestis, is favored by a robust early innate imm
189 biothreat agents such as Bacillus anthracis, Yersinia pestis, or Burkholderia pseudomallei Convention
191 r gene products are functional receptors for Yersinia pestis, the agent of plague, as shown by overex
192 The arthropod-borne transmission route of Yersinia pestis, the bacterial agent of plague, is a rec
193 ly, there is no FDA-approved vaccine against Yersinia pestis, the causative agent of bubonic and pneu
196 hat distinguish DNA amplicons generated from Yersinia pestis, the causative agent of plague, from the
206 that includes serious pathogens such as the Yersinia pestis, which causes plague, Yersinia pseudotub
212 stis (the plague bacillus) and its ancestor, Yersinia pseudotuberculosis (which causes self-limited b
213 elated food- and waterborne enteric pathogen Yersinia pseudotuberculosis A combination of population
214 secreted in a type III-dependent manner from Yersinia pseudotuberculosis and also secreted from C. tr
216 structures, we mapped the RNA structurome of Yersinia pseudotuberculosis at three different temperatu
217 and core metabolism in the enteric pathogen Yersinia pseudotuberculosis by integrated transcriptome
218 virulence genes found in Yersinia pestis and Yersinia pseudotuberculosis compared to other Yersinia s
219 lymph nodes and associated lymphatics after Yersinia pseudotuberculosis infection and clearance.
220 esponses within SLOs during gastrointestinal Yersinia pseudotuberculosis infection to limit pathogen
221 vated with lipopolysaccharide (LPS) prior to Yersinia pseudotuberculosis infection, caspase-1 is acti
224 We demonstrate that, in addition to MyD88, Yersinia pseudotuberculosis inhibits TRIF signaling thro
228 e found that only a small fraction of either Yersinia pseudotuberculosis or Yersinia pestis bacteria
229 cytotoxicity induced by Yersinia pestis and Yersinia pseudotuberculosis paradoxically leads to decre
230 itating biofilm on Caenorhabditis elegans by Yersinia pseudotuberculosis represents a tractable model
231 have suggested that rfaH may be required for Yersinia pseudotuberculosis resistance to antimicrobial
233 ium evolved from an ancestral enteroinvasive Yersinia pseudotuberculosis strain by gene loss and acqu
235 itor identified by in vitro screening, using Yersinia pseudotuberculosis Using a mouse model of P. ae
236 iI complexes from Escherichia coli EC869 and Yersinia pseudotuberculosis YPIII to explore the evoluti
237 nal peptide generated by auto-proteolysis of Yersinia pseudotuberculosis YscU, is secreted by the T3S
238 acterial pathogen that evolved recently from Yersinia pseudotuberculosis, an enteric pathogen transmi
241 as the Yersinia pestis, which causes plague, Yersinia pseudotuberculosis, Yersinia enterocolitica.
250 the YersiniaBase, a robust and user-friendly Yersinia resource and analysis platform for the analysis
251 rm is the use of the Csy-type (CRISPR system yersinia) ribonuclease 4 (Csy4) and tRNA processing enzy
253 oyed by many pathogens, including the genera Yersinia, Shigella, Pseudomonas, and Salmonella, to deli
257 t contrary to hypotheses that all pathogenic Yersinia species share a recent common pathogenic ancest
259 ersinia pseudotuberculosis compared to other Yersinia species, and differences between Yersinia enter
260 E occurs in Y. pestis but not in the enteric Yersinia species, and requires the omptin Pla (plasminog
261 tical virulence component for the pathogenic Yersinia species, and the regulation of this system is t
267 ulation, while its similarity with yscW from Yersinia spp. argued in favor of a role in machinery ass
268 ncoded type three secretion system (TTSS) of Yersinia spp. is responsible for the delivery of effecto
269 hepatitis E virus (HEV) and enteropathogenic Yersinia spp. were analyzed in parallel using immobilize
270 Vibrio spp., Salmonella spp., Shigella spp., Yersinia spp., Citrobacter spp., enterotoxigenic (ETEC)
271 itors of type III secretion system (T3SS) in Yersinia spp., have an inhibitory effect on chlamydial i
272 ence of YopE, YopT, or YopO in the infecting Yersinia strain, indicating that none of the Yops report
274 quence typing-based scheme that can identify Yersinia strains to the species level to a level of reso
277 & Microbe, Chung et al. (2016) show that the Yersinia T3SS effector protein YopM counteracts this rec
282 n of effectors into mammalian cells requires Yersinia to both insert a translocon into the host cell
283 e sites may be a strategy used by pathogenic Yersinia to prevent inactivation of this important virul
284 which the initial attachment/recognition of Yersinia to/by C. elegans is followed by bacterial growt
286 r findings indicate that lysosomal damage by Yersinia translocon proteins promotes inflammasome activ
288 aperone LcrH are essential components of the Yersinia type III pathway, enabling effector translocati
294 ckade of NF-kappaB and MAPK signaling by the Yersinia virulence factor YopJ inhibits cytokine product
297 e to host defense peptides, and virulence of Yersinia, we constructed DeltarfaH mutants of Y. pseudot
298 to express the invasin surface receptor from Yersinia, which enables uptake via mammalian host beta1-
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