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1                                              S. pyogenes bound purified fibulin-1 in a dose-dependent
2                                              S. pyogenes expresses HSA-binding surface proteins, and
3                                              S. pyogenes grew from one or both swabs for 198 (37%) of
4                                              S. pyogenes MHC class II-bound peptide-specific CD4(+) T
5                                              S. pyogenes NCTC 8198(T) and CCUG 4207(T) are derived fr
6                                              S. pyogenes strains with this type of polymorphism cause
7                                              S. pyogenes-induced Th17 formation depended on TGF-beta1
8 C and 30 S. aureus, 15 S. pneumoniae, and 15 S. pyogenes isolates by disk diffusion (DD) methods.
9 e against challenge infections with M type 2 S. pyogenes.
10     In all, 1,800 Staphylococcus aureus, 259 S. pyogenes, 226 Streptococcus pneumoniae, 93 Enterococc
11 2 opsonized SOF-positive M type 2, 4, and 28 S. pyogenes in human blood but had no effect on SOF-nega
12 d but had no effect on SOF-negative M type 5 S. pyogenes.
13                                 M/emm type 6 S. pyogenes has intrinsic reduced susceptibility to fluo
14       Additionally, we analyzed M/emm type 6 S. pyogenes isolated during 1918-2003 from diverse locat
15 rated in erythromycin-resistant M/emm type 6 S. pyogenes, which raises concern for the emergence of m
16 ysis shows that in contrast to the type II-A S. pyogenes Cas9 that is widely used for genome engineer
17        Finally, we demonstrated that sloR, a S. pyogenes gene that closely resembles the Clostridium
18 t SOF evokes bactericidal antibodies against S. pyogenes in humans, rabbits, and mice.
19       Biotin tagged whole antibodies against S. pyogenes were conjugated to Ptyr amine group via biot
20 gm shift from type-specific immunity against S. pyogenes to emm-cluster based immunity for this bacte
21 f the human adaptive immune response against S. pyogenes in both children and adults.
22         Thus, human immune responses against S. pyogenes consist of a robust Th1 cellular memory resp
23 attractive antivirulence drug target against S. pyogenes infections.
24            We found that FH6-7/Fc alleviated S. pyogenes-induced sepsis in a transgenic mouse model e
25 se-dependent manner, suggesting a role as an S. pyogenes virulence factor.
26 examine this, we analyzed the behavior of an S. pyogenes mutant deficient in expression of the cytoly
27 nally, an allelic replacement analysis of an S. pyogenes strain with a naturally occurring insertion
28 ant to in vitro penetration by S. aureus and S. pyogenes and partially resistant to P. aeruginosa.
29  also prevented penetration by S. aureus and S. pyogenes; NeoForm was less effective in withstanding
30 ar adhesion and entry for B. burgdorferi and S. pyogenes.
31 tween S. dysgalactiae subsp. equisimilis and S. pyogenes alleles revealed a history of interspecies r
32  aureus was not found by culture or PCR, and S. pyogenes was not identified by any technique.
33 quences from two of these, S. pneumoniae and S. pyogenes.
34 topes contained in HIV, M. tuberculosis, and S. pyogenes.
35 he surface of Gram-positive bacteria such as S. pyogenes will enable professional phagocytes to elimi
36 y can be applied for specific agents such as S. pyogenes, or commercial multiplex NAATs for detection
37                       All cluster-associated S. pyogenes isolates were genotype emm1 and were initial
38                        The highly attenuated S. pyogenes mutant, SalY, was identified from a transpos
39                Genomic analyses of available S. pyogenes genomes revealed the presence of intact gene
40                                      Because S. pyogenes is known to release LTA and secrete at least
41 ology, and public health communities because S. pyogenes has remained universally susceptible to beta
42                             However, because S. pyogenes are only found in humans, how are new phages
43 c toxin B (SPE B) on the interaction between S. pyogenes strain NZ131 (serotype M49) and mammalian ce
44 en grown in sugar-limited Todd-Hewitt broth, S. pyogenes cells remained culturable for more than 1 ye
45 ion of promoters that cannot be activated by S. pyogenes dCas9.
46 ds, the induction of caspase-1 activation by S. pyogenes did not require exogenous ATP or the P2X7R.
47              Two postpartum deaths caused by S. pyogenes occurred within 24 h; one was characterized
48 crobiological diagnosis of empyema caused by S. pyogenes.
49 ovel vaccine to prevent infections caused by S. pyogenes.
50 ut also for invasion of endothelial cells by S. pyogenes.
51 t to promote invasion of epithelial cells by S. pyogenes.
52 in that may function in host colonization by S. pyogenes.
53                            When expressed by S. pyogenes, PFO, like SLO, had the ability to form func
54                         SpyCEP expression by S. pyogenes hindered bacterial clearance from muscle, an
55 that fluoride causes decreased expression by S. pyogenes proteins used to respond to stress, virulenc
56  IFN-beta, which is significantly induced by S. pyogenes 23S rRNA in an Irf5-dependent manner.
57 required Myd88/Trif, whereas that induced by S. pyogenes was blocked by inhibition of NF-kappaB.
58  cells prevented nasopharyngeal infection by S. pyogenes, but not by Streptococcus pneumoniae, a bact
59 y-phase culture supernatant proteins made by S. pyogenes NZ131 rgg and NZ131 speB were separated by t
60      We hypothesize that SpyA is produced by S. pyogenes to disrupt cytoskeletal structures and promo
61 Binding of complement regulatory proteins by S. pyogenes has previously been attributed to the strept
62 ed proteomic analysis of protein released by S. pyogenes into the culture supernatant and observed de
63 , and NaCl may mimic relevant cues sensed by S. pyogenes during infection; and that identification of
64 y, we investigate hemoprotein utilization by S. pyogenes.
65                       Moraxella catarrhalis, S. pyogenes, and culture-negative episodes were also sig
66              In this report, we characterize S. pyogenes DnaE polymerase and find that it is highly e
67 ellular expression of two well-characterized S. pyogenes virulence factors.
68               Finally, we assess comparative S. pyogenes and S. aureus Cas9 specificity using GUIDE-s
69 udy, we quantitatively analyzed and compared S. pyogenes proteins in the growth medium of a strain th
70 sing bioinformatics analysis of the complete S. pyogenes strain SF370 genome, we have identified a no
71 gest that under certain in vitro conditions, S. pyogenes cells can persist for greater than 1 year as
72 rtion of IgG-reactive proteins from cultured S. pyogenes are secreted.
73 ly larger amounts of the secreted cytotoxins S. pyogenes NADase (SPN) and streptolysin O (SLO).
74 ensors were also able to specifically detect S. pyogenes in 50% (v/v) human saliva, with good selecti
75 trations of saliva and plasma, and different S. pyogenes serotypes and their isogenic mutants, reveal
76 lation by MtsR are critical processes during S. pyogenes infection.
77 , illustrating the intrinsic ability of emm1 S. pyogenes to spread while retaining virulence.
78      We sequenced the genomes of 2,101 emm28 S. pyogenes invasive strains, from which we selected 492
79 ome sequences of type emm1, emm28, and emm89 S. pyogenes clinical strains recovered from intercontine
80 we successfully delivered a plasmid encoding S. pyogenes Cas9 and sgRNA to the corneal epithelium by
81  binding to fibronectin (Fn) and facilitates S. pyogenes adherence and penetration into cells.
82  transgenic mouse model expressing human FH (S. pyogenes binds FH in a human-specific manner).
83 val niche and conduit to the bloodstream for S. pyogenes, explaining the phenomenon of occult bactera
84 e clinical settings, by a throat culture for S. pyogenes to increase the sensitivity of its detection
85 roxidase in S. pyogenes and is essential for S. pyogenes pathogenesis in several murine models that m
86 enized murine vaginal colonization model for S. pyogenes.
87 based system as a standard typing scheme for S. pyogenes will facilitate the design of future studies
88 often highly related, but they differed from S. pyogenes, in that S. dysgalactiae subsp. equisimilis
89 strate that the multidomain protein Epf from S. pyogenes serotype M49 is a streptococcal adhesin.
90 nce analyses of larger regions of FnBPs from S. pyogenes and S. aureus reveal a repeating pattern of
91 his is the first methyltransferase gene from S. pyogenes to be cloned and to have its activity charac
92 o compare cytoplasmic proteins isolated from S. pyogenes wild-type strain NZ131 (serotype M49) to pro
93 sphoribosyltransferase activity of NadC from S. pyogenes allows the organism to sustain growth when Q
94 monstrated that the released M1 protein from S. pyogenes activates platelets, and this activation is
95  from those recognized by Cas9 proteins from S. pyogenes and S. thermophilus (SpCas9 and StCas9, resp
96 rated cellular and supernatant proteins from S. pyogenes cultures by high-resolution two-dimensional
97  28-kDa streptococcal protease purified from S. pyogenes processed the 40-kDa mutant zymogen to a 28-
98 ial pathogen the group A Streptococcus (GAS; S. pyogenes) as a model organism, we review the types an
99 and virulence in group A Streptococcus (GAS; S. pyogenes), the precise role of the co-transcribing se
100                                           In S. pyogenes, mutS and mutL are organized on a polycistro
101                                           In S. pyogenes, Rgg influences the expression of several vi
102  an insertionally inactivated degP allele in S. pyogenes is similar to that reported for E. coli, wit
103       To investigate the role of c-di-AMP in S. pyogenes, we generated null mutants in each of these
104 sly identified as cell surface associated in S. pyogenes.
105 sion, the elucidation of GAC biosynthesis in S. pyogenes reported here enhances our understanding of
106 tion by the Rgg2/3 quorum-sensing circuit in S. pyogenes.
107       Such genetic elements may be common in S. pyogenes since 6 of 13 completed genomes have related
108  Taken together, the CvfA-enolase complex in S. pyogenes is involved in the regulation of virulence g
109 s aureus and Listeria monocytogenes, DacA in S. pyogenes was not essential for growth in rich media.
110                Resistance to erythromycin in S. pyogenes can be as high as 48% in specific population
111 uitry governing virulence gene expression in S. pyogenes and its impact on pathogenesis.
112 to coregulate virulence factor expression in S. pyogenes.
113 pA, the gene which encodes trigger factor in S. pyogenes, produced mutant proteins deficient in PPIas
114 side cells, and the cellular role of GdpP in S. pyogenes has not been examined yet.
115 ociated with inactivation of the rgg gene in S. pyogenes strain NZ131 (serotype M49).
116 he first hemoprotein receptors identified in S. pyogenes; their possible role in iron capture is disc
117 standing of the function of the sal locus in S. pyogenes pathogenesis.
118                                 Thus, MMR in S. pyogenes SF370 is functional in exponentially growing
119 S, coordinate the transcriptional network in S. pyogenes.
120 eparate entries to a final common pathway in S. pyogenes virulence gene expression.
121 idase is the major glutathione peroxidase in S. pyogenes and is essential for S. pyogenes pathogenesi
122 acterized an intergenic VNTR polymorphism in S. pyogenes that affects toxin production and virulence.
123 gy and the function of VNTR polymorphisms in S. pyogenes.
124 e and lincosamide antibiotics are present in S. pyogenes strains in the United States.
125 itate further study of cellular processes in S. pyogenes.
126 ainst sHIP suggest a role for the protein in S. pyogenes pathogenesis.
127 rify the function of HSA-binding proteins in S. pyogenes and underline the power of the quantitative
128      Macrolide and lincosamide resistance in S. pyogenes is mediated by several different genes.
129 ion of NadD confirmed its functional role in S. pyogenes, and its potential as an antibacterial targe
130        We investigated the role of SpyCEP in S. pyogenes necrotizing fasciitis and respiratory tract
131  or induced resistance to peroxide stress in S. pyogenes, genes for a novel mechanism of managing per
132 , and removal of read-through transcripts in S. pyogenes.
133 oper response to stress and for virulence in S. pyogenes, suggesting that its signaling pathway could
134  Here, we demonstrate that nuclease-inactive S. pyogenes CRISPR/Cas9 can bind RNA in a nucleic-acid-p
135 m by which Gram-positive bacteria, including S. pyogenes, coordinate multiple environmental cues, all
136 , and some Gram-positive pathogens including S. pyogenes use this cyclic nucleotide derivative as a s
137 gainst most streptococcal species, including S. pyogenes, S. agalactiae, S. dysgalactiae, S. equi, S.
138 hat M. catarrhalis can dramatically increase S. pyogenes adherence to human epithelial cells and that
139 ne of these inhibitors efficiently inhibited S. pyogenes NadD (sp.NadD) in vitro (50% inhibitory conc
140 signaling protects the host against invasive S. pyogenes infection by restricting inflammation-driven
141 identified across four contemporary invasive S. pyogenes serotypes (M1, M3, M12 and M89).
142  pooled human immunoglobulin during invasive S. pyogenes infection, and demonstrate a potential route
143 t insights into the pathogenesis of invasive S. pyogenes infections.
144 ernatants prepared from cultures of invasive S. pyogenes strains of varying serotypes in the stationa
145  and the finding that patients with invasive S. pyogenes infection respond with antibody production a
146 ysis of samples from a patient with invasive S. pyogenes infection revealed dramatic differences in t
147   The utility of our model for investigating S. pyogenes factors contributing to mucosal carriage was
148 odulated by neonatal exposure to heat-killed S. pyogenes bacteria.
149 retion were induced by live, but not killed, S. pyogenes, and required expression of the pore-forming
150 tudy it is shown that AspA from serotype M28 S. pyogenes, when expressed on surrogate host Lactococcu
151                                    Since M49 S. pyogenes strains have been known to be associated wit
152  SPN and SLO in epidemic serotype M1 and M89 S. pyogenes strains is associated with rapid intercontin
153 0% S), and MIC(90)s ranged from 0.03 mug/ml (S. pyogenes/S. pneumoniae) to 1 mug/ml (Enterobacteriace
154 eutrophil extracellular traps, and modulates S. pyogenes virulence.
155                    Both wild-type and mutant S. pyogenes bacteria were extremely sensitive to low pH.
156 ht of reports of hypervirulent SpeB-negative S. pyogenes variants present during invasive infections.
157 s required for survival of L. lactis but not S. pyogenes.
158    In conclusion, we have identified a novel S. pyogenes enzyme with 5'-nucleotidase activity and imm
159 ain SF370 genome, we have identified a novel S. pyogenes virulence factor, which we termed streptococ
160                                          Now S. pyogenes NAATs are being used with increasing frequen
161 mbinant SOF from M types 2, 4, 28, and 75 of S. pyogenes, indicating that the fibulin-1-binding domai
162 nsporter may be an example of the ability of S. pyogenes to adapt and evolve new survival strategies
163  of zinc homeostasis inhibits the ability of S. pyogenes to cause disease in a zinc-limited host mili
164 l regulatory system governing the ability of S. pyogenes to colonize the nasopharynx and provides kno
165 s rescued, demonstrating that the ability of S. pyogenes to utilize arginine was dispensable in the a
166 in the absence of FBP, Pi is an activator of S. pyogenes LDH, E. faecalis LDH1, and L. lactis LDH1 an
167 ered metabolism, the catabolic activities of S. pyogenes strain NZ131 (serotype M49) and an isogenic
168 fibulin-1 may be involved in the adhesion of S. pyogenes to extracellular matrices of the host.
169 hould prove effective for future analyses of S. pyogenes mucosal colonization.
170 sed proteins to identify surface antigens of S. pyogenes.
171 inhibitor ifs from a worldwide collection of S. pyogenes strains.
172 factors for the survival and colonization of S. pyogenes is well established, and many of these facto
173 plicated in non-suppurative complications of S. pyogenes, including glomerulonephritis and rheumatic
174  by how SAgs contribute to the life cycle of S. pyogenes remain poorly understood.
175         We constructed mutant derivatives of S. pyogenes that lack Fba, M1 protein, or both proteins
176 ity factor (SOF), a virulence determinant of S. pyogenes, reduced binding by approximately 50%, and a
177                    However, dissemination of S. pyogenes to the lung was SpyCEP-dependent and was ass
178  the role of prophages in diversification of S. pyogenes and the close relationship between strain Ma
179 ay contribute to the phenotypic diversity of S. pyogenes.
180 ntly protected against the lethal effects of S. pyogenes.
181                      Finally, examination of S. pyogenes following murine subcutaneous infection reve
182            SOF is also a virulence factor of S. pyogenes, but it has not been previously shown to eli
183                                    Growth of S. pyogenes in blood was dependent on the presence of fi
184 ow the intracellular proteome homeostasis of S. pyogenes is influenced by the presence of human plasm
185 novel factors related to the invasiveness of S. pyogenes.
186     This study was a unique investigation of S. pyogenes factors required for successful invasive inf
187 vival of clinical and laboratory isolates of S. pyogenes and S. pneumoniae as both organisms are thou
188 ng system conserved in sequenced isolates of S. pyogenes Deletion of the QS system's transcriptional
189                     Although all isolates of S. pyogenes possess the speB gene, not all of them produ
190         We surveyed 384 clinical isolates of S. pyogenes, isolated during 2002-2003, for susceptibili
191 tion, may be present in invasive isolates of S. pyogenes.
192 proximately half of the clinical isolates of S. pyogenes.
193 on that promoted opsonophagocytic killing of S. pyogenes in vitro and provided passive immunity in vi
194  Mrp4, Emm4 and Sof4 promoted the killing of S. pyogenes, but anti-SfbX serum had no effect.
195 t important for survival in a mouse model of S. pyogenes peritoneal infection.
196 resistant isolates from a recent outbreak of S. pyogenes infection in Pittsburgh and in the Lancefiel
197 ibution the toxin has to the pathogenesis of S. pyogenes and that both versions of SPN play an import
198 ulation is necessary for the pathogenesis of S. pyogenes.
199 for the in vivo survival and pathogenesis of S. pyogenes.
200 e epitopes of importance for phagocytosis of S. pyogenes cells are localized.
201  as titin and fibronectin, the giant pili of S. pyogenes evolved to abrogate mechanical extensibility
202 otide preferences at the seventh position of S. pyogenes Cas9 PAM (5'-NGRNNNT-3'), which was experime
203 -moving outbreak highlights the potential of S. pyogenes to cause a range of diseases in the puerperi
204  comparing genomewide transcript profiles of S. pyogenes NZ131 and isogenic derivative NZ131 rgg duri
205      The well-characterized Scl1 proteins of S. pyogenes show a dichotomous switch in ligand binding
206  important contribution to the regulation of S. pyogenes virulence factors.
207                 We studied the resistance of S. pyogenes to erythromycin and clindamycin at an urban
208 re supernatants from multiple M serotypes of S. pyogenes isolates or a commercially available SLS pre
209 SLS contribute to the subcutaneous spread of S. pyogenes and to a fatal outcome of infection.
210 ophil recruitment during the early stages of S. pyogenes infection.
211 ased SpeB production in a clinical strain of S. pyogenes and relieved its growth phase dependency.
212 re infected in thigh muscle with a strain of S. pyogenes that expresses a high level of SpyCEP, or wi
213 plete genome sequences of the type strain of S. pyogenes will effectively serve as valuable taxonomic
214  aspA gene from two different M28 strains of S. pyogenes abrogated their abilities to form biofilms o
215                     Hypervirulent strains of S. pyogenes have evolved a plethora of virulence factors
216 nteractions in attachment of skin strains of S. pyogenes to keratinocytes are unique and remain unide
217 lso differ for throat versus skin strains of S. pyogenes.
218 ontributes to the immune evasion strategy of S. pyogenes.
219             Importantly, the substitution of S. pyogenes gacB with the homologous gene from Streptoco
220  the efficacy of antibiotics in treatment of S. pyogenes infections.
221  factor SpeB and to the overall virulence of S. pyogenes, as both DacA and Pde2 null mutants were hig
222 term stationary-phase survival (>4 weeks) of S. pyogenes.
223 d but not methicillin-resistant S. aureus or S. pyogenes from cellulitis tissue specimens.
224 n with S. dysgalactiae subsp. equisimilis or S. pyogenes.
225 ed a locus that is highly conserved in other S. pyogenes genomes and is homologous to an operon invol
226                         2) For L. plantarum, S. pyogenes, and E. faecalis, the effects of Pi are dist
227       MPO directly killed H(2)O(2)-producing S. pyogenes but was ineffective against non-H(2)O(2)-pro
228 ss the need for a refined model of prolonged S. pyogenes asymptomatic mucosal colonization, we have a
229 tive form of the streptococcal CXC protease, S. pyogenes cell envelope proteinase, we developed a com
230 olysin, but not SIC, a protein that protects S. pyogenes from CAPs.
231   The polC gene from Streptococcus pyogenes (S. pyogenes, strain SF370) has been cloned and expressed
232  challenged by HRG, sHIP was found to rescue S. pyogenes bacteria.
233 demonstrated that the erythromycin-resistant S. pyogenes comprised multiple strains.
234 ern for the emergence of multidrug-resistant S. pyogenes.
235 s question, we discovered that all sequenced S. pyogenes strains possess the genes for the malic enzy
236             As with the previously sequenced S. pyogenes genomes, three unique prophages are a major
237 ed in a small subset of patients with severe S. pyogenes sepsis but not in patients with any other ca
238 lar pathogen carriage by phagocytes, we show S. pyogenes remain extracellular during transit, first i
239 st report to show natural induction of sigX, S. pyogenes remained nontransformable under laboratory c
240 rial species, SaCas9 (S. aureus) and SpCas9 (S. pyogenes).
241                           The effector, SPN (S. pyogenes NAD-glycohydrolase), is capable of producing
242 mily ADP-ribosyltransferase designated SpyA (S. pyogenes ADP-ribosyltransferase).
243 AS; Streptococcus pyogenes) protease SpyCEP (S. pyogenes cell envelope protease) cleaves granulocyte
244                            Confirmation that S. pyogenes Cas9 lacks the specificity to discriminate b
245                         We demonstrated that S. pyogenes has an unusually high mRNA turnover rate, wi
246                                We found that S. pyogenes M5-specific antibodies and sera from B. burg
247                          We report here that S. pyogenes is able to bind to bovine submaxillary mucin
248   These findings justify the hypothesis that S. pyogenes infections are more important in the pathoge
249                     These data indicate that S. pyogenes can interact with fibulin-1 and that SOF is
250         Consistent with the observation that S. pyogenes is responsible for a wider variety of human
251                    In addition, we show that S. pyogenes demonstrates an inducible peroxide resistanc
252                      These data suggest that S. pyogenes diversifies during survival in stationary ph
253      Taken together, these data suggest that S. pyogenes requires glutathione peroxidase to adapt to
254  Remarkably, these observations suggest that S. pyogenes uses SAgs to manipulate Vbeta-specific T cel
255                                          The S. pyogenes M28_Spy1325 polypeptide (designated AspA) di
256                                          The S. pyogenes NAD(+) glycohydrolase (SPN) is a virulence f
257                                          The S. pyogenes tau binds PolC, but the interaction is not a
258  and Northern blot analyses to determine the S. pyogenes mRNA half-life of the transcriptome and to u
259 we examined the role of GacB, encoded in the S. pyogenes GAC gene cluster, in the GAC biosynthesis pa
260 two-cassette system expressing pieces of the S. pyogenes Cas9 (SpCas9) protein which splice together
261  system leverages the programmability of the S. pyogenes Cas9 and is based on flexible arrangements o
262 the highly recombinatorial FCT region of the S. pyogenes genome is under strong selection for change
263 pt that can detect intergenic regions of the S. pyogenes genome.
264 ed the ExPortal, a unique microdomain of the S. pyogenes membrane, specialized for protein secretion
265 rain found that between 3.7 and 28.5% of the S. pyogenes transcripts were differentially expressed, d
266 d partial inhibition of C3 deposition on the S. pyogenes surface.
267 ts with mutually permissive NGGRRT PAMs, the S. pyogenes Cas9 and S. aureus Cas9 yield indels at comp
268 between a known effector of the pathway, the S. pyogenes NAD(+) glycohydrolase (SPN), and a second se
269                     Here, we report that the S. pyogenes cell surface protein Fba can mediate binding
270                        We show here that the S. pyogenes DnaE polymerase also functions with the beta
271  similar and unique features compared to the S. pyogenes enzyme.
272 nto structure-function relationships in this S. pyogenes virulence factor.
273 f SLPI and lysozyme would be advantageous to S. pyogenes in establishing colonization on mucosal surf
274 ontrol protein modules 6 and 7) that bind to S. pyogenes, linked to the Fc region of IgG (FH6-7/Fc).
275 d structures of AcrIIA2 or AcrIIA2b bound to S. pyogenes Cas9 reveal a mode of competitive inhibition
276 and exhibits greater specificity compared to S. pyogenes Cas9.
277 ther, these data show that ME contributes to S. pyogenes' carbon source repertory, that malate utiliz
278 contribute to the binding of hemoproteins to S. pyogenes.
279 tion of Tn5-based transposome mutagenesis to S. pyogenes with initial screening for reduced expressio
280 ate that caspase-1 activation in response to S. pyogenes infection requires NF-kappaB and the virulen
281 e for pro-IL-1beta induction, in response to S. pyogenes infection.
282 both SPN and SLO contribute significantly to S. pyogenes pathogenesis in these virulence assays.
283  subsp. equisimilis isolates were similar to S. pyogenes isolates, in that strains of the same emm ty
284 r1)-deficient mice are highly susceptible to S. pyogenes infection.
285 a-lactam antibiotics, commonly used to treat S. pyogenes infections, do not readily permeate mammalia
286 fotaxime, antibiotics commonly used to treat S. pyogenes infections, were reported.
287                     In contrast to wild-type S. pyogenes, the SLS- mutant was associated with the rob
288 lerated compared to infection with wild-type S. pyogenes.
289 rmed that the cluster was caused by a unique S. pyogenes clone.
290                                         When S. pyogenes was identified in samples from the epidemic
291 tt and Robin Patel of the Mayo Clinic, where S. pyogenes NAATs have been used for well over a decade
292 ests a novel mechanism of virulence by which S. pyogenes uses its metabolism to modulate innate immun
293       Under experimental conditions in which S. pyogenes is grown in THY medium, the strength of the
294  design rules and paired S. aureus Cas9 with S. pyogenes Cas9 to achieve dual targeting in a high fra
295 l infection following a nasal challenge with S. pyogenes M serotype 14.
296 rum IgG, prevented pharyngeal infection with S. pyogenes, and promoted survival.
297 n may be a specific feature of patients with S. pyogenes-induced shock.
298                     Our current results with S. pyogenes Glu-AdT support this characterization of Glu
299  recombinant S5nA acted synergistically with S. pyogenes nuclease A to generate macrophage-toxic deox
300                              For many years, S. pyogenes testing algorithms used a rapid and specific

 
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