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1 sed in the cdhR mutant after contact with S. gordonii.
2  elevated accumulation on a substratum of S. gordonii.
3 sfer of plasmid DNA from E. faecalis into S. gordonii.
4 w-pH-dependent expression of ADS genes in S. gordonii.
5 edent oral biofilm constituent Streptococcus gordonii.
6 A from mixed cultures of S. sanguinis and S. gordonii.
7 hogenic potential of F. nucleatum than of S. gordonii.
8 . gingivalis in heterotypic biofilms with S. gordonii.
9 forms biofilms on substrata of Streptococcus gordonii.
10 of Streptococcus anginosus and Streptococcus gordonii.
11 imal coadhesion between P. gingivalis and S. gordonii.
12 ion of Streptococcus mitis and Streptococcus gordonii.
13 ely related Streptococcal species such as S. gordonii.
14 oxidative stress response (osr) operon in S. gordonii.
15 uctose phosphotransferase system (PTS) in S. gordonii.
16 tivity of another species, H2O2-producing S. gordonii.
17 ies Streptococcus sanguinis or Streptococcus gordonii.
18 in Streptococcus sanguinis and Streptococcus gordonii.
19 eptor polysaccharides (RPS) of Streptococcus gordonii 38 and Streptococcus oralis J22 was eliminated
20                Type 2Gn RPS of Streptococcus gordonii 38 and type 2G RPS of Streptococcus oralis J22
21 ransferases encoded by downstream wefC in S. gordonii 38 and wefH in S. oralis 34.
22 -Gal and UDP-GalNAc for RPS production by S. gordonii 38 depends on the dual specificity of the epime
23 o identify and partially characterize the S. gordonii 38 RPS gene cluster.
24  and wefD in the type 2Gn gene cluster of S. gordonii 38 with wefF and wefG from the type 2G cluster
25 olysaccharide in transformable Streptococcus gordonii 38.
26  produced by the wefB-deficient mutant of S. gordonii 38.
27 ently inhibits P. gingivalis adherence to S. gordonii (50% inhibitory concentration = 1.3 microM) and
28 pecies plaque interactions, the effect of S. gordonii AbpB on S. mutans Gtf-B activity was also teste
29 tudy assessed a multi-species (Streptococcus gordonii, Actinobacillus actinomycetemcomitans, and Fuso
30 cteria (Enterococcus faecalis, Streptococcus gordonii, Actinomyces naeslundii, and Lactobacillus acid
31 hesin CshA is an important determinant of S. gordonii adherence, forming peritrichous fibrils on its
32 occus oralis (RPS bearing) and Streptococcus gordonii (adhesin bearing).
33                            Next, putative S. gordonii adhesins were analyzed for contributions to int
34 at results in increased expression of the S. gordonii alpha-amylase-encoding gene amyB.
35 determinant of colonization by Streptococcus gordonii, an oral commensal and opportunistic pathogen o
36 s role in biofilm formation by Streptococcus gordonii, an organism that colonizes human tooth enamel
37  performed comparative analyses on 14 new S. gordonii and 5 S. sanguinis strains using various bioinf
38                           Contact between S. gordonii and a CdhR mutant resulted in increased transcr
39  two other initial colonizers, Streptococcus gordonii and Actinomyces oris, as well as with Veillonel
40 onal changes that accompany competence in S. gordonii and form a basis for future intra- and interspe
41 ermed P57AS3 (P57), was isolated from Hoodia gordonii and found to have homologies to the steroidal c
42 xamined their subcellular localization in S. gordonii and in Escherichia coli expressing the streptoc
43  required for disulfide bond formation in S. gordonii and indicate that this enzyme may represent a n
44  GspB is glycosylated in the cytoplasm of S. gordonii and is then transported to the cell surface via
45 n is involved in manganese acquisition in S. gordonii and manganese homeostasis and appears to modula
46 o bacterial species, commensal Streptococcus gordonii and pathogenic Streptococcus mutans.
47 rstanding of the regulation of the ADS in S. gordonii and related organisms is needed to develop ways
48 pment of anti-adhesive agents that target S. gordonii and related streptococci.
49 mab, protected 45%-88% of animals against S. gordonii and S. aureus IE (P < .05).
50                                While both S. gordonii and S. mutans were abundant colonizers of rat's
51 r, P. gingivalis grew in combination with S. gordonii and S. oralis, demonstrating its ability to ove
52                               We revealed S. gordonii and S. sanguinis harbor open pan-genomes and sh
53 hts into the genetic distinctions between S. gordonii and S. sanguinis, which yields understanding of
54 rize the related pheromone determinant in S. gordonii and show that the peptide it encodes, gordonii-
55 r activity is also secreted by Streptococcus gordonii and Staphylococcus aureus.
56                                Streptococcus gordonii and Streptococcus mutans avidly colonize teeth.
57                                Streptococcus gordonii and Streptococcus sanguinis are pioneer coloniz
58 l flora (Streptococcus mutans, Streptococcus gordonii and Streptococcus sanguinis) to determine the u
59  revealed that S. oralis, like Streptococcus gordonii and Streptococcus sanguinis, binds platelets vi
60 ively, in the S-ECC group, and Streptococcus gordonii and Streptococcus sanguinis, which were 5- and
61 ginine metabolism is tightly regulated in S. gordonii and that arginine is critical for gene regulati
62 arginine-responsive regulatory network of S. gordonii and the basis for conditional arginine auxotrop
63 ulture with the oral commensal Streptococcus gordonii and the opportunistic commensal Fusobacterium n
64 ress tolerance between the oral commensal S. gordonii and the oral pathogen Streptococcus mutans.
65  mice were first infected with Streptococcus gordonii and then challenged with P. gingivalis in the a
66             In a closed system containing S. gordonii and V. atypica, flow cytometric analysis showed
67                                Streptococcus gordonii and Veillonella atypica, two early colonizing m
68                                Streptococcus gordonii and Veillonella atypica, two early-colonizing m
69 l colonizers of dental plaque, Streptococcus gordonii and Veillonella parvula, on gene expression in
70  the binding forces between S. mutans (or S. gordonii) and C. albicans in the presence and absence of
71 on, we found that Streptococcus gordonii (S. gordonii) and Enterococcus faecalis (E. faecalis) were f
72 to Streptococcus pyogenes, S. agalactiae, S. gordonii, and Escherichia coli.
73 zed, and Streptococcus mutans, Streptococcus gordonii, and Streptococcus sanguinis were chosen to for
74 nd fruI are cotranscribed as an operon in S. gordonii, and the transposon insertion in S. gordonii fr
75 , which vastly exceeds the forces between S. gordonii andC.
76 onses of V. parvula to coaggregation with S. gordonii are dominated by oxidative stress-related proce
77      Oral streptococci such as Streptococcus gordonii are facultative anaerobes that initiate biofilm
78  asp5) essential for export in Streptococcus gordonii are missing in S. aureus.
79     Oral streptococci, such as Streptococcus gordonii, are the predominant early colonizers that init
80 on, indicating that arcB levels may limit S. gordonii arginine biosynthesis.
81 als provide encouragement that the use of S. gordonii as a live mucosal vaccine vector is a feasible
82                       By using Streptococcus gordonii as a model organism for streptococcal H(2)O(2)
83                          Using Streptococcus gordonii as a model, we now show the mechanistic basis o
84                             In Streptococcus gordonii, Asp2 is required for the transport of the SRR
85 dii, Tannerella forsythia, and Streptococcus gordonii) associated with dysbiosis of the oral microbio
86                        The data show that S. gordonii binding force to the C. albicans surface is sig
87 nent system regulated in association with S. gordonii biofilm formation in vitro.
88 ast, heterotypic P. gingivalis-Streptococcus gordonii biofilm formation was enhanced in the InlJ-defi
89 nced heterotypic P. gingivalis-Streptococcus gordonii biofilm formation.
90 sponse, some of which may be important in S. gordonii biofilm formation.
91 h altered microcolony architecture within S. gordonii biofilms formed in saliva during a time frame c
92 uses release of DNA from S. sanguinis and S. gordonii but does not result in obvious lysis of cells.
93  microcolonies on substrata of Streptococcus gordonii but not on Streptococcus mutans.
94 onstrated that cell protein extracts from S. gordonii, but not from A. naeslundii, interfered with S.
95               S. oralis coaggregated with S. gordonii by an RPS-dependent mechanism, and both strepto
96 ring early biofilm initiation compared to S. gordonii-C. albicans biofilms.
97 pA, and eep each resulted in the ablation of gordonii-cAM373 activity in culture supernatants.
98 , the last 7 residues of which represent the gordonii-cAM373 heptapeptide SVFILAA.
99 rdonii and show that the peptide it encodes, gordonii-cAM373, does indeed induce transfer of plasmid
100                                Streptococcus gordonii can mediate its platelet attachment through a c
101            Surprisingly, S. sanguinis and S. gordonii cell integrity appears unaffected by conditions
102                            The Streptococcus gordonii cell surface glycoprotein GspB mediates high-af
103                Conversely, aggregation of S. gordonii cells by fluid-phase gp340 was not affected by
104                     Following invasion by S. gordonii CH1, HUVEC monolayers showed 63% cell lysis ove
105 ly similar to Hsa, a protein expressed by S. gordonii Challis that has been characterized as a sialic
106 though Hsa is required for the binding of S. gordonii Challis to sialic acid, most of the Hsa express
107 ntaining V. atypica expressed GFP; nearby S. gordonii colonies that lacked V. atypica did not express
108   Caries induction reflected S. mutans or S. gordonii colonization abundance: the former highly cario
109  interaction has been proposed to promote S. gordonii colonization at multiple sites within the host.
110                                Streptococcus gordonii colonizes multiple sites within the human oral
111                                           S. gordonii competed with S. sanguinis more effectively tha
112   Results supported published findings on S. gordonii competence, showing up-regulation of 12 of 16 g
113 rs Fusobacterium nucleatum and Streptococcus gordonii confirmed the presence of all three species in
114 ica, flow cytometric analysis showed that S. gordonii containing the PamyB-'gfp reporter plasmid exhi
115 in this observation, we hypothesized that S. gordonii could compete with S. sanguinis to adhere to sa
116 at were infected with either 10(9) CFU of S. gordonii DL-1 or 10(7) CFU of P. gingivalis 33277 did no
117 I polypeptides and Hsa in interactions of S. gordonii DL1 (Challis) with host receptors.
118 t Hsa directs primary adhesion events for S. gordonii DL1 (Challis) with immobilized gp340, epithelia
119                               Adhesion of S. gordonii DL1 cells to gp340 was sialidase sensitive, ver
120    The accessory Sec system in Streptococcus gordonii DL1 is a specialized export system that transpo
121 milarly to sHA, yet 10- to 50-fold excess S. gordonii DL1 reduced binding of S. sanguinis SK36 by 85
122  and AgI/II proteins mediated adhesion of S. gordonii DL1 to human HEp-2 epithelial cells.
123 n and initial biofilm formation on teeth, S. gordonii DL1 was incubated with saliva-coated hydroxyapa
124                   Five strains, including S. gordonii DL1, caused severe disease, while the other two
125                             In Streptococcus gordonii DL1, inactivation of the ccpA gene and a gene e
126 r biofilm formation on sHA than wild-type S. gordonii DL1.
127 ch greater recovery of rifampin-resistant S. gordonii DLl than of streptomycin-resistant S. gordonii
128                                           S. gordonii does not appear to be a good candidate for repl
129                              In contrast, S. gordonii early CSP-responsive genes were not preceded by
130    The arginine deiminase system (ADS) of S. gordonii enables cells to produce, ornithine, ammonia, C
131        We also identified determinants in S. gordonii encoding a signal peptidase and an Eep-like zin
132 eparation for clinical trials to evaluate S. gordonii engineered to express group A streptococcal M p
133 ry Sec system in E. coli matched those in S. gordonii, establishing the validity of this approach.
134            Thus, A. naeslundii stabilizes S. gordonii expression of arginine biosynthesis genes in co
135 olated from the same intraoral sites, yet S. gordonii fails to be excluded and survives as a species
136 o participate in metabolic communication; S. gordonii ferments carbohydrates to form lactic acid, whi
137      However, infection with 10(9) CFU of S. gordonii followed by 10(7) CFU of P. gingivalis induced
138 ation of approximately 12 +/- 5 muM above S. gordonii, followed by a gradual decrease in H2O2 concent
139 gordonii, and the transposon insertion in S. gordonii fruK::Tn917-lac resulted in a nonpolar mutation
140 ase found in culture fluids of Streptococcus gordonii FSS2, was purified and characterized, and its g
141           Cell fractionation studies with S. gordonii further corroborated these microscopy results.
142 results in increased transcription of the S. gordonii gene amyB, encoding an alpha-amylase.
143                                Streptococcus gordonii genes involved in beta-glucoside metabolism are
144 used to quantify changes in expression of S. gordonii genes known or thought to be involved in biofil
145    A DNA microarray identified Streptococcus gordonii genes regulated in response to coaggregation wi
146 creening a plasmid integration library of S. gordonii, genes were identified that are crucial for the
147                                           S. gordonii glucosyltransferase (GtfG) and amylase-binding
148                  The results suggest that S. gordonii governs the development of heterotypic oral bio
149 ultures containing coaggregates, however, S. gordonii grew to high cell density at low arginine conce
150 ion by Streptococcus mutans or Streptococcus gordonii grown in human plasma.
151 , low concentrations of arginine promoted S. gordonii growth, whereas high concentrations (> 5 mM arg
152  the predicted catalytic triad of Asp2 of S. gordonii had no effect upon GspB transport but did resul
153        In mixed cultures of S. mutans and S. gordonii harbouring a shuttle plasmid, plasmid DNA trans
154 es of GspB (the SRR adhesin of Streptococcus gordonii) have shown that a glycine-rich motif in its hy
155 atory network that controls P. gingivalis-S. gordonii heterotypic communities.
156 ry for platelet aggregation, and modulate S. gordonii-host engagements into biologically productive p
157 f cdhR is elevated following contact with S. gordonii; however, regulation of cdhR did not occur in a
158 cing P. gingivalis adhesion to Streptococcus gordonii in a dual-species biofilm model.
159                    S. mutans out-competed S. gordonii in in vivo plaque biofilm.
160 n normal adhesion and biofilm function of S. gordonii in response to exogenous oxidants therefore msr
161 th beta-glucoside metabolism may regulate S. gordonii in vitro adhesion, biofilm formation, growth, a
162 ignificantly impacted by F. nucleatum and S. gordonii included the mitogen-activated protein kinase (
163                                           S. gordonii-infected mice that were subsequently challenged
164 , Streptococcus sanguinis, and Streptococcus gordonii, inhibit the growth of P. aeruginosa and that t
165 ed production of these cytokines, whereas S. gordonii inhibited secretion from the epithelial cells.
166 oneer oral bacteria, including Streptococcus gordonii, initiate the formation of oral biofilms on too
167 lis and the accessory pathogen Streptococcus gordonii interact to form communities in vitro and exhib
168  multidimensional aspect to P. gingivalis-S. gordonii interactions and establish pABA as a critical c
169   The oral commensal bacterium Streptococcus gordonii interacts with salivary amylase via two amylase
170 ntal plaque colonizers such as Streptococcus gordonii interfere with the subsequent colonization of S
171 ggregation regulator (ScaR) of Streptococcus gordonii is a manganese-dependent transcriptional regula
172                                Streptococcus gordonii is a pioneer colonizer of the teeth, contributi
173                                Streptococcus gordonii is a primary colonizer of the human oral cavity
174                                Streptococcus gordonii is a primary colonizer of the multispecies biof
175                                Streptococcus gordonii is an oral commensal and an early coloniser of
176    The accessory Sec system of Streptococcus gordonii is comprised of SecY2, SecA2, and five proteins
177                                 In vitro, S. gordonii is conditionally auxotrophic for arginine in mo
178 r findings illustrate that H2O2-producing S. gordonii is dominant while the buffering capacity of sal
179    The accessory Sec system of Streptococcus gordonii is essential for transport of the glycoprotein
180            Platelet binding by Streptococcus gordonii is mediated in large part by GspB, a high-molec
181          Interaction of Mfa fimbriae with S. gordonii is necessary to initiate signalling through Cdh
182 A and CylB system by the alpha-haemolytic S. gordonii is presented.
183                            Like wild-type S. gordonii, isogenic mutants with mutations in antigen I/I
184                                Mutants of S. gordonii lacking components of the CiaRH, ComDE, or VicR
185 etence sigma factor, were found preceding S. gordonii late responsive genes.
186  (P < .005) but failed to protect against S. gordonii (&lt;30% protection).
187 d primer extension analyses revealed that S. gordonii luxS is monocistronic.
188 face glycoprotein expressed by Streptococcus gordonii M99 that mediates binding of this organism to h
189                                Streptococcus gordonii (mitis group) has been shown to bind avidly to
190 -glycosyltransferase GtfA/B of Streptococcus gordonii modifies the Ser/Thr-rich repeats of adhesin.
191 trongly (10- to 100-fold) up-regulated in S. gordonii monocultures after 3 h of growth when exogenous
192             The oral commensal Streptococcus gordonii must adapt to constantly fluctuating and often
193 d to be coupled with the induction of the S. gordonii natural competence system.
194 ted singly, S. mutans always out-competed S. gordonii on the teeth, independent of diet, strain of S.
195 9.8-50.5), S sanguinis OR 59.1 (32.6-107), S gordonii OR 80.8 (43.9-149), and S mutans OR 81.3 (37.6-
196 2 days before inoculation with Streptococcus gordonii or Staphylococcus aureus.
197 e local microenvironment in biofilms when S. gordonii or V. parvula immigrate into the system.
198 +) supplementation significantly improves S. gordonii oral colonization in mice.
199  the crucial role AbpB appears to play in S. gordonii oral colonization.
200 e Streptococcus sanguinis than Streptococcus gordonii organisms are consistently isolated from the sa
201 hus, Hsa confers a selective advantage to S. gordonii over S. sanguinis in competitive binding to sHA
202 the high degree of similarity between the S. gordonii paralogues, analysis of SecA-SecA2 chimeras ind
203                                       The S. gordonii PepV gene is homologous to the PepV gene family
204                 Overall, F. nucleatum and S. gordonii perturbed the gingival epithelial cell transcri
205  The ADS of the oral bacterium Streptococcus gordonii plays major roles in physiologic homeostasis, a
206                              Contact with S. gordonii propagates a tyrosine phosphorylation-dependent
207 ls Streptococcus sanguinis and Streptococcus gordonii release DNA in a process induced by pyruvate ox
208             We have investigated genes of S. gordonii required to support a heterotypic biofilm commu
209 idative stress-related processes, whereas S. gordonii responses are more focussed on carbohydrate met
210         Zymographic analysis of wild-type S. gordonii revealed peptidoglycan hydrolase activities wit
211     In addition, we found that Streptococcus gordonii (S. gordonii) and Enterococcus faecalis (E. fae
212 tion, or presence/absence of mutations of S. gordonii's abpA and gtfG genes known to negatively or po
213 l BSIs is species dependent with S mutans, S gordonii, S sanguinis, S gallolyticus, and S mitis/orali
214 ius (two strains); and one strain each of S. gordonii, S. sanguis, S. sobrinus, and S. vestibularis.
215                         Comparison of the S. gordonii SecA and SecA2 proteins in vitro revealed that
216 biochemical methods to assess whether the S. gordonii SecA2 functions similarly to SecA.
217                      To test this theory, S. gordonii secY2, asp4, and asp5 were co-expressed in Esch
218                              In biofilms, S. gordonii selectively expresses the msrA gene.
219 n Porphyromonas gingivalis and Streptococcus gordonii serves to constrain development of dual species
220 n peroxide in solution above a Streptococcus gordonii (Sg) bacterial biofilm was studied in real time
221 65 +/- 10 muM H2O2 produced by Streptococcus gordonii (Sg) in a simulated biofilm at 50 mum above its
222 t a peptide (BAR) derived from Streptococcus gordonii (Sg) potently inhibited adherence of Pg to stre
223 commensal streptococci such as Streptococcus gordonii (Sg).
224                                Streptococcus gordonii (Sg)/S. oralis (So)/S. sanguinis (Ss) and Sg/Fu
225   By contrast, an hsa-deficient mutant of S. gordonii showed significantly reduced binding and compet
226                                Streptococcus gordonii shows promise as a live mucosal vaccine vector
227 rdonii DLl than of streptomycin-resistant S. gordonii SK12 from the hearts of animals coinfected with
228 e, while the other two strains, including S. gordonii SK12, caused minimal or no disease.
229                                       The S. gordonii SspA and SspB polypeptides mediated higher bind
230 thin the C-terminal portion of Streptococcus gordonii SspB (AgI/II) is bound by Porphyromonas gingiva
231 treptococcus mutans AgI/II and Streptococcus gordonii SspB in their interaction with the SRCRs.
232  e.g., Veillonella parvula and Streptococcus gordonii, stimulated higher levels of ROS and NET releas
233                                      Each S. gordonii strain aggregated with human platelets and boun
234      The gspB-secY2A2 locus of Streptococcus gordonii strain M99 encodes the platelet-binding glycopr
235            Platelet binding by Streptococcus gordonii strain M99 is dependent on expression of the ce
236            Platelet binding by Streptococcus gordonii strain M99 is mediated predominantly by the cel
237            Platelet binding by Streptococcus gordonii strain M99 is predominantly mediated by the 286
238            Platelet binding by Streptococcus gordonii strain M99 is strongly correlated with the expr
239 imately 1.5 x 10(9) CFU of SP204(1-1), an S. gordonii strain not bearing vaccine antigens.
240          Adhesin-mediated binding of each S. gordonii strain to PMNs also triggered phagocytosis.
241       On the contrary, genomic islands of S. gordonii strains contain additional copies of comCDE quo
242 -rich surface glycoproteins of Streptococcus gordonii strains M99 and Challis, respectively, that med
243 nce among seven representative Streptococcus gordonii strains were observed by using the rat model of
244 , one of which was exclusively present in S. gordonii strains.
245 , Corynebacterium matruchotii, Streptococcus gordonii, Streptococcus cristatus, Capnocytophaga gingiv
246 y polypeptides from strains of Streptococcus gordonii, Streptococcus intermedius and Streptococcus mu
247 reus, Streptococcus sanguinis, Streptococcus gordonii, Streptococcus oralis, and Streptococcus pneumo
248 ng of accessory Sec systems in Streptococcus gordonii, Streptococcus parasanguinis, Mycobacterium sme
249  closely related oral species, Streptococcus gordonii, Streptococcus sanguinis, and cariogenic Strept
250 produced by the oral bacterium Streptococcus gordonii, suggesting the potential for cross-feeding in
251 t also glucosyltransferase G (Gtf-G) from S. gordonii supernatants.
252 rough a cell wall glycoprotein termed GspB ('gordonii surface protein B').
253 ly on the sgc protease knockout mutant of S. gordonii than on the parent biofilms.
254 nes developed more abundant biofilms with S. gordonii than the parental strain developed.
255  cascade dominantly control phenotypes of S. gordonii that are critical to colonization, persistence,
256 ogous surface glycoproteins of Streptococcus gordonii that bind sialic acid moieties on platelet memb
257 uorescence levels 20-fold higher than did S. gordonii that had not been incubated with V. atypica.
258 e-rich glycoprotein adhesin of Streptococcus gordonii that is exported to the bacterial surface by th
259           In the gram-positive Streptococcus gordonii, the ability to form disulfide bonds affected a
260                             In Streptococcus gordonii, the SRR glycoprotein GspB has a 90-residue ami
261                                        In S. gordonii, there was a high degree of inter-sample variat
262 , Streptococcus sanguinis, and Streptococcus gordonii, they exhibited antibacterial effect only in ac
263  that P. gingivalis adheres to Streptococcus gordonii through interaction of the minor fimbrial antig
264                               An isolated S. gordonii::Tn917-lac biofilm-defective mutant contained a
265                                        An S. gordonii::Tn917-lac biofilm-defective mutant was isolate
266 trast, did not significantly compete with S. gordonii to adhere.
267 sp5 are necessary for optimal adhesion of S. gordonii to glycoproteins gp340 and fibronectin, known H
268 le nutrient showed that V. atypica caused S. gordonii to increase expression of a PamyB-'gfp transcri
269 I/II family proteins) can bind Streptococcus gordonii to other oral bacteria and also to salivary agg
270 constraint against S. sanguinis, enabling S. gordonii to persist within the oral cavity, despite the
271 huttle plasmid, plasmid DNA transfer from S. gordonii to S. mutans was observed in a CSP and mutacin
272 3 also resulted in an impaired ability of S. gordonii to secrete GspB.
273 ution of GspB and Hsa to the adherence of S. gordonii to selected glycoproteins.
274                      Thus, the ability of S. gordonii to survive in PMNs following adhesin-mediated p
275                           The capacity of S. gordonii to synthesize arginine was assessed using a che
276  of pioneer organisms, such as Streptococcus gordonii, to tooth surfaces.
277 icated by transformation frequencies, the S. gordonii transcriptome was analyzed at various time poin
278                 Comparison of CSP-induced S. gordonii transcriptomes to results published for Strepto
279                             In Streptococcus gordonii, transport of the serine-rich glycoprotein GspB
280 emonstrated an increased DNA release from S. gordonii upon addition of the partially purified mutacin
281 ing aerotolerant ones, such as Streptococcus gordonii, use pyruvate dehydrogenase to decarboxylate py
282                          S. sanguinis and S. gordonii used oxygen availability and the differential p
283 o simulate pioneer colonization of teeth, S. gordonii V288 was incubated with sHA for 4 h in THB with
284 rmation, a plasmid integration library of S. gordonii V288 was used.
285 lysis, the entire accessory Sec system of S. gordonii was expressed in Escherichia coli.
286  maximum AI-2 induction was detected when S. gordonii was grown in the presence of serum and carbonat
287 s, Streptococcus sanguinis, or Streptococcus gordonii was investigated using flow cell devices that a
288                      Biofilm formation by S. gordonii was observed to be influenced by the presence o
289  expression of argC, argG, and pyrA(b) in S. gordonii was partially up-regulated although arginine wa
290  in a dose-dependent manner while that of S. gordonii was unaffected.
291        In coaggregation assays, SspB from S. gordonii was unique in mediating coaggregation with only
292 ncoding a major autolysin from Streptococcus gordonii, was identified and characterized.
293 te disulfide bond formation in Streptococcus gordonii, we identified five putative TDORs from the seq
294 adhesins of the oral bacterium Streptococcus gordonii were differentially expressed depending on whet
295                                Streptococcus gordonii were spotted onto the membranes and the plates
296 o the platelet adhesin GspB in Streptococcus gordonii, were identified.
297 sis, the 20-kDa AbpA protein is unique to S. gordonii, whereas the 82-kDa AbpB protein appears to sha
298 rast, type 1 fimbriated A. naeslundii and S. gordonii, which bound purified proline-rich proteins (PR
299  both species and well-defined mutants of S. gordonii with interrupted abpA and gtfG genes were studi
300               Furthermore, communities of S. gordonii with P. gingivalis or with A. actinomycetemcomi

 
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