ライフサイエンスコーパス: Fusobacteria

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1 is likely to play a role in the virulence of fusobacteria.

2 ria, Epsilonproteobacteria, Bacteroidia, and Fusobacteria.

3 be used as a marker to detect orally related fusobacteria.

4 rmicutes (62.9%), Proteobacteria (29.9%) and Fusobacteria (9.6%).

5 ide and fusobacterial lectin that explicates fusobacteria abundance in CRC.

6 pared to adjacent normal mucosal tissue, and fusobacteria and beta-Proteobacteria levels increased wi

7 The abundances of Fusobacteria and Proteobacteria were also remarkably inc

8 wn, with examples throughout the Firmicutes, Fusobacteria and Proteobacteria.

9 lostridium group and in the deeply branching Fusobacteria and Thermotogales lineages.

10 Bacteroides, Actinobacteria, Proteobacteria, Fusobacteria, and TM7, were represented.

11 However, fusobacteria are core members of the human oral microbio

12 Fusobacteria are found to be overrepresented in the colo

13 A core alligator gut microbiome comprised of Fusobacteria, but depleted in Bacteroidetes and Proteoba

14 rs supported altered abundances in the phyla Fusobacteria, Firmicutes, Actinobacteria and Proteobacte

15 ruitment of tumor-infiltrating immune cells, fusobacteria generate a proinflammatory microenvironment

16 cer microbiota; however, the precise role of Fusobacteria in colorectal carcinoma pathogenesis requir

17 tively with the relative abundance of phylum Fusobacteria in the guts of tadpoles.

18 the healthy gut, raising questions about how fusobacteria localize to CRC.

19 ) describe a novel homing mechanism by which fusobacteria localize to tumors by recognizing a host po

20 cterial diversity and relative abundances of Fusobacteria might have lasting positive effects on amph

21 Fusobacteria (p < 0.007) and epsilon- Proteobacteria (p

22 in HOMIM scores of firmicutes (P </=0.001), fusobacteria (P = 0.003), proteobacteria (P </=0.001), s

23 rmicutes, Actinobacteria, Bacteroidetes, and Fusobacteria phyla.

24 Fusobacteria play a central role as physical bridges tha

25 In patients with AA, Fusobacteria populations proliferate and often persist d

26 pression signature that is shared with human fusobacteria-positive colorectal carcinomas.

27 ap2 or host epithelial Gal-GalNAc may reduce fusobacteria potentiation of CRC.

28 ral biofilm formation and pathogenesis, with fusobacteria proposed to serve as central 'bridging orga

29 in addition to the previously characterized fusobacteria, proteobacteria, firmicutes, and bacteroide

30 iae, Chloroflexi, Euryarchaeota, Firmicutes, Fusobacteria, Proteobacteria, Spirochaetes, SR1, Synergi

31 Clinical fusobacteria strains naturally lacking Fap2 or inactivat

32 normal human appendix harbors populations of Fusobacteria that are generally absent in fecal samples

33 These capabilities allow Fusobacteria to survive in a mixed culture in the mouth.

34 in a Fap2-dependent manner, suggesting that fusobacteria use a hematogenous route to reach colon ade

35 esin, a system for transposon mutagenesis in fusobacteria was created.

36 Fusobacteria was only present 12 h post-infection.

37 Fusobacteria were also visualized within colorectal tumo

38 icutes, Proteobacteria, Verrucomicrobia, and Fusobacteria were significantly increased, whereas Bacte

39 Faecalibacterium spp. and Fusobacteria were, however, decreased in the dogs with c

40 Clostridia and Fusobacteria, widely pathogenic to other vertebrates, do

41 ive adhesin might mediate the interaction of fusobacteria with many partners and targets.

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