ライフサイエンスコーパス: formigenes

1 plasmic membrane of the organism Oxalobacter formigenes.

2 he oxalate/formate antiporter of Oxalobacter formigenes.

3 transporting membrane protein in Oxalobacter formigenes.

4 :formate exchange transporter of Oxalobacter formigenes.

5 late/formate exchange protein of Oxalobacter formigenes.

6 rt, by the intestinal bacterium, Oxalobacter formigenes.

7 6%) of 43 CF patients were colonised with O. formigenes.

8 d, was cloned from the bacterium Oxalobacter formigenes.

9 proton-motive metabolic cycle in Oxalobacter formigenes.

10 wed even greater sensitivity in detecting O. formigenes and provided support for further division of

11 We investigated whether the absence of O. formigenes and the presence of hyperoxaluria are correla

12 aged healthy volunteers were examined for O. formigenes by culture and DNA analysis.

13 retion in hyperoxaluric mice treated with O. formigenes CM reflects the in vivo retention of biologic

14 oxaluria type 1, rectal administration of O. formigenes CM significantly reduced (>32.5%) urinary oxa

15 Compared with control medium, O. formigenes CM significantly stimulated oxalate uptake (>

16 Treating the O. formigenes CM with heat or pepsin completely abolished t

17 as no specific therapy, although Oxalobacter formigenes colonization is associated with reduced stone

18 The difficulties in sustaining O. formigenes colonization underscore the need to identify

19 ot differ with the presence or absence of O. formigenes colonization.

20 ent kidney stone episodes and the lack of O. formigenes colonization.

21 It was hypothesized that the absence of O. formigenes could lead to increased colonic absorption of

22 We therefore evaluated the effects of O. formigenes culture conditioned medium (CM) on apical (14

23 We conclude that O. formigenes-derived bioactive factors stimulate oxalate t

24 trafiltration of the CM revealed that the O. formigenes-derived factors have molecular masses of 10-3

25 The prevalence of O. formigenes, determined by stool culture, was 17% among c

26 obligate anaerobe Oxalobacter formigenes, O. formigenes formyl coenzyme A transferase (FRC).

27 Absence of O. formigenes from the intestinal tract of CF patients appe

28 All seven CF patients colonised with O. formigenes had normal urinary oxalate levels, but 19 (53

29 he oxalate:formate antiporter of Oxalobacter formigenes, has a lone charged residue, lysine 355 (Lys-

30 To confirm the importance of O. formigenes in regulating hyperoxaluria, laboratory rats

31 Detection of O. formigenes in six of these seven patients required DNA-b

32 Detection of O. formigenes in the gastrointestinal tract has attracted a

33 les from an individual not colonized with O. formigenes, indicating unique specificity.

34 O. formigenes interacts with colonic epithelium and induces

35 Oxalobacter formigenes is a Gram-negative, anaerobic bacterium that

36 Oxalobacter formigenes is a specific oxalate-degrading, anaerobic ba

37 Oxalobacter formigenes is an obligate anaerobe that colonizes the hu

38 se results suggest that colonization with O. formigenes is associated with a 70% reduction in the ris

39 The role of Oxalobacter formigenes is herein discussed.

40 taken together, support the concept that O. formigenes is important in maintaining oxalate homeostas

41 he oxalate/formate antiporter of Oxalobacter formigenes, lysine 355 is within transmembrane helix no.

42 abolism in the obligate anaerobe Oxalobacter formigenes, O. formigenes formyl coenzyme A transferase

43 e multivariable model, the odds ratio for O. formigenes remained 0.3 (95% confidence interval 0.1 to

44 As expected, the lack of O. formigenes revealed a clear association with prophylacti

45 quences of oxc or frc were able to divide O. formigenes strains into at least two groups, consistent

46 consistent with the current separation of O. formigenes strains into groups I and II on the basis of

47 th detection as well as classification of O. formigenes strains.

48 of oxalate-degrading enzymes derived from O. formigenes to determine any subsequent increased resista

49 and the CF patient with normal numbers of O. formigenes was the only one of the 43 patients who had n

50 late:formate exchange protein of Oxalobacter formigenes, was established by site-directed fluorescenc

51 /formate exchange transporter of Oxalobacter formigenes, was purified as a histidine-tagged variant,

52 9 (53%) of 36 patients not colonised with O. formigenes were hyperoxaluric, with the most severe hype

53 nomic DNAs of various strains of Oxalobacter formigenes were subjected to restriction endonuclease fr