ライフサイエンスコーパス: K. kingae

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1 K. kingae produces a toxin of the RTX group, RtxA.

2 K. kingae strains also show significant association with

3 Although K. kingae exhibits noteworthy genetic heterogeneity, a l

4 ylococcus epidermidis, Candida albicans, and K. kingae.

5 he draft genome sequence of septic arthritis K. kingae strain PYKK081.

6 sent study, we examined interactions between K. kingae and cultured respiratory epithelial cells and

7 ul model for understanding disease caused by K. kingae and for elucidating diagnostic parameters in h

8 rmed a paracentesis on himself and developed K. kingae peritonitis and bacteremia.

9 A total of 32 different K. kingae clones were identified by PFGE, of which 5 (B,

10 on of either PilC1 or PilC2 is necessary for K. kingae piliation and bacterial adherence.

11 he genetic requirements for encapsulation in K. kingae and demonstrate an atypical organization of ca

12 y differences in PilC1 and PilC2 function in K. kingae and provide insights into the biology of the P

13 lipB (kpsS)-like gene, and the csaA gene in K. kingae capsule production.

14 The disruption of either rpoN or pilR in K. kingae resulted in a marked reduction in the level of

15 PilA1 is the major pilus subunit in K. kingae type IV pili and is essential for pilus assemb

16 A collection of 181 invasive K. kingae strains, isolated between 1991 and 2012 from I

17 , our results demonstrate that RtxA is a key K. kingae virulence factor.

18 C homologs play important roles in mediating K. kingae adherence.

19 as conducted to determine the association of K. kingae genotypes with specific clinical syndromes and

20 f the largest intercontinental collection of K. kingae strains to date.

21 The comprehensive description of K. kingae evolution would help to detect new emerging cl

22 out to determine the genetic determinants of K. kingae encapsulation.

23 Despite the increasing frequency of K. kingae disease, little is known about the mechanism b

24 the current study, we examined the genome of K. kingae strain 269-492 and identified homologs of the

25 od may serve in the initial investigation of K. kingae outbreaks.

26 The pathogenesis of K. kingae disease begins with bacterial adherence to res

27 roles for this toxin in the pathogenesis of K. kingae disease include breaching of the epithelial ba

28 The pathogenesis of K. kingae disease is believed to begin with colonization

29 ies associated with clinical presentation of K. kingae disease in humans and suggests that the toxin

30 These data suggest that the regulation of K. kingae type IV pilus expression is complex and multil

31 evelop a better understanding of the role of K. kingae type IV pili during colonization and invasive

32 IV pili may confer a selective advantage on K. kingae early in infection and a selective disadvantag

33 in infection and a selective disadvantage on K. kingae at later stages in the pathogenic process.

34 We concluded that K. kingae expresses an RTX toxin that has wide cellular

35 Recent work has demonstrated that K. kingae expresses type IV pili that mediate adherence

36 Previous work established that K. kingae expresses type IV pili that mediate adherence

37 Previous work showed that K. kingae expresses long surface fibers that vary in sur

38 that the biofilm inhibition activity in the K. kingae extract was due to polysaccharide.

39 Upon examination of the K. kingae genome, we identified two genes in physically

40 of mutant strains revealed that both of the K. kingae PilC homologs are essential for a wild-type le

41 Disruption of the K. kingae RTX locus resulted in a loss of cytotoxicity f

42 A cluster of three K. kingae genes encoding UDP-galactopyranose mutase (ugm

43 ole of RtxA in disease pathogenesis in vivo, K. kingae strain PYKK081 and its isogenic RtxA-deficient

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