ライフサイエンスコーパス: rough mutant

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1 accharide was truncated, like that of a deep-rough mutant.

2 ned concerning the intracellular survival of rough mutants.

3 sposon mutagenesis using Brucella melitensis rough mutant 16M delta manBA as the parental strain.

4 macrophages, we have monitored the uptake of rough mutants and survival in vitro by using the murine

5 Rough mutants are easily identifiable by appearance, are

6 These deep rough mutants are novobiocin susceptible until complemen

7 infected with Brucella abortus S2308-derived rough mutant CA180.

8 Since deep rough mutants contain bacterial phospholipid (BPL) as we

9 inner saccharide core, whereas Ra LPS, from "rough" mutants, contains a longer polysaccharide region.

10 Rd LPS, from more sensitive "deep rough" mutants, contains only an inner saccharide core,

11 mutagenesis was used to generate B. abortus rough mutants defective in O-antigen presentation.

12 oth, virulent B. melitensis 16M results in a rough mutant designated WRR51.

13 All of the B. abortus rough mutants exhibited a 4- to 5-log-unit increase, com

14 Several recent publications report that rough mutants exhibited increased macrophage uptake rela

15 Treatment with wild-type and rough mutant forms of LPS and synthetic lipid A resulted

16 In conclusion, Brucella rough mutant infection induces necrotic and oncotic macr

17 rgue that the increased permeability of deep rough mutants is due to structural modifications caused

18 Transposon-derived rough mutants isolated in our laboratory were previously

19 We constructed a rough mutant of Brucella abortus 2308 by transposon (Tn5

20 sis and B. bronchiseptica and the first deep rough mutants of any of the bordetellae.

21 Rough mutants of Brucella spp. are attenuated for surviv

22 Unlike previously described avirulent rough mutants of L. monocytogenes that secrete diminishe

23 ough) mutant, unlike an inner core LPS (deep rough) mutant or O-antigen-expressing recombinant of E.

24 confirm a 10- to 20-fold-increased uptake of rough mutants over that of smooth organisms under standa

25 Recovery of the rough mutants persisted up to 8 h postinfection, but at

26 for efficiently by lipoteichoic acid and by rough mutant (Ra and Rc) forms of LPS, which differ in p

27 Complementation of these rough mutants returned O-antigen expression and suscepti

28 lls, revealed survival differences among the rough mutants similar to those observed in the mouse.

29 hybridomas were more reactive to heat-killed rough mutants than to heat-killed smooth strains, as mea

30 that an outer core lipopolysaccharide (LPS) (rough) mutant, unlike an inner core LPS (deep rough) mut

31 Not surprisingly, each of the rough mutants was attenuated for survival in mice, but u

32 of [(3)H] Escherichia coli LPS from the deep rough mutant, which contains a covalently linked, photoa

33 lytic death of macrophages infected with the rough mutants, which was confirmed by the release of lac

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