ライフサイエンスコーパス: competitive fitness

1 n was dispensable for growth, virulence, and competitive fitness.

2 rom its contribution to Treg homeostasis and competitive fitness.

3 ompetitive fitness is similar to that of non-competitive fitness.

4 relation between mutations for body size and competitive fitness.

5 pecific aging-acquired mutations, may have a competitive fitness advantage after induction chemothera

6 at while the rpoS819 allele confers a strong competitive fitness advantage at basic pH, it confers a

7 ere that each of these polymerases confers a competitive fitness advantage during the stationary phas

8 Moreover, the GAL lncRNAs confer a competitive fitness advantage to yeast cells because exp

9 nt against mutations affecting hermaphrodite competitive fitness agree to within two-fold, 0.33-0.5%.

10 AS locus are frequent in cancer and modulate competitive fitness and MEK dependency.

11 expression by CD8(+) T cells inhibits their competitive fitness and results in a slightly reduced ra

12 Potential roles in competitive fitness are discussed.

13 al variance (VM) for male mating success and competitive fitness are not significantly different from

14 In a competitive fitness assay in human PC-3 tumors growing i

15 tes complex pools of barcoded mutants, whose competitive fitness can be measured during infection of

16 ains would be if these strains had increased competitive fitness compared to strains of other ribotyp

17 resistance is universally associated with a competitive fitness cost and that this cost is determine

18 ance, implying mutants in this gene may have competitive fitness costs.

19 heir natural environments where survival and competitive fitness depend upon both growth rate when co

20 f bacillaene and other antibiotics optimizes competitive fitness for B. subtilis.

21 ere used to score complex phenotypes such as competitive fitness in a chemostat, DNA repair proficien

22 g these compensatory mutations showed a high competitive fitness in vitro.

23 enhanced proliferation, and profound loss of competitive fitness in vivo.

24 ions in the assay experiment, from which new competitive fitness indices or parameters are defined.

25 is 0.17%/generation; that of hermaphrodite competitive fitness is 0.11%/generation.

26 The rate of mutational decay of male competitive fitness is 0.17%/generation; that of herma

27 rent from zero, whereas VM for hermaphrodite competitive fitness is similar to that of non-competitiv

28 BCR(-) lymphoma variants that restore competitive fitness normalize GSK3beta activity after co

29 tance plasmids and measured their effects on competitive fitness of a Pseudomonas fluorescens SBW25 h

30 ing these systems may also contribute to the competitive fitness of B. pseudomallei.

31 ects were most apparent as a decrease in the competitive fitness of cells lacking 6S RNA.

32 roducible, systematic assay to determine the competitive fitness of HIV-1 drug-resistant mutants.

33 exhibited normal thymic Treg generation, the competitive fitness of peripheral Tregs was severely com

34 Mechanistically, the competitive fitness of S. aureus is a result of both agr

35 required for maintaining the homeostasis and competitive fitness of T(reg) cells in vivo.

36 enhance acid tolerance and contribute to the competitive fitness of the organism at low pH.

37 xp3-dependent regulation of miR155 maintains competitive fitness of Treg cell subsets by targeting SO

38 odel approach for more-accurate estimates of competitive fitness parameters from multiple data points

39 A competitive fitness study failed to reveal any differenc

40 le number have a quadratic relationship with competitive fitness, suggesting stabilizing selection fo

41 Competitive fitness tests in generations 50 and 85 showe

42 over the population had significantly lower competitive fitness than two clones with mutations that

43 Wild-type nematodes exhibited greater competitive fitness than unc-22(sf21) mutants.

44 Competitive fitness, viability and fertility of the chro

45 mal locus required for copper resistance and competitive fitness was cloned from a strain of Pseudomo

46 dent Rbs(-) mutants were isolated, and their competitive fitnesses were measured relative to that of

47 n in the intestine, suggesting they may lose competitive fitness when grown outside the gut.

48 at deletion of type IV SCCmec did not affect competitive fitness, whereas deletion of ACME significan