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These mutants may also point to the future of humans, particularly athletes.

This suggests that the other mutants may also alter rRNA structure, but that these were too slight to be detected by the methods employed.

Conversely, the low ROS levels in the ΔMovam7 mutants may also be due to a block for targeting the cytosol ROS into proper vacuoles.

Since the Gfox cell line expresses both CD134 and CXCR4, it may well be that some of the reduction observed in the CD134 binding assay for some mutants may also contribute to reduced infectivity observed in figure 6.

L137P and P283L mutants may also be stabilized by the glucosamine treatment, however this could not be verified experimentally because in the available patient cell lines they were present together with the responsive mutations S518F and R344C, respectively.

However, these mutants may also have been O-antigen deficient because F. tularensis LVS lacking O-antigen and/or O-antigen capsule is highly serum-sensitive [10], [11], [12], [13], [30].

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This suggests that the S18Y mutant may also behave like damaged UCH-L1.

Therefore, the reduction in YopE and YopH synthesis observed in the ΔrelA ΔspoT mutant may also contribute to attenuation.

Because biofilm formation on abiotic and biological surfaces may be regulated by similar processes we hypothesized that a bcr1/bcr1 mutant may also be defective in oral mucosal biofilm development.

However, the observed phenotype of the Arg301Ala mutant may also be attributed to removal of an important electrostatic effect.

The absence of CR in the crl1 mutant may also modify the nutrient and water status of the plant.

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