Sentence examples for mutants may explain from inspiring English sources

While drug resistant viral mutants may explain at least some failures with RBV treatments, recent reports propose that cell-based resistance to RBV could be an important factor explaining the low antiviral activity of RBV in at least some experimental and clinical systems [6].

Thus, we asked whether differences in protein charge among the ALS mutants may explain the variability in the relative rates of mutant SOD1 aggregation.

The upregulation of a novel isoform from the tardbpl locus shown in our studies supports the idea that compensation by the tardbpl locus in the tardbp mutants may explain the viability of these mutants.

The susceptibility to ER stress displayed by atg mutants may explain why NPR1 mutation suppresses both the visible spread of lesions triggered by immune responses, as well as senescence-associated cell death in atg mutants: the protein flux through the endoplasmatic reticulum is significantly lowered in npr1 backgrounds.

The reduced capacity to produce an interfascicular cambium in the pxc1 mutants may explain the reduction in PXY/TDR and WOX4 transcript levels, or vice versa, the reduced expression of PXY/TDR and WOX4 may be the underlying cause of the lack of interfascicular cambium.

The surface change of the mutant may explain why crystal violet-stained ecs mutant cells looked optically smaller than corresponding wild-type cells.

The absence of the stabilizing hydrogen bond in the S119A mutant may explain the reduced affinity of this mutant for CBZ.

The differential interaction and processing of an aggregation-prone, disease-associated transthyretin variant with human cardiac cells, compared with a non-disease associated transthyretin mutant may explain the basis of the early events of tissue damage in the transthyretin amyloidoses.

Sac6 is also upregulated in scp1 ∆ mutants, which may explain why the scp1 ∆ phenotype is not stronger (Gheorghe et al. 2008).

These findings expand our knowledge on the previously described molecular mechanisms of action of natural hGR mutants, and may explain the differences observed in the clinical phenotype of subjects with Chrousos syndrome [ 27- 45, 47- 49].

Notably, this group of 16 genes that we expect to be directly targeted by MOP1 was not represented in our prior analyses of nucleosome position in mop1-1 mutands, and may explain the small number of genes that we observed to be effected in that study.