Sentence examples for mutants led us from inspiring English sources
Analysis of competitive STD-NMR experiments between erythromycin A and a chromogenic substrate (pNP-β-d-glucose) with the hydrolytically inactive nucleophile mutants led us to discover a family of unprecedented glycosidase inhibitors.
The robust effects of CR on yeast mitochondrial mutants led us to pose the question: Are the beneficial effects of CR in the setting of mitochondrial deficiency conserved in mammals?
Examination of existing sc mutants led us to one such mutant: scHwUa.
Genetic and biochemical analyses of kog1 mutants led us the unexpected finding that TORC1 is involved in mitotic entry via regulation of polo-like kinase, Cdc5.
The decreased p53 abundance in the context of PTEN ATP-binding mutants led us to investigate the p53-mediated transcriptional activation.
The similarity of the anatomical and behavioral phenotypes of the Jna/+ mice to the Dcx, Lis1, and reeler mouse mutants led us to consider whether mutations in the human homolog of Tuba1 might cause lissencephaly in humans.
The decreased vesicle production in the sec4-2 mutant led us to analyze the kinetics of vesicle release by these cells, in comparison to the WT strain.
Decreased resistance to oxidative stress, delayed production of several virulence factors, together with the decreased growth rate of the mutant led us to measure the sensitivity of bacterial cells to macrophage-mediated killing.
This finding, along with the observation that CR does not further extend the CLS of an ade4∆ mutant, led us to hypothesize there was overlap between the mechanisms required for CLS extension induced by either CR or the ade4∆ mutation [ 9].
This mild Jag1 phenotype contrasts with the strong neurogenic phenotype detected in Dll1 mutants and led us to hypothesize that neighbouring Dll1-expressing cells signal to V1 and dI6 progenitors and restore neurogenesis in the absence of Jag1.
These findings suggested that muscle cells are present and correctly localized but internally disorganized in y241 mutants, which led us to examine the subcellular architecture of myofibers.
