Sentence examples for mutants we suggest from inspiring English sources
From the structural and MD simulation data for the seven allosteric site mutants, we suggest the following depiction of caspase 3 as part of the inactive ensemble, where one or more of these changes result in inactivation.
Combining the high percentage of T. pallidum mutants, we suggest that the macrolide-resistant T. pallidum mutation was induced by macrolide pressure that did not result from treating syphilis, but rather, from the abuse of macrolides for other infections.
Given the increased levels of C-circles in ceob2 mutants, we suggest that this likely happens due to increased telomeric recombination events, which in certain instances can lead to the generation of survivor strains.
Since the above proposed function of Med8-Med18-Med20 might not account for the decrease in siRNA or H3K9me in the mutants, we suggest that the Med8-Med18-Med20 submodule also facilitates the processing of long non-coding RNAs into siRNA.
Because eat-2; nlp-24 mutants do not pump as slowly as eat-2; egl-3 mutants, we suggest that there may be other neuropeptides that act together with nlp-24 to stimulate pumping in the absence of MC neuron activity.
Despite the very different phenotypes of pcs1 and csm1 mutants, we suggested that the two proteins might nevertheless have similar physiological functions, namely to clamp together microtubule binding sites.
Since accumulation of other carbohydrates synthesized from the UDP-glucose precursor, such as cellulose and β-glucan, were unaffected in the mutant, we suggest that the increased expression of the genes for sucrose synthase 4 and UDPase 1 may be also associated with amylopectin synthesis.
Finally, because organotins have similar effect on LNCaP cells (containing wild-type p53 gene), MDA-MB-231 (mutant p53) cells, and Jurkat T cells (mutant p53), we suggest that organotins kill cells via a p53-independent pathway.
Given the strong interaction between MEIG1 and PACRG, and the fact that Pacrg-deficient male mice are infertile and the reproductive phenotype mirrors that of the Meig1 mutant mice, we suggest that PACRG might be the protein that recruits MEIG1.
As wg transcription in wing discs is controlled by Notch signaling and was not affected in Dsnx3 mutant cells, we suggest that DSNX3 activity is also not required for Notch signaling.
Whether either or both of these possible mechanisms is driving phenotype in the Y64H mutant mice, we suggest that failure to secrete matrix proteins would lead to cell stress and disruption of normal ameloblast organization and behaviour.
