Sentence examples for mutant we show from inspiring English sources

Using a computational model of ChR2(H134R mutant), we show that both stimulation modalities produce similar-in-morphology APs in human cardiomyocytes, and that electrical and optical excitability vary with cell type in a similar fashion.

Using this mutant, we show that NE is important for arousal that is induced by either genetic overexpression of the Hcrt neuropeptide or optogenetic activation of Hcrt neurons.

Using an SXIP defective mutant, we show that the SXIP-motif is important for proper mitotic microtubule growth rates and SKAP overexpression induced delay in anaphase onset.

Exploiting this mutant, we show that the C2A domain regulates the release probability of SVs, likely through positioning UNC-13L to the active zone.

Using these two mutants, and particularly the conditional rescue of cell elongation by GA in the ga1-3 mutant, we show that active cell elongation is associated with a higher average level of pectin esterification.

Using the K270A mutant, we show that hydrolysis is dispensable for RIG-I activation, meaning that the physical transition from an autorepressed state to an activated, signaling competent state does not depend on the ability of the protein to hydrolyze ATP.

Using the phr1 mutant, we showed that SULTR1 3 up-regulation following phosphate deficiency was dependent on PHR1.

Together with biochemical and crystallographic analysis of HD deletion mutants, we show that the HD is an autoinhibitory domain that blocks productive NAD+ binding.

In the case of cos2/kif7mw406 mutants, we show that early defects in Hedgehog signaling lead to a general, non-photoreceptor-specific delay of retinal neurogenesis, which in turn causes the secondary phenotype of delayed outer segment morphogenesis.

Using DMPK mutants, we show that DMPK is required for a correct intracellular trafficking of insulin and IGF-1 receptors, providing a mechanism to explain the molecular and metabolic phenotype of dmpk−/− mice.

Using conditional deletion mutants, we show here that c-Myc plays an important role in endochondral ossification and bone growth by promoting efficient proliferative expansion of both chondrocyte and osteoblast lineages.