Sentence examples for mutant and observed from inspiring English sources

We compared the transcript levels of GNS4 between WT and the gns4 mutant, and observed a slightly lower level of GNS4 transcripts in the mutant.

We created a degP mutant and observed a release of proteins at 37° to the culture supernatant similar to that of virK.

In vitro results above suggested a dominant negative-like inhibition of WT-CFTR by ΔF-CFTR that was specific to this most common ER retention folding mutant and observed in native human airway epithelial cells.

We obtained estimates of the apparent affinity for each mutant, and observed a wide range of different phenotypes, from small changes in affinity to almost 400-fold weakening of toxin affinity for Kv2.1.

To this end we overexpressed DnSIZ1 under the control of the CaMV35S promoter in the siz1-2 mutand and observed that the mutant phenotypes were indeed partially functionally complemented (Fig.  6).

To test this, we made cells stably expressing a dominant-negative AMPK-α2 mutant and observed that the A23187-induced increase in AMPK activity was reduced by an amount (≈70%) similar to that of the increase in ACC phosphorylation; ACC phosphorylation induced by A769662 was similarly decreased.

We restored crtc-1 cDNA in the ASI neurons in the aak-2 crtc-1 double mutaak-2 crtc-1ervedoublebust partial restoration of the increased FLP-7mutants secretion (Fig. 6and), similar tobservedeen in the aak-2 mutants alone.

To evaluate the possibility that AMPK signalling regulates 5-HT-mediated FLP-7 secretion, we crossed the flp-7mCherry secretion line with the aak-2 mutants, and observed a robust increase in FLP-7mCherry secretion (Fig. 6a c).

We tested these mutants and observed that E346K mutant undergoes autoactivation and causes AKT Tyr/Ser/Thr-phosphorylation in serum starved cells (Fig. S5B and C).

We further investigated flower development in lif2 mutants and observed several defects in lif2-1, lif2-2 and lif2-3 mutants (Fig. 4), but none in lif2-4.

We crossed the transgene into rpm-1 mutants and observed a significant increase in GFP DLK-1 fluorescence (the same transGFP DLK-1e is shown in fluorescenceJ).