Sentence examples for mutant cells exposed from inspiring English sources

Similarly, an increase in cell size was observed for a smaller fraction of the ctk1Δ mutant cells exposed to DOX (Fig. 3A).

As shown in Figure 6, in rat GFP-S18A-α1-subunit mutant cells exposed to high CO2 levels the Na,K-ATPase protein abundance at the plasma membrane was unchanged suggesting that the phosphorylation of the Ser18 was necessary for the CO2-induced endocytosis.

Mutant cells exposed to DOX in G1 demonstrated either prolonged arrest in G1 (ctf4Δ), arrested predominantly as budded cells following G1/S transition (bem1Δ, ctk1Δ, hfi1Δ and tho2Δ) or progressed to form a mixture of budded cells and small inviable microcolonies (nup133Δ).

In CSB mutant cells exposed to hypoxia-mimicking agents, the p53 pathway is indeed massively activated, as is the recruitment of RNA polymerase II at the promoter of p53 target genes.

Importantly, analyses were also performed on mutant cells exposed to inactive CORM-3 (i.e., CORM-3 depleted of CO) (11, 41, 48) to address the critical question: are the observed effects CO specific?

Since its release was unaffected in UNC93b1-mutant cells exposed to NSV, signals delivered by a non-endosomal TLR as well as some non-TLR pathway must both be involved in the induction of this mediator.

Similarly we observed a 57 ± 13% (P ≤ 0.01) increase in ROS in mutant PC12 cells exposed to ligand (Fig.  4B).

A) SF2 for the panel of wild-type (blue) and mutant (red) medulloblastoma cells exposed to radiation.

As shown in Fig. 1A, non-farnesylated prelamin A, produced by the LA-C661M mutant, accumulated in cells exposed to CQ.

We developed a novel protocol to measure the time-course ratios between mono-, di- and tri-ubiquitylated PCNA isoforms on a single western blot, which were used as the wet readout for PRR events in wild type and mutant S. cerevisiae cells exposed to acute UV radiation doses.

In contrast, only 4 of 30 (13.3%) of mutants derived from cells exposed to DPE (20 μg/mL) + UVA (0.5 J/ cm) retained all the marker genes examined, whereas 26 of 30 (86.7%) of the mutants had lost at least one additional marker, which included 8 of 30 (26.7%) that lost the proximal APO-A1 located on the long arm of the chromosome.