Sentence examples for timing of deletion from inspiring English sources

Consistent with an important role for timing of deletion, germline heterozygous ΔE Tor1a knock-in mice exhibit increased LCI cell body area, though these mutants show no difference in the number of LCIs (Song et al., 2013).

The imperfect nature of the genetic deletion event using this system (∼ 80%), and the fact that the timing of deletion is post-DNA replication (because the recombinase is under the control of a trophozoite-stage promoter) means that many of the schizonts will include a mixture of merozoites that are genetically null and wild type for the Pfama1 gene.

In March, the chairman of the Benghazi committee Rep. Trey Gowdy (R-South Carolina) released a statement questioning the timing of her deletion of her messages.

Both of these models mimic intestinal tumourigenesis; however, the timing of Src deletion is different.

The Tbx4-rtTA inducible system allowed us to closely regulate the timing of Sox9 deletion.

Alternatively, it is possible that the difference in the timing of the deletion of the ppp4c gene may allow the generation of colitogenic cells in the CD4cre:PP4f/f thymus but not in the Lckcre:PP4f/f thymus.

We conclude that LKB1 and AMPK play distinct roles in the control of insulin secretion and that the timing of LKB1 deletion, and/or its loss from extrapancreatic sites, influences the final impact on β-cell function.

Further control of the timing of gene deletion can be achieved by using a CreERT or CreERT2 recombinase, in which the recombinase is fused to a modified estrogen receptor and thus is only targeted to the nucleus upon injection of tamoxifen [ 1].

This novel system allows temporal control over the timing of gene deletions in the prostatic epithelium.

The importance of the timing of Pten deletions was also highlighted by Backman et al. [5] using the MMTVCre×Ptenfl/fl mouse model.

To determine whether these markedly divergent phenotypes may reflect true biological differences in the roles of LKB1 and AMPK in the pancreatic β-cell rather than being the result of differences in the timing and sites of deletion, using the RIP2.Cre transgene, we have therefore generated mice in which LKB1 is deleted in the β-cell.