Sentence examples for mice we now from inspiring English sources

With the advances of genetic engineering and conditional knockout (CKO) mice, we now understand hematopoiesis is a dynamic stepwise process starting from hematopoietic stem cells (HSCs) which are responsible for replenishing all blood cells.

Using TRPV4−/− mice, we now investigated whether the absence of endothelial TRPV4 alters shear-stress-induced arterial vasodilation.

Using muscle-specific gene deletion in mice, we now show that p38γ mitogen-activated protein kinase (MAPK), but not p38α and p38β, is required for endurance exercise-induced mitochondrial biogenesis and angiogenesis, whereas none of the p38 isoforms are required for IIb-to-IIa fiber-type transformation.

Although immunogold electron microscopy had been unable to demonstrate alpha-synuclein aggregates in our A53T-SNCA overexpressing mice, we now used an antibody (Mc42) specifically directed against the alpha-synuclein NAC fragment which is involved in the aggregation and analyzed the presence of insoluble alpha-synuclein species.

Further validating the observations made in the YapKI mice, we now show that mosaic Yap activation is insufficient for clonal expansion in another model of Yap activation in hepatocytes: mosaic deletion of Mst2flox/flox allele on Mst1-/ background (new Figure 2 Figure Supplement 4).

We have conducted many associative studies of this type with long-lived, somatotrophic signaling-defective mutant mice; we now progress to the first steps in testing the necessity for enhanced insulin sensitivity for the delayed senescence of these mice or the sufficiency of improved blood glucose homeostatic control for delayed aging in their normal counterparts.

For the mouse, we now have phenotypes for around 8500 genes, and 40,000 genotypes with phenotypic annotations, in the Mouse Genome Informatics database (Blake et al., 2011).

Having established the orthology of bidirectional promoters between human and mouse, we now shift our attention to the problem of discriminating functional elements in the human genome.

In these mice we have now the opportunity to follow PDAC evolution in the living animal in a time frame process.

By crossing these mice with AspM-CreERT2 mice, we could now kill virtually all AspM/Nestin expressing cells of the developing forebrain.

With the recent advances in genetic manipulation in mice, we are now able to selectively knock out a tumor suppressor gene or overexpress an oncogene which results in the spontaneous development of tumors in specific tissues [6], [10], [11].