Sentence examples for mouse cardiac development from inspiring English sources

Based on the hypothesis that NRSF negatively regulates HCN4 gene activity in cardiomyocytes [ 12], we asked how NRSF is regulated during mouse cardiac development.

We found remarkable differences in the HCN isotype transcription throughout mouse cardiac development that may contribute significantly to changes that determine the properties of pacemaker channels and thereby influence the heart rate.

We calculated target gene expression relative to that of the housekeeping gene GAPDH, which was shown to be expressed relatively stable throughout mouse cardiac development, between different cardiac tissues and in cardiomyocytes under various conditions [ 32; supplement Fig. 2].

Taken with the absence of cardiac phenotypes associated with the previously described AHDC1 truncation mutations, these results make a major role for AHDC1 in human or mouse cardiac development unlikely and allowed us to prioritize Matr3 for gene targeting in mouse.

Volz et al. have studied cardiac development in mice and used fluorescent labels to observed individual cells of the epicardium as they divided and moved.

Accordingly, in the mouse vinculin loss leads to defects in adhesion complexes that compromise embryonic cardiac development [3] and vinculin+/− mice develop dilated cardiomyopathy [4].

To determine the temporal expression patterns of Smyd-family members during vertebrate heart development, we collected mouse cardiac ventricles at sequential developmental stages from embryonic (E) days 12.5 to 18.5, postnatal (P) days 1 to 7 and adult and determined the relative mRNA expression levels of Smyd1-5.

Moreover, it has been recently demonstrated that cardiac development in the mouse is characterised by a hypoxic environment with high levels of Hif1α protein [ 37].

Wnt signaling has been identified as a downstream target of Notch1 that regulates expression of cardiac transcription factors during mouse cardiogenesis and is essential for cardiac development facilitating transcription of target genes involved in cell fate regulation [ 75, 76].

The most likely scenario is that an ancestral, single Tie gene was required for heart development and that, after genome duplication, functional divergence occurred within the vertebrate lineage: in fish, functional redundancy has been conserved between Tie-1 and Tie-2 in respect to cardiac development, whereas, in mice, Tie-1 cannot substitute for a loss of Tie-2 function in the early heart.

The mouse embryo is ideal for studying human cardiac development.