Sentence examples for mouse embryonic hearts from inspiring English sources

The results revealed that both the RCAN1.1 and RCAN1.4 were expressed in mouse embryonic hearts and human hearts (Fig. 1B).

(B) Western blot of RCAN1.1 and RCAN1.4 proteins in mouse embryonic hearts and heads at embryonic day 10.5 (E10.5) and in a human foetal heart (20 weeks).

To investigate if the RCAN1.4 plays a role in heart development, we evaluated the expression of the RCAN1.1 and RCAN1.4 proteins in E10.5 mouse embryonic hearts and human hearts.

In the present study, we investigated the effects of ANP (rat ANP 3 28) on ICaL in cardiomyocytes derived from mouse ES cells as well as isolated myocytes from mouse embryonic hearts.

To improve imaging of the blood islands in mouse embryonic hearts, we used the method described by Mukouyama et al. (2012) with our own modification.

To gain insight into the molecular mechanism of the increased heart size, we performed microarray expression analysis on E17.5 Snrk WT, HET and KO mouse embryonic hearts, a developmental stage that was close enough to birth to avoid implication associated with neonatal lethality.

We determined the spatial expression of selected candidates by in situ hybridization at mouse E7.5, E8.5, and E9.5, critical time points for mouse embryonic heart development.

These results indicate that mouse embryonic heart enhancers experienced more frequent or more intense, positive selections during their evolution.

Furthermore, Ets1 and Erg were shown to directly regulate Gata4 in the mouse embryonic heart by binding to a distal enhancer region within the Gata4 gene.

Therefore, our aim was to locate within the mouse embryonic heart and characterize putative progenitor cells bearing hematopoietic and vasculogenic markers, using morphological and immunohistochemical methods.

The disruption of fusion in mouse embryonic heart and in embryonic stem cells results in disruption of mouse heart development and impaired differentiation of embryonic stem cells into cardiomyocytes due to increased Ca2+-dependent calcineurin activity and Notch1 signaling [ 78].