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The complex, partially redundant gene regulatory architecture underlying vertebrate heart formation has been difficult to characterize.
LATS1/2 or SAV loss also affect heart development[75, 78], supporting the notion that Hippo signalling is required for normal heart formation.
From this pioneer work many research developments were led on role of EMT in gastrulation, heart formation (including endothelial mesenchymal transition), neural crest.
These findings suggest that Yap and TEAD1 may have redundant functions during early embryonic development, one of which may be the regulation of heart formation in mice.
ADMSCs can differentiate into cardiomyocytes, and it has been shown that over-expression of a cocktail of factors can induce ectopic heart formation and program cardiogenesis in ESCs.
Understanding its particular role in heart formation has helped to develop pluripotent stem cell differentiation protocols that produce relatively pure cardiomyocyte populations.
The cells in question express a protein, called Islet 1, which is present in the early stages of fetal heart formation.
Mesp1 and Mesp2 double-knockout embryo showed a complete defect of mesodermal migration and heart formation which confirmed the compensation effect of Mesp2 for Mesp1 (Kitajima et al., 2000).
Taken together, these findings demonstrate the critical involvement of Hippo signaling during cardiogenesis and suggest that a balance of Yap activity is required for proper heart formation (see Table 1 for overview of Hippo-related mouse models and cardiac phenotypes).
Inhibition of canonical Wnt signaling induces heart formation [6].
This suggests that XNkx2.5 and XNkx2.3 act redundantly during heart formation [24].
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