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Sprouty negatively modulates branching morphogenesis in the Drosophila tracheal system.
3D culture models for studying branching morphogenesis in the mammary gland and mammalian lung.
Title 3D culture models for studying branching morphogenesis in the mammary gland and mammalian lung.
Recent computational models of branching morphogenesis in the lung have helped uncover the biological mechanisms that construct this ramified architecture.
We have investigated whether the Drosophila FGF receptor homolog, Breathless (BTL), whose activity is necessary for each phase of branching morphogenesis in the embryonic tracheal system, might play a role in guiding the directed migration of tracheal cells.
During the embryonic stage, the lung bud separates from the gut followed by the branching morphogenesis in the pseudoglandular stage until 17 weeks of gestation.
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For example, loss of FGF signaling in the mammalian lung or the Drosophila trachea severely disrupts branching morphogenesis in these organs [2] [7].
FGFs are required for the branching morphogenesis in several organs including the lungs and salivary glands [ 76, 77].
This process has been studied in detail and includes endothelial cell migration towards the concentration gradient of growth factors such as vascular endothelial growth factor [39]. Migration is directed by "leader" endothelial cells that, similarly to branching morphogenesis in other tissues, direct the movement of the cells of the stalk.
In particular, specific temporal changes in the expression of certain TGFβ superfamily members (for example Bmp4 during the initiation of ureteric branching morphogenesis in betaglycan+/− metanephroi) may underlie the contrasting phenotypes.
During early lung branching morphogenesis in mice, connexin 43 is highly expressed in the distal tip endoderm of the embryonic lung at E11.5, and after birth, connexin-43 is expressed between adjacent AT-I cells in rats and mice.
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