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Thomas Gridley

Researcher at Maine Medical Center

Publications -  126
Citations -  16091

Thomas Gridley is an academic researcher from Maine Medical Center. The author has contributed to research in topics: Notch signaling pathway & Cellular differentiation. The author has an hindex of 63, co-authored 123 publications receiving 15127 citations. Previous affiliations of Thomas Gridley include Tufts University & University of Maine.

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Notch signaling is essential for vascular morphogenesis in mice.

TL;DR: An essential role for the Notch signaling pathway in regulating embryonic vascular morphogenesis and remodeling is revealed and it is indicated that whereas the NotCh4 gene is not essential during embryonic development, the notch4 and Notch1 genes have partially overlapping roles during embryogenesis in mice.
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Embryonic Lethality and Vascular Defects in Mice Lacking the Notch Ligand Jagged1

TL;DR: The phenotype of Cm /+ mice is established as a contiguous gene deletion syndrome and it is demonstrated that Jag1 is essential for remodeling of the embryonic vasculature.
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Roles for Nkx3.1 in prostate development and cancer

TL;DR: It is shown that the murine Nkx3.1 homeobox gene is the earliest known marker of prostate epithelium during embryogenesis and is subsequently expressed at all stages of prostate differentiation in vivo as well as in tissue recombinants.
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The mouse snail gene encodes a key regulator of the epithelial-mesenchymal transition.

TL;DR: In the case of mouse embryos deficient for the Snail (Sna) gene, a mesoderm layer forms and mesodermal marker genes are induced, and cells lining these lacunae retain epithelial characteristics.
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Haploinsufficient lethality and formation of arteriovenous malformations in Notch pathway mutants

TL;DR: It is demonstrated that vascular remodeling in the mouse embryo is sensitive to Dll4 gene dosage and that Notch activation in endothelial cells is essential for embryonic vascular remodels.