D
Damian Medici
Researcher at Brown University
Publications - 24
Citations - 4096
Damian Medici is an academic researcher from Brown University. The author has contributed to research in topics: Mesenchymal stem cell & Epithelial–mesenchymal transition. The author has an hindex of 16, co-authored 24 publications receiving 3614 citations. Previous affiliations of Damian Medici include Harvard University & Beth Israel Deaconess Medical Center.
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Journal ArticleDOI
Signaling mechanisms of the epithelial-mesenchymal transition
TL;DR: This review discusses how intracellular pathways and extracellular signals that regulate gene expression to induce EMT crosstalk and respond to signals from the microenvironment to regulate the expression and function of EMT-inducing transcription factors in development, physiology, and disease.
PatentDOI
Conversion of vascular endothelial cells into multipotent stem-like cells
Damian Medici,Bjorn R. Olsen +1 more
TL;DR: In this article, a method of producing multipotent cells, comprising, activating ALK2 of isolated endothelial cells in a serum starved environment, to thereby produce isolated multipotent cell.
Journal ArticleDOI
Snail and Slug Promote Epithelial-Mesenchymal Transition through β-Catenin–T-Cell Factor-4-dependent Expression of Transforming Growth Factor-β3
TL;DR: Evidence is provided for a unified signaling mechanism driven by convergence of multiple TGF-beta and TCF signaling molecules that confers loss of cell-cell adhesion and acquisition of the mesenchymal phenotype.
Journal ArticleDOI
Suppressed NFAT-dependent VEGFR1 expression and constitutive VEGFR2 signaling in infantile hemangioma.
Masatoshi Jinnin,Damian Medici,Lucy Park,Nisha Limaye,Yanqiu Liu,Elisa Boscolo,Joyce Bischoff,Miikka Vikkula,Eileen Boye,Bjorn R. Olsen +9 more
TL;DR: Normalization of the constitutive VEGfr2 signaling in hemECs with soluble VEGFR1 or antibodies that neutralize VEGF or stimulate β1 integrin suggests that local administration of these or similar agents may be effective in hemangioma treatment.
Journal ArticleDOI
Transforming growth factor-β2 promotes Snail-mediated endothelial-mesenchymal transition through convergence of Smad-dependent and Smad-independent signalling.
TL;DR: It is shown that TGF-β2 stimulates EndMT through the Smad, MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase], PI3K (phosphinositide 3-kinase) and p38 MAPK signalling pathways, which are essential for increasing expression of the cell-adhesion-suppressing transcription factor Snail.