S
Stefano Zanotti
Researcher at University of Connecticut Health Center
Publications - 55
Citations - 2131
Stefano Zanotti is an academic researcher from University of Connecticut Health Center. The author has contributed to research in topics: Notch signaling pathway & Osteoclast. The author has an hindex of 26, co-authored 54 publications receiving 1831 citations. Previous affiliations of Stefano Zanotti include University of Genoa & Saint Francis University.
Papers
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Journal ArticleDOI
Notch Signaling and the Skeleton.
Stefano Zanotti,Ernesto Canalis +1 more
TL;DR: Notch plays a critical role in skeletal development and homeostasis, and serious skeletal disorders can be attributed to alterations in Notch signaling.
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Notch Inhibits Osteoblast Differentiation And Causes Osteopenia
Stefano Zanotti,Anna Smerdel-Ramoya,Anna Smerdel-Ramoya,Lisa Stadmeyer,Deena Durant,Freddy Radtke,Ernesto Canalis,Ernesto Canalis +7 more
TL;DR: Notch signaling in osteoblasts causes osteopenia and impairs osteo-blastogenesis by inhibiting the Wnt/beta-catenin pathway, and the effects of notch1 deletion in vivo are determined.
Journal ArticleDOI
Notch and the Skeleton
TL;DR: Dysregulation of Notch signaling is the underlying cause of diseases affecting the skeletal tissue, including Alagille syndrome, spondylocostal dysostosis, and possibly, osteosarcoma.
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Conditional deletion of gremlin causes a transient increase in bone formation and bone mass
Elisabetta Gazzerro,Elisabetta Gazzerro,Anna Smerdel-Ramoya,Anna Smerdel-Ramoya,Stefano Zanotti,Lisa Stadmeyer,Deena Durant,Aris N. Economides,Ernesto Canalis,Ernesto Canalis +9 more
TL;DR: Deletion of grem1 in the bone microenvironment results in sensitization of BMP signaling and activity and enhanced bone formation in vivo.
Journal ArticleDOI
Osteoblast Lineage-Specific Effects of Notch Activation in the Skeleton
TL;DR: Notch effects in the skeleton are cell-context-dependent and when expressed in osteocytes, it causes an initial suppression of bone resorption and increased bone volume, a phenotype that evolves as the mice mature.