J
Joan C. Marini
Researcher at National Institutes of Health
Publications - 172
Citations - 9680
Joan C. Marini is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Osteogenesis imperfecta & Type I collagen. The author has an hindex of 49, co-authored 162 publications receiving 8762 citations. Previous affiliations of Joan C. Marini include Johns Hopkins University School of Medicine & Johns Hopkins University.
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Journal ArticleDOI
In utero transplantation of adult bone marrow decreases perinatal lethality and rescues the bone phenotype in the knockin murine model for classical, dominant osteogenesis imperfecta
Cristina Panaroni,Roberta Gioia,Anna Lupi,Roberta Besio,Steven A. Goldstein,Jaclynn M. Kreider,Sergey Leikin,Juan Carlos Vera,Edward L. Mertz,Egon Perilli,Fabio Baruffaldi,Isabella Villa,Aurora Farina,M. Casasco,Giuseppe Cetta,Antonio Rossi,Annalisa Frattini,Joan C. Marini,Paolo Vezzoni,Antonella Forlino +19 more
TL;DR: It is suggested that the engrafted cells form bone with higher efficiency than the endogenous cells, supporting IUT as a promising approach for the treatment of genetic bone diseases.
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Structural heterogeneity of type I collagen triple helix and its role in osteogenesis imperfecta.
Elena Makareeva,Edward L. Mertz,Natalia V. Kuznetsova,Mary Beth Sutter,Angela M. DeRidder,Wayne A. Cabral,Aileen M. Barnes,Daniel J. McBride,Joan C. Marini,Sergey Leikin +9 more
TL;DR: Two large, flexible regions deduced from the ΔTm map aligned with the regions important for collagen fibril assembly and ligand binding, and one of these regions also aligned with a lethal region for Gly substitutions in the α1(I) chain.
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Near‐infrared fluorescent probe traces bisphosphonate delivery and retention in vivo
TL;DR: Findings support a role for FRFP as an effective in vivo marker for bisphosphonate site‐specific deposition, turnover, and long‐term retention in the skeleton.
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Cellular mechanism of decreased bone in Brtl mouse model of OI: imbalance of decreased osteoblast function and increased osteoclasts and their precursors.
Thomas E Uveges,Patricia Collin-Osdoby,Wayne A. Cabral,Felicia Ledgard,Leah Goldberg,Clemens Bergwitz,Clemens Bergwitz,Antonella Forlino,Antonella Forlino,Philip Osdoby,Gloria Gronowicz,Joan C. Marini +11 more
TL;DR: It is concluded that osteoblasts and osteoclasts are unsynchronized in Brtl bone, which results in declining BFR as Brtl ages, consistent with reduced femoral geometry.
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Molecular mechanism of alpha 1(I)-osteogenesis imperfecta/Ehlers-Danlos syndrome: unfolding of an N-anchor domain at the N-terminal end of the type I collagen triple helix.
TL;DR: As in Ehlers-Danlos syndrome (EDS) VIIA/B, fibrils containing pN-collagen are thinner and weaker causing EDS-like laxity of large and small joints and paraspinal ligaments, however, distinct structural consequences of N-anchor destabilization result in a distinct alpha1(I)-osteogenesis imperfecta (OI)/EDS phenotype.