Correction of a mineralization defect by overexpression of a wild-type cDNA for COL1A1 in marrow stromal cells (MSCs) from a patient with osteogenesis imperfecta: a strategy for rescuing mutations that produce dominant-negative protein defects-Reference-Cited by-同舟云学术

Correction of a mineralization defect by overexpression of a wild-type cDNA for COL1A1 in marrow stromal cells (MSCs) from a patient with osteogenesis imperfecta: a strategy for rescuing mutations that produce dominant-negative protein defects

Published:2005-04-07 Issue:14 Volume:12 Page:1119-1125
ISSN:0969-7128
Container-title:Gene Therapy
language:en
Short-container-title:Gene Ther

Author:

Pochampally R R,Horwitz E M,DiGirolamo C M,Stokes D S,Prockop D J

Publisher

Springer Science and Business Media LLC

Subject

Genetics,Molecular Biology,Molecular Medicine

Link

http://www.nature.com/articles/3302514.pdf

Reference24 articles.

1. Kuivaniemi H, Tromp G, Prockop DJ . Mutations in fibrillar collagens (types I, II, III, and XI), fibril-associated collagen (type IX), and network-forming collagen (type X) cause a spectrum of diseases of bone, cartilage, and blood vessels. Hum Mutat 1997; 9: 300–315.

2. Myllyharju J, Kivirikko KI . Collagens and collagen-related diseases. Ann Med 2001; 33: 7–21.

3. Pereira RF et al. Marrow stromal cells as a source of progenitor cells for nonhematopoietic tissues in transgenic mice with a phenotype of osteogenesis imperfecta. Proc Natl Acad Sci USA 1998; 95: 1142–1147.

4. Horwitz EM et al. Clinical responses to bone marrow transplantation in children with severe osteogenesis imperfecta. Blood 2001; 97: 1227–1231.

5. Horwitz EM et al. Transplantability and therapeutic effects of bone marrow-derived mesenchymal cells in children with osteogenesis imperfecta. Nat Med 1999; 5: 309–313.

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