@article{f11985f0533f4eceb280be46438105c3,
title = "Normal long bone growth and development in type X collagen-null mice",
abstract = "To investigate the role of type X collagen in skeletal development, we have generated type X collagen-null mice. Surprisingly, mice without type X collagen were viable and fertile and had no gross abnormalities in long bone growth or development. No differences were detected between the type X collagen-null mice and controls when growth plates of both newborn and 3-week old mice were examined by histology and by immunostaining for extracellular matrix components of bone including osteopontin, osteocalcin and type II collagen. Our results suggest that type X collagen is not required for long bone development. However, mice and humans with dominant acting type X collagen mutations have bone abnormalities, suggesting that only the presence of abnormal type X collagen can modify bone growth and development.",
author = "Rita Rosati and Horan, \{Gerald S.B.\} and Pinero, \{Gerald J.\} and Silvio Garofalo and Keene, \{Douglas R.\} and Horton, \{William A.\} and Eero Vuorio and \{de Crombrugghe\}, Benoit and Behringer, \{Richard R.\}",
note = "Funding Information: To investigate the role of the cartilage-specific expressed a2(XI) chain, we isolated two cosmid clones from a 129sv mouse genomic library that each contain the entire COL11A2 gene. The gene was partially sequenced and two minigene versions constructed that contain an internal deletion in the triplehelical part of the molecule. Transgenic mouse lines have been generated by microinjection of the constructs into fertilized mouse eggs, and are currently being studied for their phenotype. In another line of experiments, a targeting vector for gene knock-out experiments has been assembled and electroporated into mouse embryonic stem cells. The targeting frequency after double selection was found to be 1/15, and these cells are being injected into blastocysts. By performing both dominant negative and gene knock-out experiments we hope to define more precisely the function of this minor collagen in cartilage and the consequences of its mutation. (Supported in part by NIH grants AR39740 and AR38188, and by a grant from the Lucille B. Markey Charitable Trust).",
year = "1994",
month = oct,
doi = "10.1038/ng1094-129",
language = "English (US)",
volume = "8",
pages = "129--135",
journal = "Nature Genetics",
issn = "1061-4036",
publisher = "Nature Research",
number = "2",
}