Mouse models of abnormal skeletal development and homeostasis.
Studies of a number of mouse mutations with skeletal defects have contributed significantly to the understanding of bone development and homeostasis. In many cases, such mutants are also genetic models of disorders in humans, characterized by reduced bone mass (osteoporosis), increased bone mass (osteopetrosis), or abnormalities in endochondral ossification (chondrodysplasias).
McLean
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Dept of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA.
Olsen
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BR
D000818:Animals; D001846:Bone Development / Q000235:genetics*; D001848:Bone Diseases, Developmental / Q000209:etiology / Q000235:genetics*; D004195:Disease Models, Animal; D006706:Homeostasis; D006801:Humans; D051379:Mice; D008817:Mice, Mutant Strains; D010009:Osteochondrodysplasias / Q000235:genetics; D010022:Osteopetrosis / Q000235:genetics; D010024:Osteoporosis / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics
D014157:Transcription Factors