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• W1990509225 abstract "The approach of gene-targeted animal models is likely the most important experimental tool contributing to recent advances in skeletal biology. Modifying the expression of a gene in vivo, and the analysis of the consequences of the mutation, are central to the understanding of gene function during development and physiology, and therefore to our understanding of the gene's role in disease states. Researchers had been limited to animal models primarily involving pharmaceutical manipulations and spontaneous mutations. With the advent of gene targeting, however, animal models that impact our understanding of metabolic bone disease have evolved dramatically. Interestingly, some genes that were expected to yield dramatic phenotypes in bone, such as estrogen receptor-α or osteopontin, proved to have subtle phenotypes, whereas other genes, such as interleukin-5 or osteoprotegerin, were initially identified as having a role in bone metabolism via the analysis of their phenotype after gene ablation or overexpression. Particularly important has been the advance in knowledge of osteoblast and osteoclast independent and dependent roles via the selective targeting of genes and the consequent disruption of bone formation, bone resorption, or both. Our understanding of interactions of the skeletal system with other systems, ie, the vascular system and homeostatic controls of adipogenesis, has evolved via animal models such as the matrix gla protein, knock-out, and the targeted overexpression of ΔFos B. Challenging transgenic models such as the osteopontin-deficient mice with mediators of bone remodeling like parathyroid hormone and mechanical stimuli and extending phenotype characterization to mechanistic in vitro studies of primary bone cells is providing additional insight into the mechanisms involved in pathologic states and their potentials for therapeutic strategies. This review segregates characterization of transgenic models based on the category of gene altered, eg, reproductive hormones, calcitropic hormones, growth factors and cytokines, signaling molecules, extracellular matrix molecules and “other” genes. Models are also segregated based on phenotypes that are primarily osteoclastic, osteoblastic or mixed. As the technical ability to alter gene expression negatively or positively and in a tissue-specific and temporal manner continues to evolve, there are endless possibilities for generating genetically altered animal models with which to gain insight into metabolic bone diseases." @default.
• W1990509225 created "2016-06-24" @default.
• W1990509225 creator A5010672369 @default.
• W1990509225 date "2001-07-01" @default.
• W1990509225 modified "2023-10-15" @default.
• W1990509225 title "Transgenic mouse models of metabolic bone disease" @default.
• W1990509225 cites W1491950503 @default.
• W1990509225 cites W1524345526 @default.
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• W1990509225 cites W1534645474 @default.
• W1990509225 cites W1599501164 @default.
• W1990509225 cites W1963690512 @default.
• W1990509225 cites W1964066819 @default.
• W1990509225 cites W1972305384 @default.
• W1990509225 cites W1977830503 @default.
• W1990509225 cites W1993064864 @default.
• W1990509225 cites W1996682859 @default.
• W1990509225 cites W1997812904 @default.
• W1990509225 cites W2000647744 @default.
• W1990509225 cites W2012440354 @default.
• W1990509225 cites W2016411107 @default.
• W1990509225 cites W2016484384 @default.
• W1990509225 cites W2025046506 @default.
• W1990509225 cites W2026207114 @default.
• W1990509225 cites W2029739184 @default.
• W1990509225 cites W2036368043 @default.
• W1990509225 cites W2040542461 @default.
• W1990509225 cites W2041455826 @default.
• W1990509225 cites W2044543197 @default.
• W1990509225 cites W2047727235 @default.
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• W1990509225 cites W2058579856 @default.
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• W1990509225 cites W2059562380 @default.
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• W1990509225 doi "https://doi.org/10.1097/00002281-200107000-00014" @default.
• W1990509225 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11555736" @default.
• W1990509225 hasPublicationYear "2001" @default.
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