Targeted Deletion of the Sclerostin Gene in Mice Results in Increased Bone Formation and Bone Strength
By Xiaodong Li, M. Ominsky, Qing‐Tian Niu, Ning Sun, B. Daugherty, Diane M. D’Agostin, C. Kurahara, Yongming Gao, Jin Cao, Jianhua Gong and 12 more. Journal of Bone and Mineral Research, 2008
956 citations recorded by the source corpus.
Subfields: Genetics, Orthopedics and Sports Medicine, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/2a86be6156bc5c6332a55bfda137111368d25052
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In Genetics
In Orthopedics and Sports Medicine
Citations in the corpus
- Romosozumab in postmenopausal women with low bone mineral density (2014, neutral): “Serious adverse event 7 (14) 4 (8) 5 (9) 5 (10) 17 (7)”
- Single‐dose, placebo‐controlled, randomized study of AMG 785, a sclerostin monoclonal antibody (2011, background): “Similar to the human SOSTmutation phenotype, SOST knockout mice have high bone mass and bone strength as a result of increased bone formation.((19)) Rats treated with a sclerostin antibody not only experience complete reversal of estrogen deficiency–induced bone loss atmultiple skeletal sites but al”
- The Amazing Osteocyte (2010, background): “Mutations of SOST causes high bone mass in humans,((46)) as does deletion in mice.((47))”
- Sclerostin Antibody Treatment Increases Bone Formation, Bone Mass, and Bone Strength in a Rat Model of Postmenopausal Osteoporosis (2009, background): “rosteosis, and in SOST knockout mice, results in increased bone formation and high bone mass.((3,4,11)) What is not clear from these genetic deficiencies is the extent to which sclerostin might regulate bone formation and bone mass in”
- Sclerostin Mediates Bone Response to Mechanical Unloading Through Antagonizing Wnt/β‐Catenin Signaling (2009, background): “2C), as reported in the other Sost-null mice.((14))”