Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST).

By W. Balemans, M. Ebeling, Neela M. Patel, E. Hul, P. Olson, M. Dioszegi, C. Lacza, W. Wuyts, J. Ende, P. Willems and 11 more. Human Molecular Genetics, 2001

1,145 citations recorded by the source corpus.

Subfields: Molecular Biology, Nutrition and Dietetics, Oncology

View Paper: https://www.semanticscholar.org/paper/aaf823e7ea73d8ce721b9e009d64134614ff5598

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In Molecular Biology

1. Christof Niehrs
2. Fanxin Long
3. L. Bonewald
4. Xi He
5. Cristina Cruciat
6. D. Ornitz
7. S. Manolagas
8. Mark L. Johnson

In Oncology

1. L. Bonewald
2. S. Manolagas
3. Mark L. Johnson
4. Fanxin Long
5. E. Eriksen
6. D. Lacey
7. W. S. Simonet
8. P. Kostenuik

Citations in the corpus

• Osteoblast-Osteoclast Interactions (2017, background): “Sclerostin is a protein that is encoded by the SOST gene in humans (52).”
• LDL receptor-related proteins 5 and 6 in Wnt/β-catenin signaling: Arrows point the way (2004, background): “Intriguingly, SOST is most related to WISE (38% identical; see Fig.”
• The Amazing Osteocyte (2010, background): “Mutations of SOST causes high bone mass in humans,((46)) as does deletion in mice.”
• Romosozumab in postmenopausal women with low bone mineral density (2014, neutral): “Injection-site reaction† 2 (4) 1 (2) 1 (2) 3 (6) 31 (12)”
• Single‐dose, placebo‐controlled, randomized study of AMG 785, a sclerostin monoclonal antibody (2011, background): “Individuals who are homozygous for null mutations in SOST, the gene that encodes sclerostin, have sclerosteosis.((8,9)) This syndrome is characterized by progressive bone thickening that results in significant increases in bone mass and bone mineral density (BMD) throughout the skeleton.”
• SOST is a target gene for PTH in bone. (2005, neutral): “This is consistent with reported SOST expression in kidney and cells of the bone-forming lineage [31,47].”
• Osteocytes, mechanosensing and Wnt signaling. (2008, background): “Mutations in Sost and Dkk-1 in humans and/or mice have been shown to result in increased bone mass (10)(9)(111)(84) consistent with a role of the Wnt/βcatenin signaling pathway in bone mass regulation.”
• Development of the endochondral skeleton. (2013, background): “…bone formation, loss-of-function or loss-of-expression mutations in Sost, which are expected to enhance LRP5 signaling, result in the bone-thickening diseases known as sclerosteosis or van Buchem disease, respectively (Balemans et al. 2001, 2002; Brunkow et al. 2001; Staehling-Hampton et al. 2002).”