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Article

Targeted deletion of <i>Sost</i> distal enhancer increases bone formation and bone mass

10 Aug 2012

Abstract excerpt

The Wnt antagonist Sost has emerged as a key regulator of bone homeostasis through the modulation of Lrp4/5/6 Wnt coreceptors. In humans, lack of Sclerostin causes sclerosteosis and van Buchem (VB) disease, two generalized skeletal hyperostosis disorders that result from hyperactive Wnt signaling. Unlike sclerosteosis, VB patients lack SOST coding mutations but carry a homozygous 52 kb noncoding deletion that is...

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PMID: 22886088
DOI: 10.1073/pnas.1207188109

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Related research

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Research trail→

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Targeted deletion of <i>Sost</i> distal enhancer increases bone formation and bone massPMID 22886088Read ↗

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Osteocyte-Derived Sclerostin Inhibits Bone Formation: Its Role in Bone Morphogenetic Protein and Wnt SignalingSemantic proximity Read ↗

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SOST/sclerostin, an osteocyte-derived negative regulator of bone formationSemantic proximity Read ↗

Sclerostin: Current Knowledge and Future PerspectivesSemantic proximity Read ↗

An Additional Lrp4 High Bone Mass Mutation Mitigates the Sost-Knockout Phenotype in Mice by Increasing Bone Remodeling.Semantic proximity Read ↗

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