WNT signaling in bone homeostasis and disease: from human mutations to treatments

By R. Baron, M. Kneissel. Nature Medicine, 2013

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How researchers see this paper

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Romosozumab in postmenopausal women with low bone mineral density (2014, neutral): “Injection-site reaction† 2 (4) 1 (2) 1 (2) 3 (6) 31 (12)”
The biology of YAP/TAZ: hippo signaling and beyond. (2014, background): “For example, in mesenchymal stem cells, Wnt-induced bone differentiation requires nuclear YAP/TAZ (9), while the role of -catenin remains unclear (11).”
Wnt signaling in development and tissue homeostasis (2018, background): “…multipass transmembrane escort protein GPR177, the vertebrate homolog of Drosophila Wingless/Evi/Sprinter, which mediates endosome trafficking to the plasma membrane and the release of Wnt proteins into the extracellular space (Bänziger et al., 2006; Bartscherer et al., 2006; Goodman et al., 2006).”
Wnt/ b -Catenin Signaling, Disease, and Emerging Therapeutic Modalities (2017, background): “The best-known disorders are mutations in the SOST and LRP6 genes causing sclerosteosis and hereditary osteoporosis (Baron and Kneissel, 2013).”
YAP/TAZ incorporation in the β-catenin destruction complex orchestrates the Wnt response. (2014, background): “for canonical Wnt signaling in bone differentiation, it has been reported that b-catenin deletion fails to recapitulate the phenotype of LRP5mutants, indicating the involvement of factors other than b-catenin downstream of Wnt (Baron and Kneissel, 2013).”