{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T09:34:12Z","timestamp":1779183252114,"version":"3.51.4"},"reference-count":54,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2014,8,4]],"date-time":"2014-08-04T00:00:00Z","timestamp":1407110400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"NIH\/NIAMS","award":["R01-AR055913"],"award-info":[{"award-number":["R01-AR055913"]}]},{"name":"NIH\/NIAMS","award":["P30-AR057235"],"award-info":[{"award-number":["P30-AR057235"]}]},{"name":"Washington University Musculoskeletal Research Center"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,2,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n               <jats:sec>\n                  <jats:title>\u2003<\/jats:title>\n                  <jats:p>Interaction between parathyroid hormone\/parathyroid hormone\u2013related peptide receptor 1 (PTHR1) and low-density lipoprotein receptor\u2013related protein 6 (Lrp6) is important for parathyroid hormone (PTH) signaling and anabolic action. Because N-cadherin has been shown to negatively regulate canonical Wnt\/\u03b2-catenin signaling, we asked whether N-cadherin alters PTH signaling and stimulation of bone formation. Ablation of the N-cadherin gene (Cdh2) in primary osteogenic lineage cells resulted in increased Lrp6\/PTHR1 interaction in response to PTH1-34, associated with enhanced PTH-induced PKA signaling and PKA-dependent \u03b2-catenin C-terminus phosphorylation, which promotes \u03b2-catenin transcriptional activity. \u03b2-catenin C-terminus phosphorylation was abolished by Lrp6 knockdown. Accordingly, PTH1-34 stimulation of Tcf\/Lef target genes, Lef1 and Axin2, was also significantly enhanced in Cdh2-deficient cells. This enhanced responsiveness to PTH extends to the osteo-anabolic effect of PTH, as mice with a conditional Cdh2 deletion in Osx+ cells treated with intermittent doses of PTH1-34 exhibited significantly larger gains in trabecular bone mass relative to control mice, the result of accentuated osteoblast activity. Therefore, N-cadherin modulates Lrp6\/PTHR1 interaction, restraining the intensity of PTH-induced \u03b2-catenin signaling, and ultimately influencing bone formation in response to intermittent PTH administration. \u00a9 2014 American Society for Bone and Mineral Research.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1002\/jbmr.2323","type":"journal-article","created":{"date-parts":[[2014,8,4]],"date-time":"2014-08-04T08:41:22Z","timestamp":1407141682000},"page":"274-285","source":"Crossref","is-referenced-by-count":41,"title":["N-cadherin Restrains PTH Activation of Lrp6\/\u03b2-catenin Signaling and Osteoanabolic Action"],"prefix":"10.1093","volume":"30","author":[{"given":"Leila","family":"Revollo","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Division of Bone and Mineral DiseaseWashington University School of MedicineSt. 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