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homeostasis. Upon binding of 1\u03b1,25-dihydroxyvitamin D\n                    <jats:sub>3<\/jats:sub>\n                    to the VDR, the activation function 2 (AF2) domain repositions and recruits coactivators for the assembly of the transcriptional machinery required for gene transcription. In contrast to coactivator-induced transcriptional activation, the functional effects of coactivator-independent VDR signaling remain unclear. In humans, mutations in the AF2 domain are associated with hereditary vitamin D-resistant rickets, a genetic disorder characterized by impaired bone mineralization and growth. In the present study, we used mice with a systemic or conditional deletion of the VDR-AF2 domain (\n                    <jats:italic>Vdr<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u0394AF2<\/jats:italic>\n                    <\/jats:sup>\n                    ) to study coactivator-independent VDR signaling. We confirm that ligand-induced transcriptional activation was disabled because the mutant VDR\n                    <jats:sup>\u0394AF2<\/jats:sup>\n                    protein was unable to interact with coactivators. Systemic\n                    <jats:italic>Vdr<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u0394AF2<\/jats:italic>\n                    <\/jats:sup>\n                    mice developed short, undermineralized bones with dysmorphic growth plates, a bone phenotype that was more pronounced than that of systemic\n                    <jats:italic>Vdr<\/jats:italic>\n                    knockout (\n                    <jats:italic>Vdr<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    ) mice. Interestingly, a rescue diet that is high in calcium, phosphate, and lactose, normalized this phenotype in\n                    <jats:italic>Vdr<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    , but not in\n                    <jats:italic>Vdr<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u0394AF2<\/jats:italic>\n                    <\/jats:sup>\n                    mice. However, osteoblast- and osteoclast-specific\n                    <jats:italic>Vdr<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u0394AF2<\/jats:italic>\n                    <\/jats:sup>\n                    mice did not recapitulate this bone phenotype indicating coactivator-independent VDR effects are more important in other organs. In addition, RNA-sequencing analysis of duodenum and kidney revealed a decreased expression of VDR target genes in systemic\n                    <jats:italic>Vdr<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u0394AF2<\/jats:italic>\n                    <\/jats:sup>\n                    mice, which was not observed in\n                    <jats:italic>Vdr<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    mice. These genes could provide new insights in the compensatory (re)absorption of minerals that are crucial for bone homeostasis. In summary, coactivator-independent VDR effects contribute to mineral and bone homeostasis.\n                  <\/jats:p>","DOI":"10.1038\/s41413-024-00343-7","type":"journal-article","created":{"date-parts":[[2024,8,20]],"date-time":"2024-08-20T01:02:03Z","timestamp":1724115723000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Coactivator-independent vitamin D receptor signaling causes severe rickets in mice, that is not prevented by a diet high in calcium, phosphate, and lactose"],"prefix":"10.1038","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8096-9310","authenticated-orcid":false,"given":"Stefanie","family":"Doms","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lieve","family":"Verlinden","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iris","family":"Janssens","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justine","family":"Vanhevel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roy","family":"Eerlings","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ren\u00e9","family":"Houtman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shigeaki","family":"Kato","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chantal","family":"Mathieu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brigitte","family":"Decallonne","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8324-4462","authenticated-orcid":false,"given":"Geert","family":"Carmeliet","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annemieke","family":"Verstuyf","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,8,20]]},"reference":[{"key":"343_CR1","doi-asserted-by":"publisher","first-page":"45","DOI":"10.1007\/s11154-011-9198-9","volume":"13","author":"JW Pike","year":"2012","unstructured":"Pike, J. 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