{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T17:55:16Z","timestamp":1790790916073,"version":"4.1.0"},"reference-count":39,"publisher":"National Academy of Sciences","issue":"13","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2005,3,29]]},"abstract":"<jats:p>\n                    The vitamin D receptor (VDR) is a nuclear transcription factor responsible for mediating the biological activities of 1,25-dihydroxyvitamin D\n                    <jats:sub>3<\/jats:sub>\n                    [1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D\n                    <jats:sub>3<\/jats:sub>\n                    ]. Renal and parathyroid gland VDR content is an important factor in calcium homeostasis, vitamin D metabolism, and the treatment of secondary hyperparathyroidism and renal osteodystrophy. In these tissues, VDR expression is highly regulated by the calcium and vitamin D status. Although 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D\n                    <jats:sub>3<\/jats:sub>\n                    up-regulates VDR expression, hypocalcemia and vitamin D deficiency result in drastically reduced expression of the receptor. The generation of 25-hydroxyvitamin D\n                    <jats:sub>3<\/jats:sub>\n                    -1\u03b1-hydroxylase-null mice, which are incapable of endogenously producing 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D\n                    <jats:sub>3<\/jats:sub>\n                    , has allowed us to investigate the influence of parathyroid hormone (PTH) on VDR expression independent of PTH-mediated increases in 1,25(OH)\n                    <jats:sub>2<\/jats:sub>\n                    D\n                    <jats:sub>3<\/jats:sub>\n                    . Administration of human PTH (1-34) (110 \u03bcg\/kg per day) for 48 h reduced renal VDR levels from 515 to 435 fmol\/mg protein (15%,\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.03) in wild-type mice. In the 25-hydroxyvitamin D\n                    <jats:sub>3<\/jats:sub>\n                    -1\u03b1-hydroxylase-null mice, PTH administration strongly reduced renal VDR levels, from 555 to 394 fmol\/mg protein (29%,\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.001). These results demonstrate that PTH is a potent down-regulator of VDR expression\n                    <jats:italic>in vivo<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.1073\/pnas.0501312102","type":"journal-article","created":{"date-parts":[[2005,3,15]],"date-time":"2005-03-15T22:28:28Z","timestamp":1110925708000},"page":"4724-4728","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":35,"title":["Parathyroid hormone decreases renal vitamin D receptor expression\n                    <i>in vivo<\/i>"],"prefix":"10.1073","volume":"102","author":[{"given":"Kevin D.","family":"Healy","sequence":"first","affiliation":[{"name":"Department of Biochemistry, University of Wisconsin, Madison, WI 53706"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janeen L.","family":"Vanhooke","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, University of Wisconsin, Madison, WI 53706"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean M.","family":"Prahl","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, University of Wisconsin, Madison, WI 53706"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hector F.","family":"DeLuca","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, University of Wisconsin, Madison, WI 53706"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2005,3,15]]},"reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(18)61172-X"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.69.7.1673"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.95.4.1387"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1753-4887.1998.tb01686.x"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.89.17.8097"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(19)68967-2"},{"key":"e_1_3_2_7_2","first-page":"2103","volume":"44","year":"1984","unstructured":"Dokoh, S., Donaldson, C. 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