31 citations
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January 2007 in “Journal of biological chemistry/The Journal of biological chemistry” This study found that c-Jun is essential for vitamin D receptor expression, and the vitamin D receptor inhibits c-Jun-dependent cell death through non-classical mechanisms independent of vitamin D3.
42 citations
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July 2007 in “Journal of Biological Chemistry” This study found that most pathogenic HR mutants associated with atrichia with papular lesions had abolished corepressor activity due to defective interactions with histone deacetylases.
277 citations
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July 2002 in “Molecular Endocrinology” In this study, homozygous VDR null mutant mice exhibited nonfunctional vitamin D receptors, leading to growth abnormalities and revealing the limited physiological importance of vitamin D pathways outside the classical receptor.
148 citations
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May 2008 in “The journal of investigative dermatology/Journal of investigative dermatology” This study found that mice lacking the vitamin D receptor (VDR) developed skin tumors more rapidly than those with normal VDR activity, regardless of 1,25-dihydroxyvitamin D(3) presence.
510 citations
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August 2006 in “Endocrinology” This minireview discusses a proposed model of the vitamin D receptor that explains how 1alpha,25(OH)2D3 can mediate both genomic and rapid responses through different ligand shapes and cellular locations, without presenting new research findings.