Vitamin D Receptor in Normal and Hormone-Resistant Cells

Feldman, David

Abstract

Funding Agency

• Agency: National Institute of Health (NIH)
• Institute: National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
• Type: Research Project (R01)
• Project #: 5R01DK041246-03
• Application #: 3241900
• Study Section: General Medicine B Study Section (GMB)
• Project Start: 1989-12-15
• Project End: 1993-11-30
• Budget Start: 1992-02-01
• Budget End: 1993-11-30
• Support Year: 3
• Fiscal Year: 1992

Institution

• Name: Stanford University
• Type: Schools of Medicine
• DUNS #: 800771545
• City: Stanford
• State: CA
• Country: United States
• Zip Code: 94305

Publications

Lin, N U; Malloy, P J; Sakati, N et al. (1996) A novel mutation in the deoxyribonucleic acid-binding domain of the vitamin D receptor causes hereditary 1,25-dihydroxyvitamin D-resistant rickets. J Clin Endocrinol Metab 81:2564-9

Madani, N D; Malloy, P J; Rodriguez-Pombo, P et al. (1994) Candida albicans estrogen-binding protein gene encodes an oxidoreductase that is inhibited by estradiol. Proc Natl Acad Sci U S A 91:922-6

Malloy, P J; Weisman, Y; Feldman, D (1994) Hereditary 1 alpha,25-dihydroxyvitamin D-resistant rickets resulting from a mutation in the vitamin D receptor deoxyribonucleic acid-binding domain. J Clin Endocrinol Metab 78:313-6

Krishnan, A V; Feldman, D (1991) Stimulation of 1,25-dihydroxyvitamin D3 receptor gene expression in cultured cells by serum and growth factors. J Bone Miner Res 6:1099-107

Krishnan, A V; Feldman, D (1991) Activation of protein kinase-C inhibits vitamin D receptor gene expression. Mol Endocrinol 5:605-12