VDR (Vitamin D3 receptor) variants and mutations

VDR (also known as Vitamin D3 receptor) is a human protein-coding gene encoding a vitamin D3 receptor protein. It converts active vitamin D binding into transcriptional programs that regulate calcium and phosphate balance, bone mineralization, and many tissue-specific functions. Biallelic loss-of-function variants cause hereditary vitamin-D-resistant rickets with hypocalcemia, secondary hyperparathyroidism, and impaired bone mineralization. This analysis covers 755 VDR variants and mutations. Of these, 79% have computational variant effect predictions. Disease context includes Hypocalcemic vitamin D-resistant rickets, psoriasis, and chronic kidney disease. Example VDR variants include M1?, M1R, and M1T.

Variant analysis overview

Variant and mutation evidence

Clinical, disease, and population context

Protein structure and variant hotspots

Data sources

Evidence in this analysis draws on EBI Proteins Variation, UniProt, gnomAD v4, EuropePMC, 3D Hotspot Analysis, Interaction Network Analysis, Protein Data Bank, AlphaFold DB, gnomAD constraint, Open Targets, MaveDB, LitVar.

Notable VDR variants

Examples include M1?, M1R, M1T, E2D, E2K, A3E, A3T, M4V. Listed records include available protein-change notation, database identifiers, clinical classifications, computational predictions, population evidence, experimental measurements, and disease context.