Human vitamin K epoxide reductase (VKOR) has a four transmembrane domain topology that supports the use of a homology model, enabling identification of active site residues and human variant impact.

Embryonic lethality associated with deficiency of UBIAD1, which synthesizes a vitamin K₂ subtype, results from aberrant ER-associated degradation of the cholesterol biosynthetic enzyme HMG CoA reductase.

The inhibition of sterol-accelerated degradation of HMG CoA reductase by the vitamin K2 synthetic enzyme UBIAD1 may contribute to the accumulation of cholesterol that is associated with Schnyder corneal dystrophy.

The dietary vitamin riboflavin provides the chemical backbone to generate essential substrates that support liver glucose metabolism during low-nutrient conditions.

UBIAD1 mediates a unique geranylgeranyl pyrophosphate-sensing mechanism that when disrupted, inhibits degradation of HMG CoA reductase and triggers overproduction of corneal cholesterol that characterizes the eye disease Schnyder Corneal Dystrophy.

A membrane protein complex in the endoplasmic reticulum is a key factor for the biogenesis of multi-pass transmembrane proteins, including Rh1, and its loss causes retinal degeneration.

Active uptake and metabolism of maternal vitamin D by the placenta determine fetal exposure to vitamin D and how vitamin D regulates the placental transcriptome, which is also determined by its underlying epigenetic landscape, and proteome.

Gut macrophages produce complement component C1q, which modulates neurogenic activity of gut peristalsis and is thus a key regulator of gastrointestinal motility.

A peptide motif targeting tumor-infiltrating macrophage in triple-negative breast cancer delays tumor growth and favors an antitumor immune response.

The human gut bacterial lipoprotein BtuG binds vitamin B12 with femtomolar affinity, can remove vitamin B12 from human intrinsic factor, and is required for commensal fitness in the gut.