Amnionless protein (AMN)

Amnionless protein (AMN) is a type I transmembrane protein that acts as a coreceptor within the Cubam receptor complex, partnering with the peripheral membrane protein cubilin. This receptor is critical for the endocytic uptake of vitamin B12 in the intestinal tract and for reabsorption of proteins (such as albumin) from the kidney filtrate. AMN provides structural anchoring and helps with the trafficking and surface expression of cubilin, and it is also implicated in modulating bone morphogenetic protein (BMP) receptor activity as an accessory protein. Mutations in the AMN gene cause Imerslund–Gräsbeck syndrome, a rare autosomal recessive disorder resulting in vitamin B12 deficiency and renal protein loss. No drugs currently target AMN directly; interventions typically address downstream consequences such as vitamin B12 deficiency. AMN's primary function is essential for nutrient absorption and normal kidney protein handling, and its loss of function leads directly to disease.

Other names

Amnion associated transmembrane proteinProtein amnionlessSoluble protein amnionlessAMNUNQ513/PRO1028amnionlessIGS2PRO1028amnionless homologvisceral endoderm-specific type 1 transmembrane protein

Not applicable (no direct targeted drugs). Therapeutic approaches focus on replacing vitamin B12 due to receptor defect.