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heterozygous mutations in AMN in a family from the United Kingdom with clinical features of Imerslund-Grasbeck Syndrome
Our genetic screening of 154 families of patients with inherited cobalamin malabsorption revealed population-specific mutations, mutational hotspots, and functionally distinct regions in the three causal genes: CUBN (show CUBN Proteins), AMN, and GIF (show GIF Proteins).
amnionless is essential for the correct luminal expression of cubilin (show CUBN Proteins) in humans.
homozygous mutations affecting exons 1-4 of human AMN lead to megaloblastic anemia 1
cubilin (show CUBN Proteins) and amnionless are subunits of a novel cubilin (show CUBN Proteins)/amnionless (cubam) complex
Recurrent spontaneous abortions may be caused by mutations in the Amnionless gene.
This review summarizes recent data on the biological function of amnionless and focuses on its implication in embryonic nutrition and central nervous system malformations.
AMN (show TRAF3 Proteins) may participate in meiosis in early spermatocytes and in functional differentiation of adult Leydig cells through the mediation of vitamin B(12) transport in the mouse testes
Amn (show TRAF3 Proteins) is an essential component of the Cubn (show CUBN Proteins) receptor complex
The protein encoded by this gene is a type I transmembrane protein. It is thought to modulate bone morphogenetic protein (BMP) receptor function by serving as an accessory or coreceptor, and thus facilitates or hinders BMP binding. It is known that the mouse AMN gene is expressed in the extraembryonic visceral endoderm layer during gastrulation, but it is found to be mutated in amnionless mouse. The encoded protein has sequence similarity to short gastrulation (Sog) and procollagen IIA proteins in Drosophila.
, protein amnionless
, visceral endoderm-specific type 1 transmembrane protein
, type I transmembrane protein