PMID: 23236605

 

    Legend: Sugar

Title : Modification of N-glycosylation modulates the secretion and lipolytic function of apoptosis inhibitor of macrophage ( AIM )

Abstract :

1. The mouse macrophage-derived apoptosis inhibitor of macrophage ( AIM ), which is incorporated into adipocytes and induces lipolysis by suppressing fatty acid synthase ( FAS ) activity, possesses three potential N-glycosylation sites
2. Inactivation of N-glycosylation sites revealed that mouse AIM contains two N-glycans in the first and second scavenger receptor cysteine-rich domains , and that depletion of N-glycans decreased AIM secretion from producing cells
3. Interestingly, the lack of N-glycans increased AIM lipolytic activity through enhancing AIM incorporation into adipocytes
4. Although human AIM contains no N-glycan , attachment of N-glycans increased AIM secretion
5. Thus, the N-glycosylation plays important roles in the secretion and lipolytic function of AIM