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

► The first and second SRCR domain of mouse AIM contains N-glycan. ► Depletion of N-glycans decreased mouse AIM secretion from producing cells. ► Depletion of N-glycans enhanced lipolytic activity of mouse AIM. ► Adding a N-glycan increased secretion of human AIM but not its lipolytic activity.