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

Article ID	Journal	Published Year	Pages	File Type
10871365	FEBS Letters	2012	6 Pages	PDF

Abstract

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

Keywords

IBMX SRCR Fsp27 Fatty acid synthase (FAS)TLR CD36 FAS qPCR DEX IL-6 N-Glycan quantitative RT-PCR fatty acid synthase isobutylmethylxanthine interleukin-6 Toll-like receptor Dexamethasone Lipolysis AIM fat-specific protein 27 Scavenger receptor cysteine-rich