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Inhibition of ADP-ribosylation Suppresses Aberrant Accumulation of Lipidated Apolipoprotein B in the Endoplasmic Reticulum

Yuki Ohsaki, Jinglei Cheng, Kazushi Yamairi, Xiaoyue Pan, M Mahmood Hussain, Toyoshi Fujimoto

FEBS Lett. 2013 Nov 15;587(22):3696-702.

PMID: 24100140

Abstract:

ApoB-crescent, an endoplasmic reticulum (ER)-lipid droplet amalgamation structure, is a useful marker to indicate aberrant lipidated apolipoprotein B accumulation in the hepatocyte ER. Blockade of the ER-to-Golgi transport by either vesicle transport inhibitors or dominant-negative Arf1 caused a significant increase in ApoB-crescents. However, a low concentration of Brefeldin A induced the same result without affecting protein secretion, suggesting ADP-ribosylation as an additional mechanism. ADP-ribosylation inhibitors not only suppressed the increase of ApoB-crescents, but also rapidly dissolved existing ApoB-crescents. These results implicate the involvement of ADP-ribosylation in the ApoB-crescent formation and maintenance process at the ER.

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