CLCC1 promotes hepatic neutral lipid flux and nuclear pore complex assembly.

A preprint abstract from biorxiv.org discusses the role of CLCC1 in promoting hepatic neutral lipid flux and nuclear pore complex assembly. Imbalances in lipid storage and secretion can lead to the accumulation of lipid droplets in hepatocytes, causing hepatic steatosis. Through CRISPR-Cas9 screens, researchers identified CLCC1 as a critical regulator of neutral lipid storage and secretion. Loss of CLCC1 resulted in the buildup of large lipid droplets in hepatoma cells and liver steatosis in mice. Additionally, CLCC1 was found to be homologous to yeast Brl1p and Brr6p, which are involved in nuclear pore complex assembly. The study suggests that CLCC1-mediated membrane remodeling plays a role in both hepatic neutral lipid flux and nuclear pore complex assembly. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]