CIDEB

Description

The CIDEB (cell death inducing DFFA like effector b) is a protein-coding gene located on chromosome 14.

CIDEB is a human gene. Individuals with rare loss-of-function mutations in CIDEB are protected against various liver diseases. CIDEB knockout mice exhibit decreased lipogenesis and are resistant to high-fat diet-induced obesity and liver steatosis. These mice also show improved insulin sensitivity and enhanced hepatic fatty acid oxidation and whole body metabolism. CIDEB plays a critical role in determining lipid droplet size; its overexpression leads to fat accumulation by inducing larger lipid droplets, while CIDEB knockout results in smaller lipid droplets.

CIDEB is a lipid transferase specifically expressed in hepatocytes, where it promotes unilocular lipid droplet formation by mediating lipid droplet fusion. This fusion process leads to the enlargement of lipid droplets, restricting lipolysis and favoring lipid storage. CIDEB localizes on the lipid droplet surface at focal contact sites between droplets and mediates atypical lipid droplet fusion by promoting directional net neutral lipid transfer from smaller to larger droplets. The transfer direction may be driven by the internal pressure difference between the contacting droplet pairs. CIDEB promotes lipid exchange and lipid droplet fusion in both small and large lipid droplet-containing hepatocytes. In addition to its role in lipid droplet fusion, CIDEB is also involved in cytoplasmic vesicle biogenesis and transport. It is required for very-low-density lipoprotein (VLDL) lipidation and maturation. CIDEB is likely involved in the biogenesis of VLDL transport vesicles by forming a COPII vesicle coat and facilitating the formation of endoplasmic reticulum-derived large vesicles. It is also involved in the sterol-regulated export of the SCAP-SREBP complex, composed of SCAP, SREBF1/SREBP1, and SREBF2/SREBP2, by promoting loading of SCAP-SREBP into COPII vesicles. CIDEB may also activate apoptosis.

CIDEB is also known as -.

Associated Diseases

WES Whole Exome Sequencing