Recombinant Human Cell death activator CIDE-A (CIDEA)

Uniprot Id

O60543

Target Species

Human

Target Name

CIDEA

Target Full Name

Lipid transferase CIDEA

Target Function

Acts as a CEBPB coactivator in mammary epithelial cells to control the expression of a subset of CEBPB downstream target genes, including ID2, IGF1, PRLR, SOCS1, SOCS3, XDH, but not casein. By interacting with CEBPB, strengthens the association of CEBPB with the XDH promoter, increases histone acetylation and dissociates HDAC1 from the promoter. Binds to lipid droplets and regulates their enlargement, thereby restricting lipolysis and favoring storage. At focal contact sites between lipid droplets, promotes directional net neutral lipid transfer from the smaller to larger lipid droplets. The transfer direction may be driven by the internal pressure difference between the contacting lipid droplet pair and occurs at a lower rate than that promoted by CIDEC. When overexpressed, induces apoptosis. The physiological significance of its role in apoptosis is unclear.

Target Involvement

In omental and subcutaneous adipose tissue of obese patients matched for BMI, expression levels correlate with insulin sensitivity. Expression is increased 5-6 fold in the group of patients with high insulin sensitivity, compared to the insulin-resistant group. This observation is consistent with the idea that triglyceride storage in adipocytes plays an important role in sequestering triglycerides and fatty acids away from the circulation and peripheral tissues, thus enhancing insulin sensitivity in liver and muscle.

Target Subcellular Location

Lipid droplet. Nucleus.

Target Tissue Specificity

Expressed in omental and subcutaneous adipose tissue (at protein level).

Target Synonyms

CIDEACell death activator CIDE-A; Cell death-inducing DFFA-like effector A

Target Background

This gene encodes the homolog of the mouse protein Cidea that has been shown to activate apoptosis. This activation of apoptosis is inhibited by the DNA fragmentation factor DFF45 but not by caspase inhibitors. Mice that lack functional Cidea have higher metabolic rates, higher lipolysis in brown adipose tissue and higher core body temperatures when subjected to cold. These mice are also resistant to diet-induced obesity and diabetes. This suggests that in mice this gene product plays a role in thermogenesis and lipolysis. Alternatively spliced transcripts have been identified.