CIDEA

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. [provided by RefSeq, Aug 2010]

Cell Death-Inducing DFFA-Like Effector A

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 (By similarity).

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.

Apoptotic process Source: UniProtKB-KW
Cell death Source: BHF-UCL
Cellular response to cold Source: Ensembl
Lipid droplet organization Source: Reactome
Lipid metabolic process Source: BHF-UCL
Lipid storage Source: BHF-UCL
Negative regulation of cold-induced thermogenesis Source: YuBioLab
Negative regulation of cytokine production Source: BHF-UCL
Negative regulation of execution phase of apoptosis Source: BHF-UCL
Negative regulation of lipid catabolic process Source: BHF-UCL
Negative regulation of transforming growth factor beta receptor signaling pathway Source: BHF-UCL
Negative regulation of tumor necrosis factor production Source: BHF-UCL
Positive regulation of sequestering of triglyceride Source: BHF-UCL
Regulation of apoptotic DNA fragmentation Source: BHF-UCL
Regulation of apoptotic process Source: GO_Central
Response to stilbenoid Source: Ensembl
Temperature homeostasis Source: BHF-UCL

Nucleus; Lipid droplet. Enriched at lipid droplet contact sites. Has been shown to localize to mitochondria, where it could interact with UCP1 and hence inhibit UCP1 uncoupling activity (By similarity). These data could not be confirmed (PubMed:18509062).

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.