The apolipoprotein D (APOD) gene is transcribed to yield mRNA and the mRNA is translated to yield protein. APOD is an atypical apolipoprotein that belongs to the lipocalin family, and is expressed by a wide variety of cells and tissues (Drayna D et al. 1986). The liver X receptor α (LXRα, NR1H3) and LXRβ (NR1H2) were found to regulate the expression of the APOD gene in cultured cells and in vivo (Hummasti S et al. 2004; Lai C-J et al. 2017). Synthetic LXR agonist treatment of mouse adipocytes (3T3-L1 cells) and human umbilical vein endothelial cells (HUVECs) resulted in increased mRNA and protein levels of APOD (Hummasti S et al. 2004; Lai C-J et al. 2017). An LXR response element (LXRE) was identified in the human APOD gene promoter, and binding of LXRα (NR1H3):RXRa heterodimers was demonstrated by electrophoretic mobility shift assay (EMSA) and luciferase cell reporter assay (Hummasti S et al. 2004). Mice treated with synthetic LXR agonists exhibited increased APOD mRNA levels in adipose tissue, skeletal muscle and cerebellum, but not liver (Hummasti S et al. 2004; Repa JJ et al. 2007). In humans, APOD is found in the plamsa, associated with high-density lipoprotein (HDL), and polymorphisms have been linked to metabolic disease. APOD has also been suggested to be neuroprotective (Pascua-Maestro R et al 2019).
Chuu, CP, Chen, TH, Lai, CJ, Chang, CH, Wang, HD, Huang, SH, Cheng, HC, Chung, CJ, Lin, CY
Chao, LC, Hummasti, S, Ramamurthy, L, Galardi, C, Tontonoz, P, Moore, JT, Laffitte, BA, Watson, MA
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