Tropomyosin-receptor kinase fused gene (TFG) regulates lipid production in human sebocytes.
So-Ra ChoiYul-Lye HwangSoo Jung KimKyung-Cheol SohnChong Won ChoiKyung Duck ParkYoung LeeYoung-Joon SeoJeung-Hoon LeeSeung-Phil HongSeong Jun SeoSeong Jin KimChang-Deok KimPublished in: Scientific reports (2019)
The endoplasmic reticulum (ER) is an organelle in which important cellular events such as protein synthesis and lipid production occur. Although many lipid molecules are produced in the ER, the effect of ER-organizing proteins on lipid synthesis in sebocytes has not been completely elucidated. Tropomyosin-receptor kinase fused gene (TFG) is located in ER exit sites and participates in COPII-coated vesicle formation along with many scaffold proteins, such as Sec. 13 and Sec. 16. In this study, we investigated the putative role of TFG in lipid production in sebocytes using an immortalized human sebocyte line. During IGF-1-induced lipogenesis, the level of the TFG protein was increased in a time- and dose-dependent manner. When TFG was over-expressed using recombinant adenovirus, lipid production in sebocytes was increased along with an up-regulation of the expression of lipogenic regulators, such as PPAR-γ, SREBP-1 and SCD. Conversely, down-regulation of TFG using a microRNA (miR) decreased lipid production and the expression of lipogenic regulators. Based on these data, TFG is a novel regulator of lipid synthesis in sebocytes.
Keyphrases
- endoplasmic reticulum
- fatty acid
- poor prognosis
- binding protein
- transcription factor
- estrogen receptor
- long non coding rna
- cell proliferation
- machine learning
- skeletal muscle
- insulin resistance
- gene expression
- metabolic syndrome
- genome wide
- oxidative stress
- small molecule
- breast cancer cells
- adipose tissue
- big data
- long noncoding rna
- deep learning
- electronic health record
- atomic force microscopy