Tmem182-KO Mouse

TMEM182, a transmembrane protein, is notably expressed in muscle and adipose tissues. It plays crucial roles in cell differentiation, metabolism, and signaling pathways. In myogenesis, it may be involved in pathways related to cell adhesion and muscle formation. Genetic models, like knockout mice, have been valuable in studying its functions [1,3,4].

In TMEM182-knockout mice, significant increases in body weight, muscle mass, muscle fibre number, and diameter were observed, and skeletal muscle regeneration was accelerated. This indicates that TMEM182 is a negative regulator of myogenic differentiation and muscle regeneration, possibly through its interaction with integrin beta 1 (ITGB1) [1]. In human induced pluripotent stem cells (hiPSCs), overexpressing TMEM182 inhibits their differentiation into cardiomyocytes by maintaining the activated state of Wnt/β-catenin signaling through increased ILK expression [2]. In fat metabolism, TMEM182 overexpression promotes fat deposition, as seen by increased expression of fat-synthesis-related genes and preadipocyte differentiation, while its knockout in mice reduces abdominal fat deposition [3].

In conclusion, TMEM182 serves as a key regulator in myogenic differentiation, muscle regeneration, myocardial differentiation, and fat deposition. Studies using KO mouse models have provided insights into its role in these biological processes, suggesting its potential as a target for treating obesity-related diseases, muscle disorders, and for applications in animal breeding [1,2,3].

References:

1. Luo, Wen, Lin, Zetong, Chen, Jiahui, Nie, Qinghua, Zhang, Xiquan. 2021. TMEM182 interacts with integrin beta 1 and regulates myoblast differentiation and muscle regeneration. In Journal of cachexia, sarcopenia and muscle, 12, 1704-1723. doi:10.1002/jcsm.12767. https://pubmed.ncbi.nlm.nih.gov/34427057/

2. Morihara, Hirofumi, Yokoe, Shunichi, Wakabayashi, Shigeo, Takai, Shinji. 2024. TMEM182 inhibits myocardial differentiation of human iPS cells by maintaining the activated state of Wnt/β-catenin signaling through an increase in ILK expression. In FASEB bioAdvances, 6, 565-579. doi:10.1096/fba.2024-00086. https://pubmed.ncbi.nlm.nih.gov/39512841/

3. Chen, Genghua, Lin, Zetong, Peng, Haoqi, Nie, Qinghua, Luo, Wen. 2024. The transmembrane protein TMEM182 promotes fat deposition and alters metabolomics and lipidomics. In International journal of biological macromolecules, 259, 129144. doi:10.1016/j.ijbiomac.2023.129144. https://pubmed.ncbi.nlm.nih.gov/38181918/

4. Wu, Yu, Smas, Cynthia M. 2008. Expression and regulation of transcript for the novel transmembrane protein Tmem182 in the adipocyte and muscle lineage. In BMC research notes, 1, 85. doi:10.1186/1756-0500-1-85. https://pubmed.ncbi.nlm.nih.gov/18803820/