| First Author | Lee CS | Year | 2010 |
| Journal | Cell Death Differ | Volume | 17 |
| Issue | 8 | Pages | 1254-65 |
| PubMed ID | 20139895 | Mgi Jnum | J:186368 |
| Mgi Id | MGI:5432090 | Doi | 10.1038/cdd.2010.1 |
| Citation | Lee CS, et al. (2010) TRIM72 negatively regulates myogenesis via targeting insulin receptor substrate-1. Cell Death Differ 17(8):1254-65 |
| abstractText | Lipid rafts have been known to be platforms to initiate cellular signal transduction of insulin-like growth factor (IGF) inducing skeletal muscle differentiation and hypertrophy. Here, tripartite motif 72 (TRIM72), with a really interesting new gene (RING)-finger domain, a B-box, two coiled-coil domains, and a SPRY (SPla and RYanodine receptor) domain, was revealed to be predominantly expressed in the sarcolemma lipid rafts of skeletal and cardiac muscles. Adenoviral TRIM72 overexpression prevented but RNAi-mediated TRIM72 silencing enhanced C2C12 myogenesis by modulating the IGF-induced insulin receptor substrate-1 (IRS-1) activation through the molecular association of TRIM72 with IRS-1. Furthermore, myogenic activity was highly enhanced with increased IGF-induced Akt activation in the satellite cells of TRIM72(-/-) mice, compared to those of TRIM72+/+ mice. Because TRIM72 promoter analysis shows that two proximal E-boxes in TRIM72 promoter were essential for MyoD- and Akt-dependent TRIM72 transcription, we can conclude that TRIM72 is a novel antagonist of IRS-1, and is essential as a negative regulator of IGF-induced muscle differentiation. |
