Abstract：
The \"Mlx\" and \"Myc\" transcription factor networks cross-communicate and share many common gene targets. Myc\'s activity depends upon its heterodimerization with Max, whereas the Mlx Network requires that the Max-like factor Mlx associate with the Myc-like factors MondoA or ChREBP. The current work demonstrates that body-wide Mlx inactivation, like that of Myc, accelerates numerous aging-related phenotypes pertaining to body habitus and metabolism. The deregulation of numerous aging-related Myc target gene sets is also accelerated. Among other functions, these gene sets often regulate ribosomal and mitochondrial structure and function, genomic stability, and aging. Whereas \"MycKO\" mice have an extended lifespan because of a lower cancer incidence, \"MlxKO\" mice have normal lifespans and a higher cancer incidence. Like Myc, the expression of Mlx, MondoA, and ChREBP and their control over their target genes deteriorate with age in both mice and humans. Collectively, these findings underscore the importance of lifelong and balanced cross-talk between the two networks to maintain proper function and regulation of the many factors that can affect normal aging.
摘要：
“Mlx”和“Myc”转录因子网络交叉交流并共享许多共同的基因靶标。Myc的活性取决于它与Max的异源二聚化，而Mlx网络要求类似Max的因子Mlx与类似Myc的因子MondoA或ChREBP相关联。目前的工作表明，全身Mlx失活，就像Myc一样,加速与身体习性和新陈代谢有关的许多衰老相关表型。许多衰老相关的Myc靶基因集的失调也加速。在其他功能中，这些基因集通常调节核糖体和线粒体的结构和功能，基因组稳定性，和衰老。而“MycKO”小鼠由于较低的癌症发病率而延长了寿命，“MlxKO”小鼠的寿命正常，癌症发病率较高。像Myc一样,Mlx的表达式，MondoA,和ChREBP及其对靶基因的控制随着小鼠和人类的年龄而恶化。总的来说，这些发现强调了两个网络之间的终身和平衡的串扰对于维持正常功能和调节可能影响正常衰老的许多因素的重要性。
