“Mlx”和“Myc”转录因子网络交叉通讯并共享许多共同的基因靶标。 Myc 的活性取决于其与 Max 的异二聚化，而 Mlx 网络要求 Max 样因子 Mlx 与 Myc 样因子 MondoA 或 ChREBP 关联。目前的工作表明，全身范围内的 Mlx 失活（如 Myc 失活）会加速许多与身体习性和新陈代谢有关的衰老相关表型。许多与衰老相关的 Myc 靶基因组的放松管制也在加速。除其他功能外，这些基因组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。 “MycKO”小鼠由于癌症发病率较低而具有较长的寿命，而“MlxKO”小鼠则具有正常的寿命和较高的癌症发病率。与 Myc 一样，Mlx、MondoA 和 ChREBP 的表达及其对靶基因的控制在小鼠和人类中都随着年龄的增长而恶化。总的来说，这些发现强调了两个网络之间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。© 2024 作者。 《Advanced Science》由 Wiley‐VCH GmbH 出版。

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.© 2024 The Author(s). Advanced Science published by Wiley‐VCH GmbH.