McKenney Connor D, Regot Sergi
The Biochemistry, Cellular, and Molecular Biology Graduate Program, Johns Hopkins University, Baltimore, MD, USA; Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Oncology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Trends Cell Biol. 2025 Jul;35(7):592-603. doi: 10.1016/j.tcb.2025.04.005. Epub 2025 May 16.
Cells must sense and respond to numerous stimuli to maintain their function. Stress-activated protein kinases (SAPKs) are part of an integrated network that responds to these stimuli and have critical roles in determining cell behavior. Over the past 5 years, ribosomes and the ribotoxic stress response (RSR) have unexpectedly emerged as critical regulators of the SAPK network and drivers of global cell fate changes. In particular, RSR-SAPK signaling has potent effects on cellular proliferation, with important implications for senescence and cancer. In this review, we discuss cell cycle regulation by the SAPK p38, with a particular focus on how ribotoxic stress affects key cell cycle transitions.
细胞必须感知并响应多种刺激以维持其功能。应激激活蛋白激酶（SAPK）是一个综合网络的一部分，该网络对这些刺激作出反应，并在决定细胞行为方面发挥关键作用。在过去5年中，核糖体和核糖体毒性应激反应（RSR）意外地成为SAPK网络的关键调节因子和全球细胞命运变化的驱动因素。特别是，RSR-SAPK信号传导对细胞增殖有强大影响，对衰老和癌症具有重要意义。在本综述中，我们讨论了SAPK p38对细胞周期的调控，特别关注核糖体毒性应激如何影响关键的细胞周期转变。
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