Circadian clocks dictate various physiological functions by brain SCN (a central clock) -orchestrating the temporal harmony of peripheral clocks of tissues/organs in the whole body, with adaptability to environments by resetting their timings. Dysfunction of this circadian adaptation system (CAS) occasionally causes/exacerbates diseases. CAS is based on cell-autonomous molecular clocks, which oscillate via a core transcriptional/translational feedback loop with clock genes/proteins, e.g., BMAL1: CLOCK circadian transcription driver and CRY1/2 and PER1/2 suppressors, and is modulated by various regulatory loops including clock protein modifications. Among mutants with a single clock gene, BMAL1-deficient mice exhibit the most drastic loss of circadian functions. Here, we highlight on numerous circadian protein modifications of mammalian BMAL1, e.g., multiple phosphorylations, SUMOylation, ubiquitination, acetylation, O-GlcNAcylation and S-nitrosylation, which mutually interplay to control molecular clocks and coordinate physiological functions from the brain to peripheral tissues through the input and output of the clocks.

昼夜节律时钟通过大脑SCN（中央时钟）指示各种生理功能-安排整个组织/器官的外围时钟的时间和谐，并通过重置其时间来适应环境。这种昼夜节律适应系统（CAS）的功能障碍有时会导致/加剧疾病。CAS基于细胞自主的分子时钟，它通过核心转录/翻译反馈环与时钟基因/蛋白质（例如BMAL1：CLOCK昼夜节律转录驱动器以及CRY1 / 2和PER1 / 2抑制剂）一起振荡，并受到各种调控因子的调控。循环，包括时钟蛋白修饰。在具有单个时钟基因的突变体中，缺乏BMAL1的小鼠表现出最大的昼夜节律功能丧失。在这里，我们重点介绍哺乳动物BMAL1的许多生物钟蛋白修饰，例如，