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Updated: Feb 6, 2026

Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Loss of circadian protein TIMELESS accelerates the progression of cellular senescence
Xiaomeng Shen1, Mingzhe Li1, Zebin Mao1
1Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, People's Republic of China.
Abstract:
TIMELESS protein is known to be essential for normal circadian rhythms. Aging is a deleterious process which affects all the physiological functions of complex organisms including the circadian rhythms. The circadian aging may produce disorganization among the circadian rhythms, arrhythmicity and even, disconnection from the environment, resulting in a detrimental situation to the organism. However, the role of circadian genes on the aging process is poorly understood. In present study, we found TIMELESS was down-regulated in cellular senescence, and further research indicated E2F1 bound to the promotor of TIMELESS and regulated its expression in cellular senescence. Knockdown of TIMELESS accelerated cellular senescence induced by ectopic expression of RasV12, and overexpression of TIMELESS delayed this kind onset of senescence. Meanwhile, micrococcal nuclease assays proved depletion of TIMELESS exacerbated genomic instability at the onset of senescence. Together, our data reveal that TIMELESS plays a role in OIS, which is associated with genome stability changing.
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