CipC, the CLOCK-interacting protein Circadian, is a negative-feedback regulator of the circadian clock [3]. It has been implicated in various biological processes. In mammals, the circadian clock, consisting of transcriptional/translational feedback loops, regulates physiological and behavioral rhythms, and CipC is part of this regulatory mechanism [2,3].

Specific deletion of Cipc in satellite cells of mdx mice alleviates myopathy, improves muscle function, and reduces fibrosis. Cipc deficiency activates the ERK1/2 and JNK1/2 signaling pathways, which in turn activates the transcription factor SP1 to trigger the transcription of Pax7 and MyoD, promoting muscle regeneration [1]. In contrast, inactivation of Cipc in mice only alters the expression of Per1 but does not affect circadian rhythms, suggesting CipC is not critically required for basic clock function [2]. Overexpressing wild-type CipC in HEK293 cells suppresses cell proliferation and retards the cell cycle, and inhibits PMA-induced Erk activation [4].

In conclusion, CipC has a complex role. It is involved in regulating the circadian clock, though not essential for basic clock function. In muscle, it acts as a negative regulator of satellite cell function. The study of CipC through gene knockout models, especially in the context of muscle-related diseases like in mdx mice, has provided valuable insights into its function and potential as a therapeutic target for muscle disorders.